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Sökning: L773:1873 2747 OR L773:0361 9230

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1.
  • Risedal, Anette, et al. (författare)
  • Environmental influences on functional outcome after a cortical infarct in the rat.
  • 2002
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 58:3, s. 315-321
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of postoperative housing conditions on functional outcome and brain-derived neurotrophic factor (BDNF) gene expression was evaluated 1 month after a distal ligation of the right middle cerebral artery (MCA) in spontaneously hypertensive rats. Two days postoperatively the rats were randomized into four groups; individually housed with no equipment (deprived group), individually housed with free access to a connected running wheel (running group), housed together in a large cage with no equipment (social group) or in the same size of cage furnished with bars, chains and various things to manipulate (enriched group). The enriched rats had significantly higher scores when crossing a rotating horizontal rod than deprived and running rats. The social group performed significantly better than the deprived group. The BDNF gene expression in the ipsi- and contralateral cortex, thalamus, hippocampus and cerebellum did not significantly differ between the groups. The weight of the adrenal glands was significantly increased in running rats suggesting that postischemic running may be stressful. We conclude that the beneficial effect of postischemic environmental enrichment is likely to be a combination of social and various physical activities, and that BDNF gene expression 1 month after a cortical infarct did not correlate with functional outcome.
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2.
  • Bergenius, J., et al. (författare)
  • The subjective horizontal at different angles of roll-tilt in patients with unilateral vestibular impairment
  • 1996
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 40:5-6, s. 385-390
  • Tidskriftsartikel (refereegranskat)abstract
    • The subjective visual horizontal is mainly dependent on the otolithic system. A group of 11 patients with sudden unilateral vestibular impairment were asked to set a dimly illuminated bar according to their subjective horizontal when they were seated upright and tilted 10, 20, and 30 degrees to the right and left in a completely darkened room (Bias test). The patients were examined within 1 week, after 3 and 6 weeks, and 9 patients consented to the 11-week follow-up. The results were compared with ENG examinations. In the acute stage of the disease all patients, when they were in upright position, set the light bar tilted towards the affected side. At roll tilt to the affected side, 9 of the 11 patients set the light bar in the same direction as their body tilt (undercorrection). At a tilt to the unaffected side 6 of the 11 patients made an undercorrection. For the group of patients the magnitude of undercorrection was larger at tilt to the affected side than to the unaffected side. The patients' ability to correctly align the light bar with the true horizontal gradually improved but was found normal in both upright and tilted positions in only three of the nine patients at the last follow-up. In four of the six patients who still demonstrated pathologic results, these were met only in tilted positions. No significant correlation was found between the intensity of spontaneous nystagmus or the degree of caloric side difference and the deviation in setting of the light bar in upright or tilted positions. The large asymmetric perceptual responses at tilt found at onset might be explained by the two-directional organisation of the utricle.
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3.
  • Johansson, Pia, et al. (författare)
  • The effect on opioid peptides in the rat brain, after chronic treatment with the anabolic androgenic steroid, nandrolone decanoate
  • 2000
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 51:5, s. 413-418
  • Tidskriftsartikel (refereegranskat)abstract
    • In recent years, an increase in abuse of anabolic androgenic steroids (AAS) has been seen among individuals not directly connected to sports. Clinical evidence suggests that abuse of these steroids may result in profound changes in personality, expressed by depressive symptoms, irritability and increased aggression. It is still unknown whether these alterations are related to changes in any particular transmitter system or whether they are persistent or reversible. In this study we focused on AAS effect on the endogenous dynorphin and enkephalin system in the brain. Male rats were given intramuscular injections of the AAS nandrolone decanoate (15 mg/kg), once daily for 2 weeks. The levels of the opioid peptide immunoreactivities (ir) were assessed by radioimmunoassay in two groups immediately after the treatment and in two other groups after additional 3 weeks without any drug treatment (recovery period). The result indicates that chronic AAS treatment increased the activity in the dynorphin B- and Met-enkephalin-Arg6Phe7-ir in the hypothalamus, striatum and periaqueductal gray (PAG) compared to controls. In addition, the steroid induced an imbalance between the dynorphin and the enkephalin opioid system in the nucleus accumbens, hypothalamus and PAG. This imbalance remained after the recovery period. Since increased peptide activity was found in brain regions regulating emotions, dependence, defensive reactions and aggression, it was suggested that the actual endogenous opioid systems are involved in previously reported AAS-induced changes in these behaviours.
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4.
  • LaForge, K. Steven, et al. (författare)
  • “Binge” cocaine differentially alters preproenkephalin mRNA levels in guinea pig brain
  • 2003
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 59:5, s. 353-357
  • Tidskriftsartikel (refereegranskat)abstract
    • Male Hartley guinea pigs were administered i.p. injections of cocaine or saline for 2 or 7 days in a "binge" paradigm. RNA was isolated from dissected brain regions and levels of preproenkephalin mRNA and total RNA were quantified by RNase protection assays. Following 2 days of "binge" cocaine administration, no significant alterations in preproenkephalin mRNA levels were detected in six brain regions. Following 7 days of cocaine administration, however, lower levels of preproenkephalin mRNA were observed in the nucleus accumbens and hypothalamus of cocaine-treated animals and higher levels in the frontal cortex and amygdala. These findings differed from previous studies in the rat, so an additional experiment was performed with animals treated at the 7 day time point. For increased statistical power, data from the two experiments were combined and examined by two-way ANOVAs; in this combined analysis, increases in preproenkephalin mRNA were observed in frontal cortex, amygdala, and hippocampus, decreases were found in the nucleus accumbens and hypothalamus, with no change in thalamus, caudate putamen, or cerebellum. These observed differences between guinea pigs and rats make this species an interesting model for neurobiological studies of cocaine-induced alterations in neuropeptide gene expression in the mammalian brain.
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5.
  • Lundh, Dan (författare)
  • A kinetic model on calcium residues and facilitation
  • 1998
  • Ingår i: Brain Research Bulletin. - : Elsevier. - 0361-9230 .- 1873-2747. ; 45:6, s. 589-597
  • Tidskriftsartikel (refereegranskat)abstract
    • The role of calcium as a regulator for neuronal function is very important. Calcium initiates many reactions that determine the behavior of the neuronal cell. In this article we use a kinetic model of the presynaptic synapsin I protein. This protein is responsible, via phosphorylation, for regulating the amount of transmitter vesicles available for release. This protein has been shown to inhibit the amount of vesicles ready for release in its dephosphorylated state, and releases its inhibitory binding due to phosphorylation. The phosphorylation of synapsin I depends on cyclic adenosine monophosphate and type II calcium/calmodulin protein kinase. Due to the duration of these two second messengers, we show that short-term facilitation does not have to depend on calcium residues. Furthermore, we show that calcium residues (in parts of μM range) promote increased facilitation due to the additional calcium reacting with the second messenger system.
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6.
  • Ploj, Karolina, et al. (författare)
  • Basal levels and alcohol-induced changes in nociceptin/orphanin FQ, dynorphin, and enkephalin levels in C57BL/6J mice
  • 2000
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 53:2, s. 219-226
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to investigate the involvement of the opioid and nociceptin/orphanin FQ (N/OFQ) system in alcohol drinking behaviour, N/OFQ and the opioid peptides dynorphin B (DYNB) and Met-enkephalin-Arg(6) Phe(7) (MEAP) were examined in the alcohol-preferring C57BL/6J mice. Basal peptide levels were compared in the brain and the pituitary gland with basal levels in the alcohol-avoiding DBA/2J mice. Furthermore, the effects of chronic alcohol self-administration on peptides were studied in the C57BL/6J mice. Compared to the DBA/2J mice, C57BL/6J mice had low immunoreactive (ir) levels of DYNB and MEAP in the nucleus accumbens, the hippocampus, and the substantia nigra, low ir-DYNB levels in the striatum and low ir-MEAP levels in the frontal cortex. Higher ir-DYNB levels in the pituitary gland and in the periaqueductal gray (PAG) and higher ir-N/OFQ levels in the frontal cortex and in the hippocampus were detected in C57BL/6J mice compared to the DBA/2J mice. After 4 weeks of voluntary alcohol consumption, only minor changes in steady-state peptide levels were identified. However, 5 days after the alcohol-drinking period, lower levels of all peptides were detected in the ventral tegmental area and ir-DYNB levels were also lower in the amygdala and in the substantia nigra. Twenty-one days after cessation of alcohol self-administration, the opioid peptides in alcohol-consuming C57BL/6J mice were lower in the PAG, the N/OFQ was lower in the frontal cortex and DYNB was higher in the amygdala and substantia nigra as compared to control C57BL/6J mice. This study demonstrates strain differences between C57BL/6J mice and DBA/2J mice that could contribute to divergent drug-taking behaviour, and it also demonstrates time- and structure-specific changes in neuropeptide levels after alcohol self-administration in the C57BL/6J mice.
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7.
  • Ploj, Karolina, et al. (författare)
  • Effects of melanocortin receptor ligands on ethanol intake and opioid peptide levels in alcohol-preferring AA rats
  • 2002
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 59:2, s. 97-104
  • Tidskriftsartikel (refereegranskat)abstract
    • Melanocortin (MC) peptides are suggested to play a role in opiate dependence, where they antagonise the addictive properties of opiates. To further study the involvement of the MCs in drug dependence, we analysed the effects of the MC(4)-receptor antagonist HS014 (1 nmol/rat), and the non-selective MC-receptor agonist MTII (1 nmol/rat), using i.c.v. administration, on ethanol intake in alcohol-preferring AA rats. The rats had access to ethanol during 40 days, resulting in a mean ethanol intake of 6.6 g/kg/day, before treatment. One group received only artificial cerebrospinal fluid solution. MTII caused a reduction in ethanol intake and ethanol preference, whereas HS014 was without effect. No effect on water intake was observed. A decrease in food intake was detected after MTII, whereas HS014 induced an increase in food intake. Analysis of dynorphin B and Met-enkephalin-Arg(6)Phe(7) immunoreactive levels revealed that MTII and HS014 altered opioid peptide levels in several brain areas and the pituitary gland of the rats with an established ethanol intake. This is the first report showing that manipulation of the MC-receptor system changes ethanol intake in chronically ethanol-drinking AA rats. In addition, manipulation of the MC system modulates ethanol-induced changes in opioid peptide levels.
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8.
  • Tribukait, Arne, et al. (författare)
  • The subjective visual horizontal for different body tilts in the roll plane : characterization of normal subjects
  • 1996
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 40:5-6, s. 375-383
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to establish a method for estimation of the perceptual horizontal as a test of otolith function in diagnosis of atypical vertigo, in a first study we have standardized a test procedure and characterized a body of normal material consisting of 72 healthy subjects, 24 of them examined with tests followed by retests. The perceptual visual horizontal in darkness was estimated in the upright body position and at body tilts of 10, 20, and 30 degrees to the right and to the left by means of a narrow luminous bar. The deviation of the perceptual horizontal relative to the gravitational horizontal is expressed as a function of body tilt. In the upright body position, 95% had a perceptual horizontal within the range of +/- 2.5 degrees. In the tilted positions, there was a tendency to set the light bar tilted oppositely with respect to the body tilt. The results suggest that roll tilt to the right and to the left is sensed by two independent functional units. Furthermore, the results imply that some other factor might be of importance and that the perceptual horizontal in the upright position and tilt perception are complementary in reflecting vestibular function. Differences between individuals were great in comparison with intraindividual variability and the test-retest variability. The results are discussed against the background of the extensive literature.
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9.
  • Aylward, E H, et al. (författare)
  • Caudate volume as an outcome measure in clinical trials for Huntington's disease : a pilot study.
  • 2003
  • Ingår i: Brain Research Bulletin. - 0361-9230 .- 1873-2747. ; 62:2, s. 137-41
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous research has demonstrated that longitudinal change in caudate volume could be observed over a period of 3 years in subjects with Huntington's disease (HD). The current pilot study was designed to determine whether measurement of caudate change on magnetic resonance imaging (MRI) is a feasible and valid outcome measure in an actual clinical trial situation. We measured caudate volumes on pre- and post-treatment MRI scans from 19 patients at two sites who were participating in CARE-HD (Co-enzyme Q10 and Remacemide: Evaluation in Huntington's Disease), a 30-month clinical trial of remacemide and co-enzyme Q(10) in symptomatic patients with HD. Results from this pilot study indicated that decrease in caudate volume was significant over time. Power analysis indicated that relatively small numbers of subjects would be needed in clinical trials using caudate volume as an outcome measure. Advantages and disadvantages of using MRI caudate volume as an outcome measure are presented. We recommend the adoption of quantitative neuroimaging of caudate volume as an outcome measure in future clinical trials for treatments of HD.
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10.
  • Binnewies, Julia, et al. (författare)
  • Lifestyle-related risk factors and their cumulative associations with hippocampal and total grey matter volume across the adult lifespan : a pooled analysis in the European Lifebrain consortium
  • 2023
  • Ingår i: Brain Research Bulletin. - : Elsevier. - 0361-9230 .- 1873-2747. ; 200
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Lifestyle-related risk factors, such as obesity, physical inactivity, short sleep, smoking and alcohol use, have been associated with low hippocampal and total grey matter volumes (GMV). However, these risk factors have mostly been assessed as separate factors, leaving it unknown if variance explained by these factors is overlapping or additive. We investigated associations of five lifestyle-related factors separately and cumulatively with hippocampal and total GMV, pooled across eight European cohorts.Methods: We included 3838 participants aged 18–90 years from eight cohorts of the European Lifebrain consortium. Using individual person data, we performed cross-sectional meta-analyses on associations of presence of lifestyle-related risk factors separately (overweight/obesity, physical inactivity, short sleep, smoking, high alcohol use) as well as a cumulative unhealthy lifestyle score (counting the number of present lifestyle-related risk factors) with FreeSurfer-derived hippocampal volume and total GMV. Lifestyle-related risk factors were defined according to public health guidelines.Results: High alcohol use was associated with lower hippocampal volume (r = −0.10, p = 0.021), and overweight/obesity with lower total GMV (r = −0.09, p = 0.001). Other lifestyle-related risk factors were not significantly associated with hippocampal volume or GMV. The cumulative unhealthy lifestyle score was negatively associated with total GMV (r = −0.08, p = 0.001), but not hippocampal volume (r = −0.01, p = 0.625).Conclusions: This large pooled study confirmed the negative association of some lifestyle-related risk factors with hippocampal volume and GMV, although with small effect sizes. Lifestyle factors should not be seen in isolation as there is evidence that having multiple unhealthy lifestyle factors is associated with a linear reduction in overall brain volume.
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11.
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12.
  • Christophersen, Nicolaj, et al. (författare)
  • Induction of dopaminergic neurons from growth factor expanded neural stem/progenitor cell cultures derived from human first trimester forebrain.
  • 2006
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 70:4-6, s. 457-466
  • Tidskriftsartikel (refereegranskat)abstract
    • Multipotent stem/progenitor cells derived from human first trimester forebrain can be expanded as free-floating aggregates, so called neurospheres. These cells can differentiate into neurons, astrocytes and oligodendrocytes. In vitro differentiation protocols normally yield γ-aminobutyric acid-immunoreactive neurons, whereas only few tyrosine hydroxylase (TH) expressing neurons are found. The present report describes conditions under which 4–10% of the cells in the culture become TH immunoreactive (ir) neurons within 24 h. Factors including acidic fibroblast growth factor (aFGF) in combination with agents that increase intracellular cyclic AMP and activate protein kinase C, in addition to a substrate that promotes neuronal differentiation appear critical for efficient TH induction. The cells remain THir after trypsinization and replating, even when their subsequent culturing takes place in the absence of inducing factors. Consistent with a dopaminergic phenotype, mRNAs encoding aromatic acid decarboxylase, but not dopamine-β-hydroxylase were detected by quantitative real time RT-PCR. Ten weeks after the cells had been grafted into the striatum of adult rats with unilateral nigrostriatal lesions, only very few of the surviving human neurons expressed TH. Our data suggest that a significant proportion of expandable human neural progenitors can differentiate into TH-expressing cells in vitro and that they could be useful for drug and gene discovery. Additional experiments, however, are required to improve the survival and phenotypic stability of these cells before they can be considered useful for cell replacement therapy in Parkinson's disease.
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13.
  • Edin, Benoni B, et al. (författare)
  • Bio-inspired sensorization of a biomechatronic robot hand for the grasp-and-lift task.
  • 2008
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 75:6, s. 785-95
  • Tidskriftsartikel (refereegranskat)abstract
    • It has been concluded from numerous neurophysiological studies that humans rely on detecting discrete mechanical events that occur when grasping, lifting and replacing an object, i.e., during a prototypical manipulation task. Such events represent transitions between phases of the evolving manipulation task such as object contact, lift-off, etc., and appear to provide critical information required for the sequential control of the task as well as for corrections and parameterization of the task. We have sensorized a biomechatronic anthropomorphic hand with the goal to detect such mechanical transients. The developed sensors were designed to specifically provide the information about task-relevant discrete events rather than to mimic their biological counterparts. To accomplish this we have developed (1) a contact sensor that can be applied to the surface of the robotic fingers and that show a sensitivity to indentation and a spatial resolution comparable to that of the human glabrous skin, and (2) a sensitive low-noise three-axial force sensor that was embedded in the robotic fingertips and showed a frequency response covering the range observed in biological tactile sensors. We describe the design and fabrication of these sensors, their sensory properties and show representative recordings from the sensors during grasp-and-lift tasks. We show how the combined use of the two sensors is able to provide information about crucial mechanical events during such tasks. We discuss the importance of the sensorized hand as a test bed for low-level grasp controllers and for the development of functional sensory feedback from prosthetic devices.
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14.
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15.
  • Grönbladh, Alfhild, et al. (författare)
  • The neurobiology and addiction potential of anabolic androgenic steroids and the effects of growth hormone
  • 2016
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 126, s. 127-137
  • Forskningsöversikt (refereegranskat)abstract
    • Anabolic androgenic steroids (AAS) are substances that mimic the hormone testosterone, and primarily act via the androgen receptor. In addition to their physiological effect on muscle tissue and growth, research from the last decade has shown that AAS have a pronounced impact on the central nervous system. A large number of studies have demonstrated that AAS affect the mesolimbic reward system in the brain. However, whether the direct effects of AAS on endorphins, dopamine, serotonin and GABA etc. and on the corresponding and related systems lead to dependence needs to be further elucidated. According to recent studies, the prevalence of AAS dependence among AAS users has been estimated to be approximately 30%, and polysubstance use, of both pharmaceutical drugs and narcotics, within this group is common. The present review primarily discusses AAS in the context of addiction and dependence, and further addresses the issue of using multiple substances, i.e. stimulants and opiates in combination with AAS. In addition, aspects of the treatment of AAS dependence, the connection between AAS abuse and cognition, and AAS-induced neurotoxicity are presented. Currently, performance enhancing drugs are frequently used in combination with AAS. Therefore, a large section on growth hormone and insulin-like growth factor is also included.
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16.
  • Hirata, Rafael Y. S., et al. (författare)
  • Platinum nanoparticle-based microreactors protect against the behavioral and neurobiological consequences of chronic stress exposure
  • 2022
  • Ingår i: Brain Research Bulletin. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0361-9230 .- 1873-2747. ; 190
  • Tidskriftsartikel (refereegranskat)abstract
    • Excitotoxicity is described as the exacerbated activation of glutamate AMPA and NMDA receptors that leads to neuronal damage, and ultimately to cell death. Astrocytes are responsible for the clearance of 80-90% of syn-aptically released glutamate, preventing excitotoxicity. Chronic stress renders neurons vulnerable to excitotox-icity and has been associated to neuropsychiatric disorders, i.e., anxiety. Microreactors containing platinum nanoparticles (Pt-NP) and glutamate dehydrogenase have shown in vitro activity against excitotoxicity. The purpose of the present study was to investigate the in vivo effects of these microreactors on the behavioral and neurobiological effects of chronic stress exposure. Rats were either unstressed or exposed for 2 weeks to an unpredictable chronic mild stress paradigm (UCMS), administered intra-ventral hippocampus with the micro -reactors (with or without the blockage of astrocyte functioning), and seven days later tested in the elevated T -maze (ETM; Experiment 1). The ETM allows the measurement of two defensive responses, avoidance and escape, in terms of psychopathology respectively related to generalized anxiety and panic disorder. Locomotor activity in an open field was also measured. Since previous evidence shows that stress inhibits adult neurogenesis, we evaluated the effects of the different treatments on the number of cells expressing the marker of migrating neuroblasts doublecortin (DCX) in the dorsal and ventral hippocampus (Experiment 2). Results showed that UCMS induces anxiogenic effects, increases locomotion, and decreases the number of DCX cells in the dorsal and ventral hippocampus, effects that were counteracted by microreactor administration. This is the first study to demonstrate the in vivo efficacy of Pt-NP against the behavioral and neurobiological effects of chronic stress exposure.
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17.
  • Holmgren, Simon, et al. (författare)
  • Neuropsychiatric symptoms in dementia : a role for neuroinflammation?
  • 2014
  • Ingår i: Brain Research Bulletin. - : Elsevier. - 0361-9230 .- 1873-2747. ; 108, s. 88-93
  • Tidskriftsartikel (refereegranskat)abstract
    • Dementia is characterized by a progressive cognitive decline and neuropsychiatric symptoms (NPSD) such as agitation, apathy and sleeping problems. There is some evidence of activation of inflammatory pathways in the brain in dementia, but little research has been performed regarding the role of neuroinflammation in NPSD, which might represent a potential novel target for treatment. The aim of this study was to examine the possible association between NPSD and cerebrospinal fluid (CSF) levels of the cytokines IL-6, TNF-α and IL-10, and the cytokine receptor sIL-1RII, in patients with dementia and NPSD. Ninety-four patients (mean age 79±8; 67% female) with a score on the neuropsychiatric inventory (NPI) ≥10 points, were included. Clinical assessment included administration of NPI, the mini-mental state examination (MMSE) and the Cohen-Mansfield agitation inventory (CMAI). The cytokine levels in CSF samples were analysed by enzyme-linked immunosorbent assay. Correlations were statistically examined using Spearman's rank correlation coefficient (r), and simple- and multiple-linear regression. The anti-inflammatory cytokine IL-10 showed reverse correlations with total NPI score (NPI-total=-0.001, t(90)= 8.50, p=0.004) and NPI sub-items agitation (agitation=-0.007, t(90)=7.02, p=0.009) and night-time behaviour (night time behaviour=-0.006, t(90)=6.34, p=0.01). There was a trend towards reverse correlation between IL-10 and depression (depression=-0.004, t(90)=2.96, p=0.09). Also, the soluble cytokine receptor sIL-1RII showed a trend towards correlation with apathy (apathy=0.82, t(82)=3.62, p=0.06). The levels of IL-6 showed no significant correlations with NPSD. Levels of TNF-α were non-detectable. In Alzheimer's disease (AD) subjects (n=33), IL-6 showed reverse correlation with anxiety (r=-0.35, p=0.049). In mixed AD subjects (n=26), IL-10 showed reverse correlations with the total NPI score (r=-0.46, p=0.02) and depression (r=-0.45, p=0.02). The findings indicate a relationship between neuroinflammation and neuropsychiatric symptoms in AD in which anti-inflammatory signalling by IL-10 is beneficial from a mental health perspective.
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18.
  • Johansson, Jenny, 1980-, et al. (författare)
  • Application of in vitro [(35)S]GTPγ-S autoradiography in studies of growth hormone effects on opioid receptors in the male rat brain
  • 2013
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 90, s. 100-106
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic treatment with opiates may inhibit cell growth and trigger apoptosis. On the contrary, growth hormone (GH) has been demonstrated to stimulate neurogenesis and counteract apoptosis. We recently demonstrated that recombinant human GH (rhGH) may reverse opiate-induced apoptosis in cells derived from prenatal mouse hippocampus. Thus, GH might be able to prevent the impaired cognitive capabilities that may occur in both humans and other mammals in connection to chronic opiate treatment. In order to explore the mechanism by which GH exerts its beneficial effects we here examined the impact of GH treatment on the levels of delta and mu opioid peptide (DOP and MOP, respectively) receptors in the male rat brain. The rats were treated with rhGH (Genotropin(®)) at two different doses (0.07 and 0.7IU/kg), twice daily, during 7 days. Following decapitation, the levels of DOP and MOP receptor functionality were determined using [(35)S]GTPγS autoradiography. The results demonstrate that rhGH affects the levels of the MOP receptor functionality in certain areas of the brain. These alterations were seen in e.g. amygdala and thalamus, i.e. regions that recently have been implicated in learning and memory. The activity level of DOP receptors was not affected. Thus, the data support that the beneficial effect of GH on counteracting apoptosis might involve a direct or indirect effect on the MOP but not the DOP receptor.
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19.
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20.
  • LaForge, K. Steven, et al. (författare)
  • Primary structure of guinea pig preprodynorphin and preproenkephalin mRNAs : multiple transcription initiation sites for preprodynorphin
  • 2004
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 63:2, s. 119-126
  • Tidskriftsartikel (refereegranskat)abstract
    • Preprodynorphin and preproenkephalin are protein precursors from which are derived two classes of opioid neurotransmitter peptides. Dynorphin A((1-17)) is produced by proteolytic processing of prodynorphin, and processing of proenkephalin yields the enkephalin peptides. We report here on the isolation and sequencing of multiple clones for these two mRNAs from a cDNA library. Two cDNA clones of preprodynorphin contained the full-length sequence (2.35 kb) with the primary structure predicted from the guinea pig gene sequence. In contrast, one clone encoded the full-length sequence but also an additional 192 nt at the 5' end. This sequence has high homology to the 5' flanking region of the human preprodynorphin gene, and RNase protection assays demonstrated that in addition to a primary initiation site, transcription of this mRNA is initiated at several sites 160-190 nt 5' with respect to the primary site. This difference may alter translational efficiency or mRNA stability. The sequence of preproenkephalin cDNA clones confirmed the structure predicted from the gene sequence. One clone, however, contained sequences encoded by exons 2 and 3, and initiated within the first intron (intron A) of the gene. We used RNase protection mapping to assess the abundance in the brain and pituitary of preproenkephalin transcripts that initiate within intron A. These studies confirmed that the primary transcription start site is 28 nucleotides downstream from the TATAA site, and that intron A sequences are not present in significant amounts in these tissues.
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21.
  • Le Grevès, Madeleine, et al. (författare)
  • Age-related effects of IGF-1 on the NMDA-, GH- and IGF-1 receptor mRNA transcripts in the rat hippocampus
  • 2005
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 65:5, s. 369-374
  • Tidskriftsartikel (refereegranskat)abstract
    • Insulin-like growth factor-1 (IGF-1) and growth hormone (GH) have been suggested to promote memory and cognitive capabilities. In a recent publication we observed that GH increase the proportion of the NR2B subunit mRNA transcript of the NMDA receptor in rat hippocampus. NR2B has been suggested to be essential for spatial learning and long-term potentiation (LTP). This effect of GH might be IGF-1-mediated or a result of a co-ordination with IGF-1. To test this hypothesis further, we examined the effects of 10 daily s.c. injections of IGF-1 on NMDA receptor subunits (NR1, NR2A, and NR2B), GH receptor (GHR), GH binding protein (GHBP) and type 1 IGF receptor (IGF-1R) gene transcripts in the hippocampus. The NR2B subunit mRNA increased in young (11 weeks) but not in older (14-16 months) rats and the expression of the NR2A mRNA was decreased in both groups. The ratio of NR2B to NR2A is suggested to mirror the potential for synaptic plasticity. In both age groups, IGF-1 treatment resulted in a significant increase of this ratio at transcription level. The GHR mRNA increased in young rats, mimicking the effect of GH, while the IGF-1R mRNA was decreased in the older group of rats after IGF-1 treatment. These results suggest that IGF-1 in many aspects may mediate the actions earlier shown for GH.
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22.
  • Lönngren, Ulrika, et al. (författare)
  • The growth factor response in ischemic rat retina and superior colliculus after brimonidine pre-treatment
  • 2006
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 71:1-3, s. 208-218
  • Tidskriftsartikel (refereegranskat)abstract
    • The α-2-adrenergic receptor agonist brimonidine has been shown to increase survival of retinal ganglion cells following ischemic injury to the rat retina. Increased expression of growth factors has been suggested to be involved in this action. We investigated expressional changes of growth factors and their receptors following transient retinal ischemia induced by selective ligature of ophthalmic vessels in rats pre-treated with vehicle or 0.5% brimonidine. In addition, analysis of expression in retinal samples following unilateral administration of brimonidine to normal tissue was performed. Tissue samples of retina and superior colliculus were collected at time points between 6 h and 14 days of retinal reperfusion. Analysis of mRNA levels of the ligands BDNF, NT3, CNTF, FGF1, FGF2, FGF9 and HGF; as well as the receptors TrkB, TrkC, p75NTR, CNTFRα, FGFR1, FGFR3, FGFR4 and HGFR were performed using qRT-PCR. The cell specific markers Thy1 and GFAP were analysed. We report transiently increased retinal levels of BDNF, NT3, p75NTR, FGFR1 and HGFR and decreased levels of FGF9, HGF, TrkB, TrkC, FGFR4 and Thy1 following ischemia. The decreases were counteracted by brimonidine. Brimonidine treatment gave an increase in BDNF, NT3 and CNTF levels compared to the vehicle treated group. In superior colliculus increased levels of growth factor mRNA were found. In conclusion, transient ischemia has a profound effect on gene expression in rat retina. Alterations can also be seen in the superior colliculus but are smaller. Brimonidine pre-treatment attenuates an acute injury-induced response by decreasing the expression of several genes, among them p75NTR. Brimonidine also causes a prolonged increase of several growth factors as well as receptors in retina and superior colliculus compared to the ischemic situation. The increased expression of several growth factors represents a coordinated growth factor system response that differs from the ischemia-induced changes and is likely part of the neuroprotective activity that is elicited by BMD pre-treatment.
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23.
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24.
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25.
  • McGrath, Aleksandra M, et al. (författare)
  • BD™ PuraMatrix™ peptide hydrogel seeded with Schwann cells for peripheral nerve regeneration
  • 2010
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 83:5, s. 207-213
  • Tidskriftsartikel (refereegranskat)abstract
    • This study investigated the effects of a membrane conduit filled with a synthetic matrix BD™ PuraMatrix™ peptide (BD) hydrogel and cultured Schwann cells on regeneration after peripheral nerve injury in adult rats. After sciatic axotomy, a 10mm gap between the nerve stumps was bridged using ultrafiltration membrane conduits filled with BD hydrogel or BD hydrogel containing Schwann cells. In control experiments, the nerve defect was bridged using either membrane conduits with alginate/fibronectin hydrogel or autologous nerve graft. Axonal regeneration within the conduit was assessed at 3 weeks and regeneration of spinal motoneurons and recovery of muscle weight evaluated at 16 weeks postoperatively. Schwann cells survived in the BD hydrogel both in culture and after transplantation into the nerve defect. Regenerating axons grew significantly longer distances within the conduits filled with BD hydrogel when compared with the alginate/fibronectin hydrogel and alginate/fibronectin with Schwann cells. Addition of Schwann cells to the BD hydrogel considerably increased regeneration distance with axons crossing the injury gap and entering into the distal nerve stump. The conduits with BD hydrogel showed a linear alignment of nerve fibers and Schwann cells. The number of regenerating motoneurons and recovery of the weight of the gastrocnemius muscle was inferior in BD hydrogel and alginate/fibronectin groups compared with nerve grafting. Addition of Schwann cells did not improve regeneration of motoneurons or muscle recovery. The present results suggest that BD hydrogel with Schwann cells could be used within biosynthetic conduits to increase the rate of axonal regeneration across a nerve defect.
  •  
26.
  • Nobel, Gerard, 1964-, et al. (författare)
  • Histaminergic and cholinergic neuron systems in the impairment of human thermoregulation during motion sickness
  • 2010
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 82:3-4, s. 193-200
  • Tidskriftsartikel (refereegranskat)abstract
    • Motion sickness (MS) exaggerates body cooling during cold-water immersion. The aim of the present study was to investigate whether such MS-induced predisposition to hypothermia is influenced by two anti-MS drugs: the histamine-receptor blocker dimenhydrinate (DMH) and the muscarine-receptor blocker scopolamine (Scop). Nine healthy male subjects were immersed in 15 degrees C water for a maximum of 90 min in five conditions: (1) control (CN): no medication, no MS provocation; (2) MS-control (MS-CN): no medication, MS provocation; (3) MS-placebo (MS-P): placebo DMH and placebo Scop, MS provocation; (4) MS-DMH: DMH and placebo Scop, MS provocation; (5) MS-Scop: Scop and placebo DMH, MS provocation. MS was induced by use of a rotating chair. Throughout the experiments rectal temperature (T-re), the difference in temperature between the non-immersed right forearm and third finger (T-ff) as an index of peripheral vasoconstriction, and oxygen uptake (VO2) as a measure of shivering thermogenesis, were recorded. DMH and Scop were similarly efficacious in ameliorating nausea. The fall in T-re was greater in the MS-CN and MS-P conditions than in the CN condition. DMH, but not Scop, prevented the MS-induced increase in body-core cooling. MS attenuated the cold-induced vasoconstriction, an effect which was fully prevented by DMH but only partially by Scop. MS provocation did not affect VO2 in any condition. The results suggest that the MS-induced predisposition to hypothermia is predominantly mediated by histaminergic mechanisms and that DMH might be useful in conjunction with maritime accidents or other scenarios where exposure to cold and MS are imminent features.
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27.
  • Norgren, Niklas, et al. (författare)
  • Cerebrospinal fluid levels of neurofilament light in chronic experimental autoimmune encephalomyelitis
  • 2005
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 67:4, s. 264-268
  • Tidskriftsartikel (refereegranskat)abstract
    • Experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) is a chronic relapsing-remitting animal model of multiple sclerosis (MS). Neurofilament light (NF-L), a structural protein expressed in neuronal cells can be used to quantify the amount of neuronal damage in MS patients. An immunoassay was used to measure levels of neurofilament light in cerebrospinal fluid (CSF) in rats with myelin oligodendrocyte glycoprotein-induced EAE. Significantly increased levels of neurofilament were found in the immunized animals compared to the controls, strengthening the similarities in the diseases and the progression pattern between the animal model and MS. The turnover of NF-L during this disease is increased since significantly elevated levels also were identified in the spinal cord of the diseased animals and immunohistochemistry gave support for this observation. Monitoring neurofilament levels in EAE can be used to follow disease progression and effects of therapy.
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28.
  • Nylander, Erik, 1986-, et al. (författare)
  • The effects of morphine, methadone, and fentanyl on mitochondria : A live cell imaging study
  • 2021
  • Ingår i: Brain Research Bulletin. - : Elsevier. - 0361-9230 .- 1873-2747. ; 171, s. 126-134
  • Tidskriftsartikel (refereegranskat)abstract
    • The important role of mitochondria in maintaining normal brain cell function has been demonstrated in several neurodegenerative diseases where mitochondrial dysfunction is a prominent feature. Accumulating evidence indicates that opioids may induce neuronal cell death and inhibit neurogenesis, two factors that are dependent on normal mitochondrial function. The aim of the present study was to examine the effects of morphine, methadone, and fentanyl on mitochondrial morphology. Cells from the neuroblastoma/glioma hybrid cell-line NG108-15 were seeded on 96-well cell culture plates and treated with MitoTracker™ for 30 min prior to opioid treatment. Morphine, methadone, and fentanyl were added at various concentrations and images of mitochondria were acquired every 30 min for four hours using a high-content imaging device. The morphological parameters total mitochondrial area, mitochondrial network, number of mitochondrial objects, and the mean area of mitochondrial objects were analyzed using automated image analysis. Methadone and fentanyl, but not morphine, decreased the mitochondrial network, the number of mitochondrial objects, and increased the mean area of mitochondrial objects. Both methadone and fentanyl altered mitochondrial morphology with no effects seen from morphine treatment. These data suggest that methadone and fentanyl disrupt mitochondrial morphology, which may contribute to neuronal cell death.
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29.
  • Pettersson, Jonas, 1979-, et al. (författare)
  • Labeling of olfactory ensheathing glial cells with fluorescent tracers for neurotransplantation
  • 2010
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 81:1, s. 125-132
  • Tidskriftsartikel (refereegranskat)abstract
    • Development of cell-based treatment strategies for repair of the injured nervous system requires cell tracing techniques to follow the fate of transplanted cells and their interaction with the host tissue. The present study investigates the efficacy of fluorescent cell tracers Fast Blue, PKH26, DiO and CMFDA for long-term labeling of olfactory ensheathing glial cells (OEC) in culture and following transplantation into the rat spinal cord. All tested dyes produced very efficient initial labeling of p75-positive OEC in culture. The number of Fast Blue-positive cells remained largely unchanged during the first 4 weeks but only about 21% of the cells retained tracer 6 weeks after labeling. In contrast, the number of cells labeled with PKH26 and DiO was reduced to 51-55% after 2 weeks in culture and reached 8-12% after 4-6 weeks. CMFDA had completely disappeared from the cells 2 weeks after labeling. AlamarBlue assay showed that among four tested tracers only CMFDA reduced proliferation rate of the OEC. After transplantation into spinal cord, Fast Blue-labeled OEC survived for at least 8 weeks but demonstrated very limited migration from the injection sites. Additional immunostaining with glial and neuronal markers revealed signs of dye leakage from the transplanted cells resulted in weak labeling of microglia and spinal neurons. The results show that Fast Blue is an efficient cell marker for cultured OEC. However, transfer of the dye from the transplanted cells to the host tissue should be considered and correctly interpreted.
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30.
  • Porto, Fabio Henrique de Gobbi, et al. (författare)
  • In vivo evidence for neuroplasticity in older adults
  • 2015
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 114, s. 56-61
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuroplasticity can be conceptualized as an intrinsic property of the brain that enables modification of function and structure in response to environmental demands. Neuroplastic strengthening of synapses is believed to serve as a critical mechanism underlying learning, memory, and other cognitive functions. Ex vivo work investigating neuroplasticity has been done on hippocampal slices using high frequency stimulation. However, in vivo neuroplasticity in humans has been difficult to demonstrate. Recently, a long-term potentiation-like phenomenon, a form of neuroplastic change, was identified in young adults by differences in visual evoked potentials (VEPs) that were measured before and after tetanic visual stimulation (TVS). The current study investigated whether neuroplastic changes in the visual pathway can persist in older adults. Seventeen healthy subjects, 65 years and older, were recruited from the community. Subjects had a mean age of 77.4 years, mean education of 17 years, mean MMSE of 29.1, and demonstrated normal performance on neuropsychological tests. 1 Hz checkerboard stimulation, presented randomly to the right or left visual hemi-field, was followed by 2 mm of 9 Hz stimulation (TVS) to one hemi-field. After 2 mm of rest, 1 Hz stimulation was repeated. Temporospatial principal component analysis was used to identify the Nib component of the VEPs, at lateral occipital locations, in response to 1 Hz stimulation pre- and post-TVS. Results showed that the amplitude of factors representing the early and late Nib component was substantially larger after tetanic stimulation. These findings indicate that high frequency visual stimulation can enhance the Nib in cognitively high functioning old adults, suggesting that neuroplastic changes in visual pathways can continue into late life. Future studies are needed to determine the extent to which this marker of neuroplasticity is sustained over a longer period of time, and is influenced by age, cognitive status, and neurodegenerative disease. (C) 2015 Elsevier Inc. All rights reserved.
  •  
31.
  • Tribukait, Arne, et al. (författare)
  • Effects of anti-histaminic and anti-cholinergic substances on human thermoregulation during cold provocation
  • 2010
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 81:1, s. 100-106
  • Tidskriftsartikel (refereegranskat)abstract
    • The roles of histaminergic and cholinergic neuron systems in the regulation of body temperature have been studied almost exclusively in animals. Recently, we have found that motion sickness, i.e. a condition where hippocampal cholinergic mismatch signals induce a release of histamine in the vomiting centre, accelerates the decline in body temperature in men during exposure to cold. In the present study we measured the thermoregulatory effects of two substances commonly used against motion sickness, i.e. the histamine (H1) receptor blocker dimenhydrinate (DMH) and the muscarine receptor blocker scopolamine (SCOP). In three trials, control (CN), DMH and SCOP, 10 male subjects were immersed in 15 degrees C water for a maximum of 90 min. The trials were separated by a minimum of three days and their order was alternated between subjects. In all trials the subject received, in a double blind fashion, a transdermal patch (SCOP or placebo) 12-14 h before immersion and a tablet (DMH or placebo) 1 h before immersion. Mean skin temperature, rectal temperature (T-rec), the difference in temperature between the non-immersed right forearm and 3rd finger of the right hand (T-ff), and oxygen uptake (VO2) were recorded. The fall in T-rec was smaller in the DMH than in the CN and SCOP conditions. The recordings of T-ff and VO2 suggest that SCOP attenuates peripheral vasoconstriction while DMH increases shivering thermogenesis. Notably, thermal discomfort was reduced in the SCOP condition. Findings are thoroughly discussed in the context of animal studies on the neuropharmacology and neurophysiology of thermoregulation and motion sickness.
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32.
  • Wu, Junfang, et al. (författare)
  • Gender differences in the bile acid profiles of APP/PS1 transgenic AD mice
  • 2020
  • Ingår i: Brain Research Bulletin. - : Elsevier. - 0361-9230 .- 1873-2747. ; 161, s. 116-126
  • Tidskriftsartikel (refereegranskat)abstract
    • Alzheimer’s disease (AD) is a neurodegenerative disease and presents in the accumulation of amyloid and neurofibrillary tangle. The association between modulations of gut symbiotic microbes with neurological disease via bidirectional gut-brain axis has been well documented. Bile acid (BA) pools in the enterohepatic circulation could be valuable for probing complex biochemical interactions between host and their symbiotic microbiota. Herein we investigated the levels of 28 BAs in several compartments in enterohepatic circulation (including jejunal, ileum, cecum, colon and feces, plasma and liver tissue) by employing an APP/PS1 induced transgenic AD mouse model. We found that BA profiles in AD mice were gender specific. We observed decreased levels of taurine-conjugated primary BAs (TUDCA, TCA, T-α-MCA and T-β-MCA) and increased levels of secondary BA (iso-DCA) in plasma and liver extracts for female AD transgenic mice. In contrast, increased levels of TDCA in liver extracts and decreased levels of T-β-MCA in jejunal content were noted in male AD mice. These observations suggested that perturbations of BA profiles in AD mice displayed clear gender variations. Our study highlighted the roles of gut microbiota on neurodegenerative disease, which could be gender specific.
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33.
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34.
  • Ågren, Thomas (författare)
  • Human reconsolidation : A reactivation and update
  • 2014
  • Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230 .- 1873-2747. ; 105, s. 70-82
  • Forskningsöversikt (refereegranskat)abstract
    • The reconsolidation hypothesis states that memories, when reactivated, enter a transient, labile state followed by a re-stabilization termed reconsolidation. By affecting the reconsolidation process, memory persistence can be influenced, leading to memory enhancement or decrement. This is a time-dependent process and the result of modulating reconsolidation is present only after the reconsolidation process is completed. Historically, reconsolidation research has been performed on non-human animals, since the methods originally used for reconsolidation disruption are not safe. However, there now exist several techniques safe for humans, and consequently, in recent years, papers on human reconsolidation have emerged. Here, the existing literature on human reconsolidation is reviewed and discussed, including studies on fear memories, appetitive memories, procedural memories, and declarative memories. Methods of memory reactivation are compared between studies, and the consistency and lack of consistency in results over reactivation methods and memory types are discussed. These results provide future challenges, both experimental and clinical, in defining the boundary conditions and mechanisms governing the reconsolidation phenomenon. This article is part of a Special Issue entitled 'Memory Enhancement'. 
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35.
  • Boer, GJ, et al. (författare)
  • Clinical neurotransplantation: Core assessment protocol rather than sham surgery as control
  • 2002
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 58:6, s. 547-553
  • Forskningsöversikt (refereegranskat)abstract
    • Basic neurotransplantation research evoked clinical trials of restorative brain surgery. Parkinson's disease was the first and primary test bed for this putative new therapeutic method. Various centers performed the grafting surgery and the behavioral evaluations in different ways, and observed a varying degree of symptomatic relief. This led to a plea for double blind placebo-controlled clinical trials, which have since been performed and of which the first outcomes were recently published. In the present paper this approach of experimental neurotransplantation in brain diseases is discussed and rejected. Neural grafting in the central nervous system is irreversible and is therefore not suitable for experimental approaches originally designed for and best suited to drug studies. For Parkinson's disease in particular, the technique is far from optimized to perform large-scale studies at this stage. Moreover, previous negative results of adrenal medulla tissue implantation in the brain of patients make placebo effects rather unlikely. Moral arguments concerning the validity of the informed consent, therapeutic misconception, and the risk/benefit ratio can be added in the plea against this control surgery. Finally, a recommendation is made for study designs that apply a disease-dedicated core assessment protocol (CAP) that can evaluate the period from pre-operative to post-convalescent stages quantitatively, and therefore, unbiased. The strength of these CAPs is that they allow comparisons of different grafting techniques, of results between centers and of other types of interventions and invasive treatments such as deep brain stimulation. On ethical grounds, it is unacceptable not to use a study design that circumvents sham or imitation surgery. It is a challenge for the neuroscience community to develop CAPs for brain diseases that are eligible for neurotransplantation in the future. (C) 2002 Elsevier Science Inc. All rights reserved.
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36.
  • Larsson, L C, et al. (författare)
  • Discordant xenografts : different outcome after mouse and rat neural tissue transplantation to guinea-pigs
  • 1999
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 49:5, s. 76-367
  • Tidskriftsartikel (refereegranskat)abstract
    • Embryonic neural tissue obtained from other species has been considered as a donor tissue source in repair strategies for human neurodegenerative disorders. The neuro- and immunobiology of distantly related species combinations, discordant xenografts, need to be characterised. For this purpose, a small animal model would be an important research tool. Adult guinea-pigs, and adult rats as controls, received intrastriatal grafts of either mouse or rat embryonic ventral mesencephalic tissue. The survival rates and types of host immune response were assessed at 2 weeks after grafting using stereological techniques and semi-quantitative evaluations. In the mouse-to-guinea-pig group, all transplants were rejected and no tyrosine hydroxylase-immuno reactive (TH-IR) cells remained. In the rat-to-guinea-pig group, there was good survival of TH-IR cells (5050 SEM+/-1550), similar to that in the rat-to-rat group (4900 SEM+/-1540). In the mouse-to-rat group, half of the animals had no surviving TH-IR cells (520 SEM+/-230 for the whole group). These species combinations offer inexpensive, efficient, and suitable conditions to study important survival factors for discordant xenogeneic neural tissue transplants. The factors responsible for the divergent graft outcomes between the two combinations might provide clues on how to manipulate xenogeneic tissue to increase survival rates in the future.
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37.
  • Petersén, Åsa, et al. (författare)
  • Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death
  • 2001
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 56:3-4, s. 331-335
  • Tidskriftsartikel (refereegranskat)abstract
    • In hereditary Huntington's disease, a triplet repeat disease, there is extensive loss of striatal neurons. It has been shown that brain-derived neurotrophic factor (BDNF) protects striatal neurons against a variety of insults. We confirmed that BDNF enhances survival and DARPP-32 expression in primary striatal cultures derived from postnatal mice. Furthermore, BDNF inhibited intracellular oxyradical stress triggered by dopamine, and partially blocked basal and dopamine-induced apoptosis. Nevertheless, BDNF failed to rescue striatal neurons from dopamine-induced cell death. Therefore, BDNF inhibits free radical and apoptotic pathways in medium spiny neurons, but does so downstream from the point of commitment to cell death.
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38.
  • Sahlin, C, et al. (författare)
  • Changes in contractile response and effect of a calcium antagonist, nimodipine, in isolated intracranial arteries of baboon following experimental subarachnoid hemorrhage
  • 1990
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 24:3, s. 355-361
  • Tidskriftsartikel (refereegranskat)abstract
    • Isolated pial arteries from a previously well-characterized model of experimental subarachnoid hemorrhage (SAH) in baboon were tested for their contractile response to 5-hydroxytryptamine (5-HT), norepinephrine (NE), and prostaglandin F2 alpha (PGF2 alpha) and the effect of the calcium antagonist, nimodipine. Autologous blood was injected cisternally at three times with one-day intervals to a total amount of 11.5-29.5 ml (mean: 18.5 ml), and the animals were killed 7 days after the first injection. Untreated animals served as controls. The degree of maximum contraction (EAm) with 5-HT and NE in the control situation was for the three arteries tested in the order middle cerebral greater than anterior cerebral greater than basilar artery. Experimental SAH markedly increased EAm, by 190-370 percent above control values (depending on type of vessel) for 5-HT and 170-185 percent for NE. In addition, the sensitivity to 5-HT was significantly increased, as evidenced by a left-shift of the concentration-response curve. Previous exposure of the artery to 10(-6) M nimodipine reduced the contractile response of both amines to approximately half, the inhibition being slightly less pronounced post-SAH. When vessels were contracted beforehand with the amines or with PGF2 alpha, followed by administration of increasing amount of nimodipine (10(-9) M to 10(-6) M), a concentration-dependent relaxation was obtained by up to 60 percent of the original level. This relaxing effect was significantly less following SAH in the experiments with NE and PGF2 alpha compared to 5-HT; the contraction in the presence of 5-HT did not differ before and after experimental SAH. The experiments show that SAH markedly enhances the intrinsic activity for both 5-HT and NE. Nimodipine inhibits the contractile response less efficiently following experimental SAH. The difference in the responsiveness to 5-HT on the one hand, and to NE and PGF2 alpha on the other, could be due to differences in the blood-induced alterations of those calcium channels that are influenced by the calcium antagonist, nimodipine.
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39.
  • Tarkowski, E, et al. (författare)
  • Cerebral pattern of pro- and anti-inflammatory cytokines in dementias
  • 2003
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 61:3, s. 255-260
  • Tidskriftsartikel (refereegranskat)abstract
    • The knowledge regarding putative inflammatory component(s) participating in Alzheimer's disease (AD) and vascular dementia (VAD) is scarce. Recently, we have demonstrated the presence of certain inflammatory cytokines in the cerebrospinal fluid (CSF) of demented patients. Although the initial event(s) triggering the neurodegenerative processes in AD versus VAD may be different and lead to different neuropathological changes, it may initiate a similar cascade of cytokine production in response to neuronal injury. The cytokines released in the central nervous system (CNS) may, in turn, act in a similar manner in both diseases, amplifying some pathological changes such as amyloidogenesis and white matter lesions or on the contrary acting as neuroprotective molecules. This review will focus on the intracerebral production of the pro- and anti-inflammatory cytokines interleukin IL-1beta, IL-1 receptor antagonist (IL-1ra), IL-6 and TNF-alpha in dementia, and their relation to gene polymorphism, to cerebral neuronal damage, apoptosis, and to clinical variables of dementia. Our results, which show for the first time strikingly increased CSF levels of TNF-alpha but not of TNF-beta, IL-1beta or IL-6 in AD and VAD, may form a conceptual framework for further studies of neuroprotective mechanisms in dementias. (C) 2003 Elsevier Science Inc. All rights reserved.
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40.
  • Zeng, J, et al. (författare)
  • Are neuronal markers and neocortical graft-host interface influenced by housing conditions in rats with cortical infarct cavity?
  • 1999
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 48:2, s. 165-171
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim was to study if exposure to an enriched environment influenced graft-host interface and neuronal markers in neocortical grafts implanted in cortical infarct cavities 3 weeks after distal ligation of the middle cerebral artery in adult hypertensive rats. Half the rats were exposed to an enriched environment for 2 h daily 5 days a week starting 1 week after the arterial ligation. The brain was fixed by perfusion 4 weeks postgrafting. The immunoreactivity to glial fibrillary acidic protein, microtubule associated protein 2, and synaptophysin was studied in coronal paraffin-embedded sections. A distinct glial border separated the infarct cavity from the surrounding brain in sham-transplanted rats. Most grafts filled the larger part of the infarct cavity. In 8 of 18 transplants, 4 in each experimental group, part of the transplants protruded through the thin glial membrane that delineated the transplant-host interface into the adjacent host brain tissue. Microtubule associated protein 2 immunostained sections indicated bridging of dendrites in the host-transplant interface. Synaptophysin immunoreactivity was significantly higher in grafts than in contralateral cortex. However, graft morphology and neuronal marker immunoreactivity did not differ between rats housed in standard and activity stimulating cages.
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