| 1. |
- Andreasen, N, et al.
(author)
-
Cerebrospinal fluid tau and Abeta42 as predictors of development of Alzheimer's disease in patients with mild cognitive impairment
- 1999
-
In: Neuroscience Letters. - 0304-3940. ; 273:1, s. 5-8
-
Journal article (peer-reviewed)abstract
- We studied CSF-tau and CSF-Abeta42 in 16 patients with mild cognitive impairment (MCI) who at follow-up investigations 6-27 months later had progressed to Alzheimer's disease (AD) with dementia. For comparison, we studied 15 age-matched healthy individuals. At baseline, 14/16 (88%) of MCI patients had high CSF-tau and/or low CSF-Abeta42 levels. These findings show that these CSF-markers are abnormal before the onset of clinical dementia and that they may help to identify MCI patients that will develop AD. This is especially important when drugs with potential effects on the progression of AD will reach the clinical phase.
|
|
| 2. |
- Blomqvist, Photjanee, et al.
(author)
-
Lesions of the locus coeruleus system aggravate ischemic damage in the rat brain
- 1985
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 58:3, s. 353-358
-
Journal article (peer-reviewed)abstract
- The possibility that the noradrenergic locus coeruleus system influences brain damage following ischemia was explored in rats. Bilateral lesions of the locus coeruleus projections to the forebrain aggravated the neuronal necrosis in the hippocampal CAI region and neocortex following complete cerebral ischemia induced by transient cardiac arrest. These findings provide evidence that the postischemic activation of the inhibitory locus coeruleus system could counteract a possible detrimental neuronal hyperexcitation, thereby limiting neuronal necrosis.
|
|
| 3. |
- Borlongan, C V, et al.
(author)
-
Cyclosporine-A enhances choline acetyltransferase immunoreactivity in the septal region of adult rats
- 2000
-
In: Neuroscience Letters. - 0304-3940. ; 279:2, s. 73-76
-
Journal article (peer-reviewed)abstract
- Cyclosporine-A (CsA) is the primary anti-rejection drug used for organ and neural transplantation therapy. In addition to its immunosuppressive action, CsA has been recently shown to exert neuroprotective and neurotrophic effects in the central nervous system when able to cross the blood-brain barrier. Postulated mechanisms for these CsA-induced beneficial effects include the drug's powerful inhibition of the calcium-dependent phosphatase calcineurin (CN) and blockade of the assembly of the mitochondrial permeability transition pore. We report here, for the first time, that adult Wistar rats treated with CsA (10 mg/kg per day, i.p. for 9 days) displayed significantly reduced septal CN expression in combination with enhanced levels of septal choline acetyltransferase (ChAT) immunoreactivity as compared to controls. The observed enhancement of septal ChAT immunoreactivity suggests potential therapeutic utility of CsA for brain disorders characterized by alterations of the cholinergic system.
|
|
| 4. |
- Bretillon, L, et al.
(author)
-
Plasma levels of 24S-hydroxycholesterol in patients with neurological diseases
- 2000
-
In: Neuroscience Letters. - 0304-3940. ; 293:2, s. 87-90
-
Journal article (peer-reviewed)abstract
- The brain is the exclusive or almost exclusive site of formation of 24S-hydroxycholesterol and we have shown that the circulating level of 24S-hydroxycholesterol is dependent upon the relation between cerebral production and hepatic clearance. In the present work we determined plasma levels of 24S-hydroxycholesterol in patients with various neurological diseases. Eleven subjects with brain death occurring 6-10 h before collection of the plasma samples had markedly reduced circulating levels of 24S-hydroxycholesterol (-43%, P<0.001). Patients with advanced Alzheimer's disease and cerebral inflammatory diseases had slightly lower levels of 24S-hydroxycholesterol in plasma when compared to matched controls. Patients with acute ischemic stroke, multiple sclerosis and primary brain tumors had levels not significantly different from those of controls. The conditions leading to reduced plasma levels of 24S-hydroxycholesterol had no significant effect on plasma levels of another side-chain oxidized oxysterol, 27-hydroxycholesterol. Except for conditions characterized by very marked destruction of the central nervous system, different severe neurological diseases seem to have relatively small effects on the flux of 24S-hydroxycholesterol from the brain.
|
|
| 5. |
- Cardell, Monika, et al.
(author)
-
Protein kinase C is translocated to cell membranes during cerebral ischemia
- 1990
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 119:2, s. 228-232
-
Journal article (peer-reviewed)abstract
- The subcellular distribution of PKC(α) and PKC(γ) was studied in homogenates of cerebral cortex from rats subjected to 10 and 15 min of ischemia and 15 min of ischemia followed by 1 h, 6 h, 24 h, 48 h, and 7 days of reperfusion. During ischemia no significant changes in the levels of PKC (α) were seen. During the first hour of reperfusion, a transient 2.5-fold (P < 0.05) increase in PKC(α) levels was observed in the particulate fraction. In contrast, a three-fold increase of PKC(γ) in the particulate fraction concomitant with a 40% decrease in the cytosol was noted during ischemia. In the postischemic phase the levels in the cytosol decreased to 35% of control values at 2 days following ischemia, with a concomitant decrease in the particulate fraction to control levels. The redistribution of PKC to the cell membranes during and following ischemia could be due to ischemia induced receptor activation, increased levels of diacylglycerols, arachidonate and intracellular calcium, and may be of importance for the development of ischemic neuronal damage.
|
|
| 6. |
- Davidsson, P, et al.
(author)
-
Differential increase in cerebrospinal fluid-acetylcholinesterase after treatment with acetylcholinesterase inhibitors in patients with Alzheimer's disease
- 2001
-
In: Neuroscience Letters. - 0304-3940. ; 300:3, s. 157-160
-
Journal article (peer-reviewed)abstract
- The clinical significance and the effects of pharmacological treatment of patients with Alzheimer's disease (AD) were evaluated by measurement of acetylcholinesterase (AChE) in the cerebrospinal fluid (CSF). CSF-AChE of AD patients was lower, not significantly, compared with controls. However, CSF-AChE was significantly increased after treatment of AD patients with AChE inhibitors (donepezil and galantamine). The increase was higher in patients treated with donezepil than in those treated with galantamine, which might be related to different mechanisms for the substances. The increase was also dose-dependent, and was especially marked in patients showing a clinical response. These data suggest that CSF biomarkers are capable not only of identifying a biochemical effect of drugs, but also of differentiating between different compounds in a dose-dependent manner.
|
|
| 7. |
- Edbladh, Magnus, et al.
(author)
-
Early regeneration in vitro of adult mouse sciatic axons is dependent on local protein synthesis but may not involve neurotrophins
- 1994
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 168:1-2, s. 37-40
-
Journal article (peer-reviewed)abstract
- The sensory axons of the adult mouse sciatic nerve were shown to regenerate after a local test crush lesion in vitro in a serum-free medium. The average outgrowth distance of the leading axons after culturing for 3 days was 2.8 ± 0.1 mm, which was shorter than in vivo (3.8 ± 0.2 mm). With the use of a compartmentalised culture system we could show that regeneration was partially dependent on local protein synthesis in the injury region. The initial stages of regeneration did not seem to involve neurotrophins since both K252a and K252b, selective and nontoxic inhibitors of the neurotrophin actions, failed to inhibit axonal growth. The present in vitro model system offers favourable conditions to investigate the early events of the regeneration process in an adult mammalian peripheral nerve.
|
|
| 8. |
- Ekström, Per A R
(author)
-
Insulin stimulates ganglionic protein synthesis and reduces thymidine incorporation in support cells of the in vitro regenerating adult frog sciatic sensory neurons
- 1991
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 132:2, s. 183-186
-
Journal article (peer-reviewed)abstract
- Insulin was tested for effects on crush injured, in vitro regenerating, adult frog sciatic sensory axons. A wide range of insulin concentrations (0.01-10 μg × ml-1) was found to stimulate incorporation of radioactive leucine into ganglionic protein by 50-80%. without affecting the regeneration distance. Simultaneously insulin inhibited the proliferation of the support cells at the crush region by 30%, as measured by thymidine incorporation. Experiments using compartmentalized culture dishes indicated that the proliferation inhibitory effect could be indirect and mediated by the neuronal cells. The results suggest that insulin influences the metabolism of adult peripheral neuronal cell bodies. The stimulated nerve cells could in turn affect the proliferation of support cells in the nerve trunk.
|
|
| 9. |
- Ekström, Per A R, et al.
(author)
-
Leukemia inhibitory factor null mice : Unhampered in vitro outgrowth of sensory axons but reduced stimulatory potential by nerve segments
- 2000
-
In: Neuroscience Letters. - 0304-3940. ; 281:2-3, s. 107-110
-
Journal article (peer-reviewed)abstract
- Leukemia inhibitory factor (LIF) is locally up-regulated after peripheral nerve injury and may be involved in the subsequent regeneration. Here, adult mice with or without LIF gene deletions were used to study the role of LIF in regeneration. The results show that axonal regeneration in vitro from dorsal root ganglia (DRGs) was unaffected by LIF deletion. However, segments from wild type mice promoted DRG axonal outgrowth better than segments from LIF deleted animals when in vivo-injured sciatic nerve segments were co-cultured with DRGs from normal adult mice. Addition of LIF could not restore the deficit. This suggests that LIF is engaged in the local regulation of regeneration but not in the regenerative events occuring at the cell body level. (C) 2000 Elsevier Science Ireland Ltd.
|
|
| 10. |
- Ekström, Peter, et al.
(author)
-
The left habenular nucleus contains a discrete serotonin-immunoreactive subnucleus in the coho salmon (Oncorhynchus kisutch)
- 1988
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 91:2, s. 121-125
-
Journal article (peer-reviewed)abstract
- By use of antibodies against serotonin, a discrete subnucleus of putatively serotoninergic neurons was observed in the dorsal subdivision of the left habenular nucleus in the brain of the coho salmon. The subnucleus was observed in salmon of different life-stages: in fingerlings, during smolt transformation, after smolt transformation (in seawater), and after spawning. This finding further emphasizes the close relationship between the pineal organ and the habenular nuclei not only in terms of topographical proximity but also in terms of cytological similarities: cells of the habenular nucleus and the pineal complex have previously been shown to be immunoreactive also with antibodies directed against retinal phototransduction proteins [5]. It also underlines the asymmetric organization of the epithalamic region.
|
|
| 11. |
|
|
| 12. |
- Grundemar, L, et al.
(author)
-
Long-lasting inhibition of the cardiovascular responses to glutamate and the baroreceptor reflex elicited by neuropeptide Y injected into the nucleus tractus solitarius of the rat
- 1991
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 122:1, s. 135-139
-
Journal article (peer-reviewed)abstract
- Neuropeptide Y (NPY) microinjected unilaterally into the nucleus tractus solitarii (NTS) of anesthetized paralyzed rats elicits a gradual dose-dependent and reversible fall in arterial pressure (AP) and heart rate (HR) lasting 20 min. It also abolished the brief (less than 1 min) dose-dependent and reversible fall of AP and HR elicited by L-glutamate (L-Glu) injected into the nucleus. The blockade of L-Glu by NPY appeared gradually and was prolonged, lasting over 2 h, and recovering by 24 h. It was not replicated by desamido-NPY or galanin. Unlike 2% lidocaine it did not block the hypotension elicited by focal electrical stimulation at the injection site indicating the response was not that of a local anesthetic. Bilateral injection of NPY into the NTS resulted, after an initial fall, in an elevation of AP (+48 +/- 10.6 mmHg). At this time the reflex bradycardia evoked by elevating AP with phenylephrine was markedly reduced. We conclude that in the NTS, NPY antagonizes the actions of L-Glu and may attenuate baroreceptor reflexes. Since the NTS is richly innervated by NPY neurons and contains many NPY binding sites and since primary baroreceptor afferents appear to be glutamatergic the results suggested that NPY may serve in NTS as a long-term regulator of baroreceptor reflex activity.
|
|
| 13. |
- Hardebo, Jan Erik, et al.
(author)
-
Origins of substance P- and calcitonin gene-related peptide-containing nerves in the internal carotid artery of rat
- 1989
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 101:1, s. 39-45
-
Journal article (peer-reviewed)abstract
- An aggregation of substance P (SP)- and calcitonin gene-related peptide (CGRP)-containing nerve cells (internal carotid mini-ganglion) is described at the junction between the greater superficial petrosal nerve and the internal carotid nerve close to the internal carotid artery. A retrograde tracer dye technique demonstrates that this ganglion and the trigeminal and superior vagal ganglia supply the internal carotid artery with SP/CGRP fibers at, above and below this level, respectively. Implications of this finding for cranial painful syndromes in man are discussed.
|
|
| 14. |
- Holmqvist, Bo I., et al.
(author)
-
Nitric oxide synthase in the brain of a teleost
- 1994
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 171:1-2, s. 205-208
-
Journal article (peer-reviewed)abstract
- The presence and distribution of the nitric oxide (NO) converting enzyme, NO synthase (NOS), was investigated in the brain of a teleost, the Atlantic salmon. Both NOS immunoreactive and NADPH diaphorase positive, non-neuronal and neuronal cell bodies, fibers and putative nerve terminals were identified throughout the brain. Even so, the staining was not identical in all regions. NO, synthesized by NOS-like enzymes, may play an important role in a diversity of cellular mechanisms in the brain of the salmon, including in neural systems related to olfactory, visual, hypophysiotrophic, viscero-sensoric and motor functions.
|
|
| 15. |
- Hornfelt, M., et al.
(author)
-
Upregulation of cytosolic phospholipase A2 correlates with apoptosis in mouse superior cervical and dorsal root ganglia neurons
- 1999
-
In: Neuroscience Letters. - 0304-3940. ; 265:2, s. 87-90
-
Journal article (peer-reviewed)abstract
- The involvement of cytosolic phospholipase A2 (cPLA2) in apoptosis of adult mouse superior cervical and dorsal root ganglia neurons has been investigated by the use of immunohistochemistry for cPLA2 and DNA nick-end labeling for apoptotic cells, respectively, cPLA2 immunoreactivity was strongly upregulated in neurons of both preparations during in vitro culturing. By double labeling it was unequivocally demonstrated that cPLA2 was present and upregulated only in neurons undergoing apoptosis. A similar picture emerged when cPLA2 immunoreactivity was compared with staining with Fluoro-Jade, a novel fluorochrome marker for neuronal degeneration. The preferential presence of cPLA2 in apoptotic and degenerating cells suggests that the enzyme is important for some mechanism involved in or intimately coupled to neuronal cell death.
|
|
| 16. |
- Hou, Mingyan, et al.
(author)
-
Capsaicin receptor immunoreactivity in the human trigeminal ganglion.
- 2002
-
In: Neuroscience Letters. - 0304-3940. ; 330:3, s. 223-226
-
Journal article (peer-reviewed)abstract
- The cloned capsaicin receptor, also known as vanilloid receptor subtype 1 (VR1) receptor, has been demonstrated to be an integral membrane protein with homology to a family of putative store-operated calcium channels. The VR1 receptor is activated not only by capsaicin but also by noxious heat and protons, and therefore it is suggested as a molecular integrator of chemical and physical stimuli that elicit pain. In the present study, indirect immunofluorescence detected a small number of neurons that are VR1 receptor immunoreactive (ir) (171 versus 1038 or 16% of all neuronal cell bodies) in the human trigeminal ganglion (TG). In addition, RT-PCR confirmed the presence of VR1 mRNA in the human TG. It has been hypothesized that TG neuronal cell bodies are the source of capsaicin-stimulated release of calcitonin gene-related peptide (CGRP), and hence co-localization experiments were performed. Around 10% of the VR1 receptor-ir is expressed on neurons that contain CGRP-ir (ten among 74) in the human TG, indicating that capsaicin may act through the VR1 receptor to modulate the release of CGRP and in turn to modulate pain. We observed that 8% of the VR1 receptor-ir neuronal cell bodies contain substance P-ir and 5% nitric oxide synthase. Capsaicin can release nitric oxide, CGRP and substance P from sensory nerves and contribute to central sensitization.
|
|
| 17. |
- Johansson, A, et al.
(author)
-
Increased frequency of a new polymorphism in the cycle 2 (cdc2) gene in patients with Alzheimer's disease frontotemporal dementia
- 2003
-
In: Neuroscience Letters. - 0304-3940. ; 340:1, s. 69-73
-
Journal article (peer-reviewed)abstract
- Recent studies show linkage between Alzheimer's disease (AD) and two loci on chromosome 10. The cell division cycle 2 (cdc2) gene is located close to one of the chromosome 10 markers, and is a candidate gene for AD since it is involved in the pathogenesis of AD. We sequenced coding exons and flanking intronic sequences and the promoter region on the cdc2 gene and found three new single nucleotide polymorphisms (SNPs). We analyzed 272 Caucasian AD cases, 160 controls and 70 cases with frontotemporal dementia (FTD) for these SNPs. Homozygosity for one of the SNPs (Ex6 + 7I/D) was more frequent in both AD and FTD cases than in controls. In the combined tauopathy (AD and FTD) group the odds ratio (OR) was 1.77 (95% CI 1.19-2.63) for the Ex6 + 7II genotype. Our findings suggest that the Ex6 + 7I allele is associated with tauopathies, both AD and FrD. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.
|
|
| 18. |
- Kokaia, Zaal, et al.
(author)
-
Changes in GABA(B) receptor immunoreactivity after recurrent seizures in rats
- 2001
-
In: Neuroscience Letters. - 0304-3940. ; 315:1-2, s. 85-88
-
Journal article (peer-reviewed)abstract
- GABA(B) receptors play an important role in the excitability of neuronal networks and can influence seizure activity. Here we demonstrate for the first time that kindling, an animal model for human temporal lobe epilepsy, leads to both early and delayed changes of GABA(B) receptor immunoreactivity in hippocampal and cortical areas. We propose that the altered GABA(B) receptor levels might be a compensatory mechanism to reduce excitability induced by recurrent kindled seizures, or alternatively, may promote the development of kindled epilepsy.
|
|
| 19. |
- Larsson, Christer, et al.
(author)
-
Desensitization of acetylcholine induced inositol 1,4,5-trisphosphate formation in neuroblastoma SH-SY5Y cells following repetitive acetylcholine stimulations
- 1993
-
In: Neuroscience Letters. - 0304-3940. ; 150:2, s. 141-144
-
Journal article (peer-reviewed)abstract
- In this study, the desensitization of acetylcholine-induced inositol 1,4,5-trisphosphate [I(1,4,5)P3] formation, upon short-time prestimulations, was investigated in cultures of human neuroblastoma SH-SY5Y cells. Four repeated stimulations for 10 seconds with 10 microM acetylcholine were necessary to induce a desensitization of the I(1,4,5)P3 formation. The desensitization was observed 4 hours after the initiation of repetitive stimulations. The same effect was obtained by a single prestimulation with 1 mM acetylcholine. Preincubation of the cells with phorbol 12-myristate 13-acetate (PMA) markedly down-regulated the acetylcholine-induced I(1,4,5)P3 formation. However, the protein kinase C (PKC) inhibitors H7 and staurosporine did not influence the desensitization induced by four repeated stimulations with 20 microM acetylcholine. These results indicate that the signal transduction can be desensitized following repeated stimulations with sub-maximal concentrations of receptor agonist and although activation of PKC can induce the same down-regulation, PKC is most likely not involved in the desensitization induced by repetitive acetylcholine-stimulations.
|
|
| 20. |
- Lillesaar, Christina, 1975-, et al.
(author)
-
Rat tooth pulp cells elicit neurite growth from trigeminal neurones and express mRNAs for neurotrophic factors in vitro
- 2001
-
In: Neuroscience Letters. - 0304-3940 .- 1872-7972. ; 308:3, s. 161-164
-
Journal article (peer-reviewed)abstract
- Molecular factors control the developmental ingrowth of axons to the tooth pulp. Here we examine the ability of pulpal cells to induce neurite outgrowth from neonatal rat trigeminal neurones (TGNs) in vitro. We found that TGNs emitted neurites and formed networks of branches in relation to pulpal cells. Neurones co-cultured with a mixture of pulpal cells and 3T3 fibroblasts formed networks exclusively in relation to the pulpal cells. Cultivated pulpal cells and pulpal tissue produced mRNAs for all neurotrophins and members of the glial cell line-derived neurotrophic factor family. Hence, rat pulpal cells have neuritogenic effects on single TGNs in vitro, that may be associated with secretion of neurotrophic factors.
|
|
| 21. |
- Magnusson, Kerstin, et al.
(author)
-
Impairment of protein ubiquitination may cause delayed neuronal death
- 1989
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 96:3, s. 264-270
-
Journal article (peer-reviewed)abstract
- The hippocampus is a brain structure specifically vulnerable to short periods of transient cerebral ischemia, and which displays delayed neuronal necrosis. Protein ubiquitination is a posttranslational modification of proteins and an important factor in heat shock response and a regulator of ATP-dependent protein degradation. Using affinity purified antibodies against ubiquitin and ubiquitin-protein conjugates we have found that the ubiquitin immunoreactivity (UIR), normally present in all neurons of the hippocampus, disappears in the early recirculation period following cerebral ischemia from all hippocampal cells except the interneurons. Later UIR reappears in the different hippocampal regions over a 72 h period in the following order: granule cells-CA3 pyramidal cells-CA2 pyramidal cells. This is the inverse order of sensitivity of these cells to ischemia. The UIR never recovers in the CA1 pyramidal neurons where a 95% neuronal necrosis is seen following three days of recovery. We propose that the loss of UIR in the pyramidal neurons in the CA1 region signifies a persistent impairment of protein ubiquitination, and thus a change in the turnover of structural and regulatory proteins, which could be an essential part of the mechanism of slow neuronal death following cerebral ischemia.
|
|
| 22. |
- Minthon, Lennart, et al.
(author)
-
The apolipoprotein E epsilon4 allele frequency is normal in fronto-temporal dementia, but correlates with age at onset of disease
- 1997
-
In: Neuroscience Letters. - 0304-3940. ; 226:1, s. 65-68
-
Journal article (peer-reviewed)abstract
- The apolipoprotein (apoE) epsilon4 allele was studied in fronto-temporal dementia (FTD), a diagnostic category including the specific disorders Pick's disease and frontal lobe degeneration of non-Alzheimer type (FLD). These dementing diseases have neuronal and synaptic degeneration in common with Alzheimer's disease (AD), for which the presence of the apoE epsilon4 allele is a known risk factor, and lowers the age of onset of disease. Previous studies on the apoE epsilon4 allele frequency in FTD have been inconclusive. The structural hallmarks of AD, allegedly linked to apoE presentation, neuritic plaques (NP), primarily composed of aggregates of beta-amyloid, and neurofibrillary tangles (NFT), primarily composed of hyperphosphorylated tau, are lacking in FTD. However, tau-positive cytoskeletal pathology is found in Pick's disease, but not in FLD. Resolving whether the epsilon4 frequency is increased in FTD or not may thus give clues to the pathogenetic mechanism of apoE in AD. We therefore studied apoE alleles in a well characterized material of FTD patients. The epsilon4 allele frequency was similar in 25 patients with FTD (14.0%) as compared with 26 healthy controls (13.5%). A post-mortem neuropathological examination was performed in 10 cases (nine had FLD and one Pick's disease). Our finding of a normal epsilon4 allele frequency in our group of FTD, principally consisting of FLD cases, support hypotheses involving differential binding of apoE to beta-amyloid and/or tau, in the development of beta-amyloid deposition and NP formation and/or tau hyperphosphorylation and NFT formation, for the pathogenetic role of apoE in AD. The age at onset was significantly lower (P < 0.01) in FTD patients possessing the epsilon4 allele (48.7 +/- 8.0 years) than in patients not possessing this allele (58.9 +/- 7.6 years). We conclude that, although the apoE epsilon4 allele frequency is not increase in FTD, the epsilon4 allele is not an etiological factor, but may rather be an accelerating factor in the degenerative process of FTD, thereby resulting in an earlier presentation of the disorder in individuals predisposed to develop FTD.
|
|
| 23. |
- Owman, Christer, et al.
(author)
-
Chronic nicotine treatment eliminates asymmetry in striatal glucose utilization following unilateral transection of the mesostriatal dopamine pathway in rats
- 1989
-
In: Neuroscience Letters. - 0304-3940. ; 102:2-3, s. 279-283
-
Journal article (peer-reviewed)abstract
- Partial hemitransection was performed through a knife lesion at the meso-diencephalic level in rats to sever the mesostriatal dopamine system. During the subsequent 2 weeks the animals received 0.125 mg/kg/h of nicotine continuously via an osmotic minipump implanted s.c. To achieve prompt high nicotine levels, 4 i.p. injections of 0.5 mg/kg nicotine were, in addition, given during the first 2 h following the lesion. The total treatment corresponded to a mean plasma level of 50 ng/ml nicotine, measured at the end of the experiment. Control animals received corresponding volumes of 0.9% saline. Quantitative autoradiographic analysis of the glucose utilization in the caudate nucleus using Sokoloff's [14C]2-deoxyglucose method demonstrated a 16% side-to-side difference in the lesioned control animals, whereas the asymmetry was counteracted by the nicotine treatment. Although there was an overall tendency to a lower rate of glucose utilization (by 6%) in the nicotine-treated animals compared to the controls receiving saline only, the difference was not statistically significant. The eliminated asymmetry probably reflects an increased survival of the dopamine neurons and/or of striatal nerve cells on the lesioned side due to protective effects of nicotine resulting from desensitization of nicotinic-type cholinergic receptors following continuous administration of the drug.
|
|
| 24. |
- Perez, M T, et al.
(author)
-
Expression of brain-derived neurotrophic factor and of its functional receptor in neonatal and adult rat retina
- 1995
-
In: Neuroscience Letters. - 0304-3940. ; 183:1-2, s. 9-96
-
Journal article (peer-reviewed)abstract
- The expression of mRNA coding for brain-derived neurotrophic factor (BDNF) and for its functional receptor, the full-length tyrosine kinase receptor trkB (trkB mRNA), was examined in early postnatal and adult rat retina by in situ hybridization using digoxygenin and radioactively-labeled oligonucleotide probes. BDNF and trkB mRNAs are expressed in the ganglion cell layer at postnatal-days (PN) 1, 4, 7, 14, 60, in proximal neuroblastic layer (PN 1, 4, 7), and proximal inner nuclear layer (PN 14, 60). Subpopulations of developing and mature retinal cells are thus capable of synthesizing BDNF.
|
|
| 25. |
- Rutherford, Diane M, et al.
(author)
-
Isolation and identification from Salvia officinalis of two diterpenes which inhibit t-butylbicyclophosphoro[35S]thionate binding to chloride channel of rat cerebrocortical membranes in vitro
- 1992
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 135:2, s. 224-226
-
Journal article (peer-reviewed)abstract
- Ethanolic extracts from dried leaves of sage (Salvia officinalis) showed inhibition of [35S]tertiary-butylbicyclophosphorothionate ([35S]TBPS) binding to rat brain membranes in vitro. This ligand is considered to bind to the chloride channel of the GABA/benzodiazepine receptor complex in brain tissue. Substances having inhibitory activity were purified and their chemical structure identified as the diterpenes carnosic acid and carnosol (IC50 values of 33 +/- 3 microM and 57 +/- 4 microM, respectively). The two compounds did not affect binding of the ligands [3H]muscimol and [3H]diazepam to the GABA/benzodiazepine complex in vitro. Saturation experiments of [35S]TBPS binding indicated that carnosic acid decreases the binding affinity.
|
|
| 26. |
- Stefanova, N, et al.
(author)
-
Ultrastructure of alpha-synuclein-positive aggregations in U373 astrocytoma and rat primary glial cells
- 2002
-
In: Neuroscience Letters. - 0304-3940. ; 323:1, s. 37-40
-
Journal article (peer-reviewed)abstract
- Abnormal alpha-synuclein-positive glial cytoplasmic inclusions are found in Parkinson's disease, multiple system atrophy and dementia with Lewy bodies. We have recently developed an in vitro model of alpha-synuclein-immunoreactive aggregations in U373 astrocytoma cells. We have additionally overexpressed wild-type and a C-terminally truncated form of alpha-synuclein in primary rat glial cells. Astrocytes and oligodendrocytes were found to form alpha-synuclein-positive aggregations in vitro perinuclearly or in the processes of the cells. The morphological studies presented here demonstrate that the aggregations we have observed in vitro are not limited by a membrane but have unclear borders. They have an amorphous dense core that is intensely alpha-synuclein-immunopositive and a predominantly filamentous halo around. Mainly filamentous structures at the border area between the halo and the core are alpha-synuclein-immunoreactive. We conclude that this in vitro model of alpha-synuclein-positive glial aggregations mimics the morphology of the abnormal glial inclusions described in neuroclegenerative disorders and could be a suitable model for studying their role in the pathogenesis of these diseases. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
|
|
| 27. |
- Suzuki, Norihiro, et al.
(author)
-
Galanin-positive nerves of trigeminal origin innervate rat cerebral vessels
- 1989
-
In: Neuroscience Letters. - 0304-3940. ; 100:1-3, s. 123-129
-
Journal article (peer-reviewed)abstract
- (GAL)-positive nerve fibers in rat cerebral vessels were demonstrated by immunohistochemistry, and their origin in the trigeminal ganglia and pathway in the nasociliary nerve to the vessels was shown by retrograde tracer technique and nerve transection. Some fibres in the vertebrobasilar system appear to originate in extracranial sources. With the antiserum used only few GAL fibers could be seen in the vessels, mostly in the vertebrobasilar system. In neonatally sympathectomized animals a rich network could be visualized in most pial arteries - still particularly in the vertebrobasilar system - probably as a result of a diminished competition for nerve growth factor. No vasomotor effect of GAL could be detected in isolated segments of pial arteries, neither in normal nor in sympathectomized animals, which rules out a direct postsynaptic effect on vascular tone. GAL did not display prejunctional modulatory action on the adrenergic nerves present in the vascular preparations. A sensory function of GAL is discussed.
|
|
| 28. |
- Svensson, Bodil, et al.
(author)
-
Increased levels of mitogen activated protein kinase (MAP-K) detected in the injured adult mouse sciatic nerve
- 1995
-
In: Neuroscience Letters. - 0304-3940. ; 200:1, s. 33-36
-
Journal article (peer-reviewed)abstract
- Adult mouse sciatic nerves (SNs) with attached dorsal root ganglia (DRG) were analysed for the presence of mitogen activated protein kinase (MAP-K) during normal and regenerative conditions. By immunohistochemistry, MAP-k was found to be present in the normal nerve at low levels in both Schwann cells and DRG nerve cell bodies, with a profoundly increased expression during regeneration. In axonal outgrowth assays, treatment with 2 mM 2-aminopurine (2-AP), a MAP-K antagonist, inhibited the regeneration of axons from the SN as well as from the cultured superior cervical ganglia. The reduced outgrowth was probably not due to toxic effects of the drug since the ganglionic protein synthesis was not inhibited. It is possible that 2-AP inteferes with regeneration-related events by inhibition of MAP-K.
|
|
| 29. |
- Terasmaa, A, et al.
(author)
-
Modulation of [(35)S]GTPgammaS binding to chinese hamster ovary cell membranes by D(2(short)) dopamine receptors
- 2000
-
In: Neuroscience Letters. - 0304-3940. ; 280:2, s. 135-138
-
Journal article (peer-reviewed)abstract
- Rat dopamine D(2short) expressed in Chinese hamster ovary (CHO) cells were characterized by means of activation of [(35)S]-guanosine 5'-O-(gamma-thiotriphosphate) ([(35)S]GTPgammaS) binding and inhibition of [(3)H]raclopride binding. Among 18 dopaminergic ligands studied dopamine, NPA, apomorphine and quinpirole were full agonists in activation of [(35)S]GTPgammaS binding, while seven ligands were partial agonists with efficacies from 16 to 69% of the effect of dopamine and seven ligands were antagonists having no effect on the basal level of [(35)S]GTPgammaS binding, but inhibited dopamine-dependent activation in a dose-response manner. Despite the different efficacies, the potencies of all 18 ligands to modulate [(35)S]GTPgammaS binding revealed a good correlation with their potencies to inhibit [(3)H]raclopride binding in the CHO cell membranes. This indicates that the binding of the ligand to the receptor determines its potency, but has no direct correlation with its intrinsic activity.
|
|
| 30. |
- Tossman, Ulf, et al.
(author)
-
γ-aminobutyric acid and taurine release in the striatum of the rat during hypoglycemic coma, studied by microdialysis
- 1985
-
In: Neuroscience Letters. - 0304-3940. ; 62:2, s. 231-235
-
Journal article (peer-reviewed)abstract
- Extracellular levels of striatal γ-aminobutyric acid (GABA) and taurine were monitored during insulin-induced hypoglycemia using microdialysis. At the onset of isoelectricity in the electroencephalogram (EEG), a transient 5-fold increase in the levels of GABA occurred. Taurine levels increased 5 min following the onset of isoelectricity and continued to increase during the entire isoelectric period. The results demonstrate that events associated with the onset of isoelectricity during hypoglycemia trigger an increase in extracellular concentrations of GABA and taurine. The discrepancy in time-course of these changes may reflect differences in compartmentation, function and metabolism of the two amino acids.
|
|
| 31. |
- Vecino, E., et al.
(author)
-
Expression of the homeobox engrailed gene during the embryonic development of the nervous system of the trout (Salmo fario L.)
- 1991
-
In: Neuroscience Letters. - 0304-3940. ; 129:2, s. 311-314
-
Journal article (peer-reviewed)abstract
- The expression of the engrailed homeobox gene during trout embryogenesis has been examined using immunohistochemistry and the monoclonal antibody 'Mab 4D9'. Engrailed has been suggested to play an important role during development by controlling position-specific characteristics in the CNS of the early embryo. In the present study we have analyzed the expression of engrailed at 5 stages of embryonic development of the trout (Salmo fario L.). The earliest stage analyzed was when the optic vesicles appear. Engrailed was then expressed in the posterior mesencephalon and anterior metencephalon, in a caudorostrally decreasing gradient. As the embryo develops, the pattern of the engrailed expression increases in spatial complexity. Thus, in the later stages of development, just before hatching, engrailed was found in hypothalamic areas, the germinative matrix layer of the cerebellum, the mesencephalic tegmentum, the caudal optic tectum and in the area of the trigeminal motor nucleus. This is similar to the distribution of engrailed in embryos of amphibians, birds and mammals.
|
|
| 32. |
- Wang, Z Y, et al.
(author)
-
Electroconvulsive treatment evokes release of preprotachykinin-A mRNA into the cerebrospinal fluid and ocular aqueous humor of rabbits
- 1997
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 226:3, s. 151-154
-
Journal article (peer-reviewed)abstract
- Following electroconvulsive treatment (ECT) of rabbits, preprotachykinin-A (PPT-A) mRNA was detected by Southern blot analysis of polymerase chain reaction (PCR)-amplified products in the cerebrospinal fluid (CSF) and aqueous humor of the eye. In contrast, no PPT-A mRNA could be detected in samples from untreated animals. In addition, several neuropeptides (substance P, neuropeptide Y, cholecystokinin, calcitonin gene-related peptide and pituitary adenylate cyclase activating peptide) were released into the CSF (and aqueous humor) following ECT. The results suggest that PPT-A mRNA was released together with neuropeptides into the CSF and aqueous humor in response to ECT. Indeed, previous studies have suggested that neurons can release neuropeptide mRNAs and that neurons are capable of taking up and expressing foreign mRNA. If neuropeptide mRNA can be taken up and utilized by another neuronal population, it might explain instances when neurons display 'phenotypic switch', i.e. the transient expression of novel neuropeptides.
|
|
| 33. |
- Westerberg, Eva, et al.
(author)
-
Excitatory amino acid receptors and ischemic brain damage in the rat
- 1987
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 73:2, s. 119-124
-
Journal article (peer-reviewed)abstract
- The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA1 hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hippocampus following transient ischemia. We report a transient reversible decrease in [3H]AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites (presumably representing quisqualate receptors) followed by a long term loss of binding at 2 days postischemia which precedes neuronal loss. In contrast, no change was noted in the N-methyl-d-aspartate or kainic acid binding sites over this time period.
|
|
| 34. |
- Wieloch, T., et al.
(author)
-
Lesions of the glutamatergic cortico-striatal projections in the rat ameliorate hypoglycemic brain damage in the striatum
- 1985
-
In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 58:1, s. 25-30
-
Journal article (peer-reviewed)abstract
- Unilateral ablations of the motor cortex were performed on rats. One to two weeks following the ablation they were subjected to 30 min of reversible insulin-induced hypoglycemic coma. The levels of glutamate, aspartate, γ-aminobutyric acid (GABA), taurine, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and phosphocreatine (PCr) were determined in frozen tissue sections from the superior half of the caudate nucleus. The lesions induced a specific reduction in the levels of glutamate by approx. 10% in the dorsal caudate nucleus ipsilateral to the lesion, while no significant differences in the levels of aspartate, GABA, taurine, ATP, ADP, AMP or PCr were noted. Neuronal necrosis in the caudate nucleus in animals subjected to 30 min of insulin-induced hypoglycemic coma and one week recovery was assessed by light microscopy. Contralateral to the lesion, extensive neuronal necrosis, mainly affecting small and medium-sized neurons, was observed in the dorsal and lateral caudate nucleus. In the caudate ipsilateral to the lesion a complete amelioration of necrosis was noted in areas subjacent to the lesion. The data suggest that hypoglycemic brain damage is induced by excitotoxins such as glutamate or related compounds.
|
|
| 35. |
- Wiklund, Peter, et al.
(author)
-
Protein kinase C inhibition has only a transient growth arresting effect on in vitro regenerating mouse sensory neurons
- 1999
-
In: Neuroscience Letters. - 0304-3940. ; 275:3, s. 155-158
-
Journal article (peer-reviewed)abstract
- Adult mice sensory ganglia were cultured in an extracellular matrix gel. Analyses of extending axons were made 48 h (long-term) or immediately (short-term) after addition of protein kinase inhibitors. Long- and short-term growth was insensitive to protein kinase A/G inhibition by HA-1004. Long-term protein kinase C inhibition by chelerythrine affected only certain, long axons. In the short-term virtually all axon growth was arrested, but largely recovered on the following day. When combined, the drugs inhibited all long- and short-term growth and largely prevented the recovery of the latter. The transient effect by chelerythrine, and the permanent inhibition after combination with HA-1004, suggests compensatory mechanisms, perhaps via other kinases. Copyright (C) 1999 Elsevier Science Ireland Ltd.
|
|
| 36. |
- Woldbye, D P D, et al.
(author)
-
Neuropeptide Y inhibits in vitro epileptiform activity in the entorhinal cortex of mice.
- 2002
-
In: Neuroscience Letters. - 0304-3940. ; 333:2, s. 127-130
-
Journal article (peer-reviewed)abstract
- Previous studies show that neuropeptide Y (NPY) inhibits in vitro seizures in rodent hippocampus. Here, we explored the effect of NPY application on epileptiform discharges induced by perfusion with magnesium-free solution in slices of entorhinal cortex from two different mouse strains. NPY significantly reduced the duration of epileptiform discharges with a peak effect of 36–50%. This is the first study showing anti-epileptiform effect of NPY in the entorhinal cortex and also the first evidence that NPY inhibits seizures in a cortical region in mice. The entorhinal cortex has a central role in transferring information between the hippocampus and the rest of the brain. Therefore our data further strengthen the concept of NPY and its receptors as widespread regulators of epileptiform activity and as a potential future target for antiepileptic therapy.
|
|
| 37. |
- Yáñez, Julián, et al.
(author)
-
Neural projections of the pineal organ in the larval sea lamprey (Petromyzon marinus L.) revealed by indocarbocyanine dye tracing
- 1993
-
In: Neuroscience Letters. - 0304-3940. ; 164:1-2, s. 213-216
-
Journal article (peer-reviewed)abstract
- The distribution of the central neural connections of the pineal organ of the larval sea lamprey was investigated by means of anterograde and retrograde tracing with the fluorescent lipophilic dye. DiI (1,1′-dioctadecyl 3,3,3′,3′-tetramethylindocarbocyanine perchlorate). Pinealofugal projections are well developed in larvae, extending from the posterior commissure into the diencephalon and mesencephalon. Small numbers of neurons were retrogradely labelled in the transition zone between the diencephalon and the mesencephalic tegmentum. These cells may consitute the first pinealopetal system described in anamniotes.
|
|
| 38. |
- Zhao, Li Ru, et al.
(author)
-
Enriched environment influences brain-derived neurotrophic factor levels in rat forebrain after focal stroke
- 2001
-
In: Neuroscience Letters. - 0304-3940. ; 305:3, s. 169-172
-
Journal article (peer-reviewed)abstract
- Tissue levels of brain-derived neurotrophic factor (BDNF) protein were studied using enzyme immunoassay in different forebrain regions in the ipsi- and contralateral hemispheres of rats housed under enriched or standard conditions after the middle cerebral artery ligation. BDNF levels in the ipsilateral to ligation side was significantly higher only in the frontal cortex of standard as compared to enriched rats. However, BDNF overall was more abundant in standard than in enriched group. In addition, BDNF levels detected in the hippocampus and frontal cortex on the ischemic side of standard rats was higher as compared to contralateral side. The present study shows that housing conditions after permanent middle cerebral artery ligation leads to differential regulation of BDNF protein levels in forebrain regions which might have important implication for post-ischemic recovery.
|
|
| 39. |
- Abelson, Klas, et al.
(author)
-
Intravenously administered lidocaine in therapeutic doses increases the intraspinal release of acetylcholine in rats
- 2002
-
In: Neuroscience Letters. - : Elsevier. - 0304-3940 .- 1872-7972. ; 317:2, s. 93-6
-
Journal article (peer-reviewed)abstract
- The local anesthetic lidocaine suppresses different pain conditions when administered systemically. Part of the antinociceptive effect appears to be mediated via receptor mechanisms. We have previously shown that muscarinic and nicotinic agonists that produce antinociception increase the intraspinal release of acetylcholine. In the present study it was hypothesized that systemically administered lidocaine is acting through the same mechanisms as cholinergic agonists and affects the intraspinal release of acetylcholine. Microdialysis probes were placed in anesthetized rats for sampling of acetylcholine. Ten and 30 mg/kg lidocaine injected intravenously significantly increased the intraspinal release of acetylcholine. The effect of lidocaine could be reduced by pretreatment with intraspinally administered atropine or mecamylamine. Our results suggest that the antinociceptive effect produced by systemically administered lidocaine is mediated through an action on muscarinic and nicotinic receptors.
|
|
| 40. |
- Adlerz, Linda, et al.
(author)
-
Down-regulation of amyloid precursor protein by peptide nucleic acid oligomer in cultured rat primary neurons and astrocytes
- 2003
-
In: Neuroscience Letters. - 0304-3940 .- 1872-7972. ; 336:1, s. 55-59
-
Journal article (peer-reviewed)abstract
- The amyloid precursor protein (APP) and its proteolytic cleavage products, the amyloid P peptides, have been implicated as a cause of Alzheimer's disease. Peptide nucleic acids (PNA), the DNA mimics, have been shown to block the expression of specific proteins at both transcriptional and translational levels. Generally, the cellular uptake of PNA is low. However, recent studies have indicated that the effect of unmodified antisense PNA uptake is more pronounced in nervous tissue. In this study we have shown that biotinylated PNA directed to the initiator codon region of the APP mRNA (-4 - +11) was taken up into the cytoplasm of primary rat cerebellar granule cells and cortical astrocytes, using fluorescence and confocal microscopy studies. Uptake of PNA was faster in neurons than in astrocytes. Western blotting analysis showed that APP was strongly down-regulated in both neurons and astrocytes. Thus, unmodified PNA can be used for studies on the function of APP in neurons and astrocytes.
|
|
| 41. |
|
|
| 42. |
|
|
| 43. |
|
|
| 44. |
|
|
| 45. |
|
|
| 46. |
|
|
| 47. |
|
|
| 48. |
- Amandusson, Åsa, et al.
(author)
-
Estrogen receptor-like immunoreactivity in the medullary and spinal dorsal horn of the female rat
- 1995
-
In: Neuroscience Letters. - 0304-3940 .- 1872-7972. ; 196:1-2, s. 25-28
-
Journal article (peer-reviewed)abstract
- Using an immunohistochemical technique, we demonstrate that large numbers of neurons in the laminar spinal trigeminal nucleus and spinal gray matter of the female rat express estrogen receptors (ER). Densely packed ER-immunoreactive neurons were present in lamina II, but labeled neurons were also present in lamina I, the neck of the dorsal horn, and in lamina X. Labeling was present throughout the length of the spinal cord, with the exception of segments caudal to S1, which were unlabeled. The distribution of ER-containing neurons to areas that are involved in processing of primary afferent nociceptive information suggests that the pain modulatory effects of estrogen may be exerted at the spinal level.
|
|
| 49. |
|
|
| 50. |
|
|
