| 1. |
- Anderson, Maria E., et al.
(författare)
-
Galanin, through GalR1 but not GalR2 receptors, decreases motivation at times of high appetitive behavior
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 239, s. 90-93
-
Tidskriftsartikel (refereegranskat)abstract
- Galanin is a 29/30-amino acid long neuropeptide that has been implicated in many physiological and behavioral functions. Previous research has shown that i.c.v. administration of galanin strongly stimulates food intake in sated rats when food is freely available, but fails to stimulate this consumption when an operant response requirement is present. Using fixed ratio (FR) schedules, we sought to further clarify galanin's role in motivated behavior by administering galanin i.c.v. to rats working on fixed ratio schedules requiring either a low work condition (FR1) or higher work conditions (FR > 1) to obtain a 0.2% saccharin reward. Rats in the FR > 1 group were assigned to either an FR3, FR5 or FR7 schedule of reinforcement. The rate of reinforcement decreased for only the FR > 1 group as compared to saline controls. Furthermore, injections of GalR1 receptor agonist M617 led to a similar, marginally significant decrease in the number of reinforcers received in the FR > 1 condition, but a decrease was not seen after injections of GalR2 receptor agonist M1153. Taken together, these results show that galanin may be playing a role in decreasing motivation at times of high appetitive behavior, and that this effect is likely mediated by the GalR1 receptor.
|
|
| 2. |
|
|
| 3. |
- Bannbers, Elin, 1984-, et al.
(författare)
-
Prefrontal activity during response inhibition decreases over time in the postpartum period
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 241, s. 132-138
-
Tidskriftsartikel (refereegranskat)abstract
- The postpartum period is characterized by complex hormonal changes, but human imaging studies in the postpartum period have thus far predominantly focused on the neural correlates of maternal behavior or postpartum depression, whereas longitudinal studies on neural correlates of cognitive function across the postpartum period in healthy women are lacking. The aim of this study was to longitudinally examine response inhibition, as a measure of executive function, during the postpartum period and its neural correlates in healthy postpartum women and non-postpartum controls. Thirteen healthy postpartum women underwent event-related functional magnetic resonance imaging while performing a Go/NoGo task. The first assessment was made within 48 h of delivery, and the second at 4-7 weeks postpartum. In addition, 13 healthy women examined twice during the menstrual cycle were included as non-postpartum controls. In postpartum women region of interest analyses revealed task-related decreased activations in the right inferior frontal gyrus, right anterior cingulate, and bilateral precentral gyri at the late postpartum assessment. Generally, postpartum women displayed lower activity during response inhibition in the bilateral inferior frontal gyri and precentral gyri compared to non-postpartum controls. No differences in performance on the Go/NoGo task were found between time-points or between groups. In conclusion, this study has discovered that brain activity in prefrontal areas during a response inhibition task decreases throughout the course of the first postpartum weeks and is lower than in non-postpartum controls. Further studies on the normal adaptive brain activity changes that occur during the postpartum period are warranted. (C) 2012 Elsevier B.V. All rights reserved.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Codita, Alina, et al.
(författare)
-
Impaired behavior of female tg-ArcSwe APP mice in the IntelliCage : A longitudinal study
- 2010
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 215:1, s. 83-94
-
Tidskriftsartikel (refereegranskat)abstract
- Transgenic animals expressing mutant human amyloid precursor protein (APP) are used as models for Alzheimer disease (AD). Ideally, behavioral tests improve the predictive validity of studies on animals by mirroring the functional impact of AD-like neuropathology. Learning and memory studies in APP transgenic models have been difficult to replicate. Standardization of procedures, automatization or improved protocol design can improve reproducibility. Here the IntelliCage, an automated system, was used for behavioral testing of APP female transgenic mice with both the Arctic and Swedish mutations, the tg-ArcSwe model. Protocols covering exploration, operant learning, place learning and extinction of place preference as well as passive avoidance tests were used for longitudinal characterization of behavior. Differences in exploratory activity were significant at four months of age, when plaque-free tg-ArcSwe mice visited less frequently the IntelliCage corners and initially performed fewer visits with licks compared to non-tg animals, inside the new environment. Fourteen months old tg-ArcSwe mice required a longer time to re-habituate to the IntelliCages than non-tg mice. At both ages tg-ArcSwe mice perseverated in place preference extinction test. Fourteen months old tg-ArcSwe mice were impaired in hippocampus-dependent spatial passive avoidance learning. This deficit was found to inversely correlate to calbindin-D28k immunoreactivity in the polymorphic layer of the dentate gyrus. Reduced water intake and body weight were observed in 4 months old tg-ArcSwe animals. The body weight difference increased with age. Thus behavioral and metabolic changes in the tg-ArcSwe APP model were detected using the IntelliCage, a system which provides the opportunity for standardized automated longitudinal behavioral phenotyping.
|
|
| 7. |
- Dahlbom, S. Josefin, et al.
(författare)
-
Aggression and monoamines : Effects of sex and social rank in zebrafish (Danio rerio)
- 2012
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 228:2, s. 333-338
-
Tidskriftsartikel (refereegranskat)abstract
- Social defeat is a common model for studies on depression. However, such models are most often used to study aggression in males and sex differences in depression may therefore be overseen. This study investigated the potential of the zebrafish (Danio rerio) as a model for male and female aggression. In addition, effects on the brain serotonergic and dopaminergic neurotransmitter systems after agonistic interaction are well studied in many species, but not in zebrafish. We wanted to explore whether the zebrafish follows the same patterns as many other species. Therefore, the effects of agonistic interaction on brain monoaminergic activity were studied in adult male and female wild-type zebrafish. The fish interacted in pairs with one of the same sex for five days during which agonistic behaviour was quantified daily. Clear dominant/subordinate relationships developed in all pairs, both in males and females. The frequency of aggressive acts increased over time but did not differ between male and female pairs. Further, we found that dyadic agonistic interaction resulted in elevated brain serotonergic activity in subordinate zebrafish, as indicated by elevated hindbrain 5-hydroxyindoleacetic acid to serotonin ratios (5-hydroxyindolacetic acid (5-HIAA)/5-hydroxytryptamine (5-HT) ratios). We also observed a sex difference in forebrain dopamine levels and forebrain 5-HIAA/5-HT ratios, with females displaying higher concentrations of dopamine but lower 5-HIAA/5-HT ratios than males. These results suggest that zebrafish is a suitable model for studies on female aggression and sex differences in brain monoaminergic neurotransmission.
|
|
| 8. |
- Enhamre-Brolin, Erika, et al.
(författare)
-
Growth hormone reverses streptozotocin-induced cognitive impairments in male mice
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 238, s. 273-278
-
Tidskriftsartikel (refereegranskat)abstract
- In recent decades, growth hormone (GH) replacement therapy in human subjects deficient in the hormone has resulted in a number of beneficial effects on cognitive performance. Studies in hypophysectomised rats report similar effects of GH treatment on learning and memory tasks. The purpose of this study was to investigate the ability of GM to reverse learning impairments in mice with streptozotocin (STZ)-induced diabetes. Diabetic and control mice were given recombinant human GM (rhGH) 0.1 IU/kg/day for ten consecutive days. In the latter phase of the treatment the cognitive abilities of the mice were tested using the Barnes maze (BM). A profound hormonal effect was seen when analysing the search patterns used by the animals in the maze. rhGH treatment significantly counteracted the cognitive disabilities expressed as lack of direct search strategies on the last day in the BM. In addition, the number of primary errors made by diabetic mice during the acquisition phase was reduced by rhGH treatment, although the primary escape latency was unchanged in these animals when compared to saline-treated diabetic animals. These results suggest that specific cognitive impairments induced by STZ, i.e. the disabilities seen in strategic behaviour, could be reversed by exogenous hormone treatment. Our findings highlight the influence of GH on brain function and in particular on cognitive behaviour related to learning and memory.
|
|
| 9. |
- Frick, Andreas, et al.
(författare)
-
Classifying social anxiety disorder using multivoxel pattern analyses of brain function and structure
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 75:9, s. 358S-358S
-
Tidskriftsartikel (refereegranskat)abstract
- Functional neuroimaging of social anxiety disorder (SAD) support altered neural activation to threat-provoking stimuli focally in the fear network, while structural differences are distributed over the temporal and frontal cortices as well as limbic structures. Previous neuroimaging studies have investigated the brain at the voxel level using mass-univariate methods which do not enable detection of more complex patterns of activity and structural alterations that may separate SAD from healthy individuals. Support vector machine (SVM) is a supervised machine learning method that capitalizes on brain activation and structural patterns to classify individuals. The aim of this study was to investigate if it is possible to discriminate SAD patients (n = 14) from healthy controls (n = 12) using SVM based on (1) functional magnetic resonance imaging during fearful face processing and (2) regional gray matter volume. Whole brain and region of interest (fear network) SVM analyses were performed for both modalities. For functional scans, significant classifications were obtained both at whole brain level and when restricting the analysis to the fear network while gray matter SVM analyses correctly classified participants only when using the whole brain search volume. These results support that SAD is characterized by aberrant neural activation to affective stimuli in the fear network, while disorder-related alterations in regional gray matter volume are more diffusely distributed over the whole brain. SVM may thus be useful for identifying imaging biomarkers of SAD.
|
|
| 10. |
- Gruden, Marina A, et al.
(författare)
-
Intranasal administration of alpha-synuclein aggregates : a Parkinson's disease model with behavioral and neurochemical correlates
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier. - 0166-4328 .- 1872-7549. ; 263, s. 158-168
-
Tidskriftsartikel (refereegranskat)abstract
- Parkinson's disease (PD) is a neurodegenerative disorder in which both alpha-synuclein (alpha-syn) and dopamine (DA) have a critical role. Our previous studies instigated a novel PD model based on nasal inoculation with alpha-syn aggregates which expressed parkinsonian-like behavioral and immunological features. The current study in mice substantiated the robustness of the amyloid nasal vector model by examining behavioral consequences with respect to DA-ergic neurochemical corollaries. In vitro generated alpha-syn oligomers and fibrils were characterized using atomic force microscopy and the thioflavin T binding assay. These toxic oligomers or fibrils administered alone (0.48 mg/kg) or their 50:50 combination (total dose of 0.48 mg/kg) were given intranasally for 14 days and "open-field" behavior was tested on days 0, 15 and 28 of the protocol. Behavioral deficits at the end of the 14-day dosing regime and on day 28 (i.e., 14 days after treatment completion) induced rigidity, hypokinesia and immobility. This was accompanied by elevated nigral but not striatal DA, DOPAC and HVA concentrations in response to dual administration of alpha-syn oligomers plus fibrils but not the oligomers by themselves. alpha-Syn fibrils intensified not only the hypokinesia and immobility 14 days post treatment, but also reduced vertical rearing and enhanced DA levels in the substantia nigra. Only nigral DA turnover (DOPAC/DA but not HVA/DA ratio) was augmented in response to fibril treatment but there were no changes in the striatum. Compilation of these novel behavioral and neurochemical findings substantiate the validity of the alpha-syn nasal vector model for investigating parkinsonian-like symptoms.(C) 2014 Elsevier B.V. All rights reserved.
|
|
| 11. |
- Gruden, Marina A., et al.
(författare)
-
Nasal inoculation with a-synuclein aggregates evokes rigidity, locomotor deficits and immunity to such misfolded species as well as dopamine
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 243, s. 205-212
-
Tidskriftsartikel (refereegranskat)abstract
- Animal models of Parkinson's disease (PD) have been widely used to investigate the pathogenesis of this neurodegenerative disorder which is typically associated with the specific and largely disordered protein alpha-synuclein (alpha-syn). In the current study, the nasal vector was used to deliver alpha-syn aggregates to the brain. Both alpha-syn oligomers and its fibrils were firstly characterized using atomic force microscopy and the thioflavin T binding assay. The toxic oligomers alone (0.48 mg/kg) or their 50:50 combination with fibrils (in a total dose of 0.48 mg/kg) were then given intranasally for ten days in mice and PD-mimetic symptoms as well as humoral immunity to these species and dopamine (DA) were evaluated simultaneously. Open-field behavioral deficits indicated by rigidity and reduced locomotor activity were induced by the dual administration of alpha-syn oligomers plus fibrils but not the oligomers by themselves under the 10-day dosing regimen. In contrast, using ELISA, high levels of serum autoantibodies to alpha-syn monomeric, oligomeric and fibrillar conformers as well as DA were observed in both treatment groups reflecting immune system activation and this substantiates previous clinical studies in Parkinson's disease patients. Thus, nasal administration of alpha-syn amyloidogenic species may be a potential experimental PD model which results not only in motor deficits but also incitement of humoral protection to mimic the disease. Such a paradigm may be exploitable in the quest for potential therapeutic strategies and further studies are warranted.
|
|
| 12. |
- Johansson, Jenny, et al.
(författare)
-
Gamma-Hydroxybutyrate (GHB) induces cognitive deficits and affects GABAB receptors and IGF-1 receptors in male rats
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 269, s. 164-174
-
Tidskriftsartikel (refereegranskat)abstract
- In recent years, the abuse of the club drug Gamma-hydroxy butyric acid (GHB) has become increasingly frequent among adolescents. The drug induces euphoria but can also result in sedation, anaesthesia as well as short-term amnesia. In addition, the abuse of GHB is reported to cause cognitive impairments. The mechanism by which GHB induces impairment in learning and memory has not been fully clarified. The present study investigates the impact on spatial learning and memory using a water maze test in rats treated with GHB. The behavioural data is combined with an autoradiographic analysis of the GABAB and the IGF-1 receptor systems. The results demonstrate that the GHB treated animals display an impaired performance in the water maze test as compared to controls. In addition, significant alterations in GABAB and IGF-1 receptor density as well as GABAB receptor functionality, were observed in several brain regions associated with cognitive functions e.g. hippocampus. To conclude, our findings suggest that GHB treatment can affect spatial learning and memory, and that this outcome at least to some extent is likely to involve both GABAB and IGF-1 receptors.
|
|
| 13. |
- Karlsson, Oskar, et al.
(författare)
-
Early hippocampal cell death, and late learning and memory deficits in rats exposed to the environmental toxin BMAA (β-N-methylamino-l-alanine) during the neonatal period
- 2011
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 219:2, s. 310-320
-
Tidskriftsartikel (refereegranskat)abstract
- We have reported previously that exposure to the cyanobacterial neurotoxin β-N-methylamino-l-alanine (BMAA) during the neonatal period causes cognitive impairments in adult rats. The aim of this study was to investigate the long-term effects of neonatal BMAA exposure on learning and memory mechanisms and to identify early morphological changes in the neonatal brain. BMAA was injected subcutaneously in rat pups on postnatal days 9-10. BMAA (50 and 200mg/kg) caused distinct deficits in spatial learning and memory in adult animals but no morphological changes. No impairment of recognition memory was detected, suggesting that neonatal exposure to BMAA preferentially affects neuronal systems that are important for spatial tasks. Histopathological examination revealed early neuronal cell death as determined by TUNEL staining in the hippocampus 24h after a high dose (600mg/kg) of BMAA whereas no changes were observed at lower doses (50 and 200mg/kg). In addition, there was a low degree of neuronal cell death in the retrosplenial and cingulate cortices, areas that are also important for cognitive function. Taken together, these results indicate that BMAA is a developmental neurotoxin inducing long-term changes in cognitive function. The risk posed by BMAA as a potential human neurotoxin merits further consideration, particularly if the proposed biomagnifications in the food chain are confirmed.
|
|
| 14. |
- Landgren, Sara, 1980, et al.
(författare)
-
Expression of the gene encoding the ghrelin receptor in rats selected for differential alcohol preference.
- 2011
-
Ingår i: Behavioural brain research. - : Elsevier BV. - 1872-7549 .- 0166-4328. ; 221:1, s. 182-8
-
Tidskriftsartikel (refereegranskat)abstract
- The mechanisms involved in alcohol use disorder, a chronic relapsing brain disorder, are complex and involve various signalling systems in the brain. Recently, the orexigenic peptide ghrelin was shown to be required for alcohol-induced reward, an effect mediated via ghrelin receptors, GHS-R1A, at the level of the cholinergic-dopaminergic reward link. Moreover, ghrelin increases and GHR-R1A antagonists reduce moderate alcohol consumption in mice, and a single nucleotide polymorphism in the GHS-R1A gene has been associated with high alcohol consumption in humans. Therefore, GHS-R1A gene expression and alcohol intake were investigated in high, AA (Alko, Alcohol), versus low, ANA (Alko, Non-Alcohol), alcohol consuming rats as well as in Wistar rats. In the AA and ANA rats plasma ghrelin levels were also measured. GHS-R1A gene expression was increased in AA compared to ANA rats in nucleus accumbens, ventral tegmental area, amygdala, prefrontal cortex and hippocampus. A similar trend was observed in the ventral tegmental area of Wistar rats consuming high amounts of alcohol. Furthermore, the AA rats had significantly smaller reduction of plasma ghrelin levels over time, after several weeks of alcohol exposure, than had the ANA rats. The present study provides further evidence for that the ghrelin signalling system, in particular at the level of the mesocortocolimbic dopamine system, is involved in alcohol consumption, and thus possibly contributes to alcohol use disorder. Therefore the GHS-R1A may constitute a novel candidate for development of new treatment strategies for alcohol dependence.
|
|
| 15. |
|
|
| 16. |
|
|
| 17. |
- Momeni, Shima, et al.
(författare)
-
Subgroup-dependent effects of voluntary alcohol intake on behavioral profiles in outbred Wistar rats
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 275, s. 288-296
-
Tidskriftsartikel (refereegranskat)abstract
- Experimental animal models are critical for understanding the genetic, environmental and neurobiological underpinnings of alcohol use disorders. Limited studies investigate alcohol-induced effects on behavior using free-choice paradigms. The aims of the present experiment were to study voluntary alcohol intake using a modified intermittent access paradigm, investigate the effects of voluntary alcohol intake on behavioral profiles in water- and alcohol-drinking rats, and select extreme low- and high-drinking animals for a more detailed behavioral characterization. Sixty outbred male Wistar rats were randomized into water and alcohol groups. Behavioral profiles in the multivariate concentric square field (TM) (MCSF) test were assessed prior to and after voluntary alcohol intake. The animals had intermittent access to 20% alcohol and water for three consecutive days per week for seven weeks. The results revealed increased alcohol intake over time. No major alcohol-induced differences on behavior profiles were found when comparing water- and alcohol-drinking animals. The high-drinking animals displayed an alcohol deprivation effect, which was not found in the low-drinking animals. High-drinking rats had lower risk-taking behavior prior to alcohol access and lower anxiety-like behavior after voluntary alcohol intake compared to low-drinking rats. In conclusion, the modified intermittent access paradigm may be useful for pharmacological manipulation of alcohol intake. With regard to behavior, the present findings highlights the importance of studying subgroup-dependent differences and add to the complexity of individual differences in behavioral traits of relevance to the vulnerability for excessive alcohol intake.
|
|
| 18. |
|
|
| 19. |
- Persson, Jonas, et al.
(författare)
-
Remembering our origin : Gender differences in spatial memory are reflected in gender differences in hippocampal lateralization
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier. - 0166-4328 .- 1872-7549. ; 256, s. 219-228
-
Tidskriftsartikel (refereegranskat)abstract
- Gender differences in spatial memory favoring men are frequently reported, and the involvement of the hippocampus in these functions is well-established. However, little is known of whether this behavioral gender difference is mirrored in a gender difference in hippocampal function. Here we assessed hippocampal activity, using functional MRI, while 24 men and women moved through three-dimensional virtual mazes (navigation phase) of varying length, and at the end-point estimated the direction of the starting-point (pointing phase). Men were indeed more accurate than women at estimating direction, and this was especially true in longer mazes. Both genders activated the posterior hippocampus throughout the whole task. During the navigation phase, men showed a larger activation in the right hippocampus than women, while in the pointing phase, women showed a larger activation in the left hippocampus than men. Right-lateralized activation during the navigation phase was associated with greater task performance, and may reflect a spatial strategy that is beneficial in this task. Left-sided activation during the pointing phase might reflect a less efficient post hoc verbal recapitulation of the route. This study is the first to identify neural correlates of the commonly observed male advantage in recalling one's original position, and points to hippocampal lateralization as a possible explanation for this behavioral gender difference. (C) 2013 Elsevier B.V. All rights reserved.
|
|
| 20. |
|
|
| 21. |
- Pontén, Emma, et al.
(författare)
-
Neonatal exposure to propofol affects BDNF but not CaMKII, GAP-43, synaptophysin and tau in the neonatal brain and causes an altered behavioural response to diazepam in the adult mouse brain
- 2011
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 223:1, s. 75-80
-
Tidskriftsartikel (refereegranskat)abstract
- Animal studies have shown that neonatal anaesthesia is associated with acute signs of neurodegeneration and later behavioural changes in adult animals. The anaesthetic effect of propofol is thought to be mediated by gamma-amino butyric acid (GABA)(A) receptors. The present study investigated the effects on proteins important for normal neonatal brain development (i.e. BDNF, CaMKII, GAP-43, synaptophysin and tau), and adult spontaneous motor and anxiety-like behaviours in response to diazepam, after neonatal exposure to propofol. Ten-day-old mice were exposed to 0, 10 or 60 mg/kg bodyweight propofol. Neonatal propofol exposure changed the levels of BDNF in the brain, 24h after exposure, but did not alter any of the other proteins. Neonatal propofol exposure significantly changed the adult response to the GABA-mimetic drug diazepam, manifest as no change in spontaneous motor activity and/or reduced sedative effect and an extinguished effect on the reduction of anxiety-like behaviours in an elevated plus maze. Although no adult spontaneous behavioural changes were detected after neonatal propofol exposure, the exposure caused an adult dose-dependent decrease in the response to the GABA-mimetic drug diazepam. These changes may be due to neonatal alterations in BDNF levels.
|
|
| 22. |
- Reefmann, Nadine
(författare)
-
Prefrontal cortex activity, sympatho-vagal reaction and behaviour distinguish between situations of feed reward and frustration in dwarf goats
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 239, s. 104-114
-
Tidskriftsartikel (refereegranskat)abstract
- Recent concepts relating to animal welfare accept that animals experience affective states. These are notoriously difficult to measure in non-verbal species, but it is generally agreed that emotional reactions consist of well-coordinated reactions in behaviour, autonomic and brain activation. The aim of the study was to evaluate whether each or a combination of these aspects can differentiate between situations presumed to differ in emotional content. To this end, we repeatedly confronted dwarf goats at short intervals with a covered and an uncovered feed bowl (i.e. presumably frustrating and rewarding situations respectively) whilst simultaneously observing their behaviour, measuring heart-rate and heart-rate variability and haemodynamic changes in the prefrontal cortex using functional near-infrared spectroscopy. When faced with a covered feed bowl, goats occupied themselves at locations away from the bowl and showed increased locomotion, while there was a general increase in prefrontal cortical activity. There was little indication of autonomic changes. In contrast, when feed was accessible, the goats reduced locomotion, focused their behaviour on the feed bowl, showed signs of sympathetically mediated arousal reflecting anticipation and, if any cortical activity at all was present, it was concentrated to the left hemisphere. We thus observed patterns in behaviour, sympathetic reaction and brain activity that distinguished between a situation of frustration and one of reward in dwarf goats. These patterns consisted of a well-coordinated set of reactions appropriate in respect of the emotional content of the stimuli used. (c) 2012 Elsevier B.V. All rights reserved.
|
|
| 23. |
- Suchankova, Petra, 1979, et al.
(författare)
-
Personality traits and the R668Q polymorphism located in the MMP-9 gene.
- 2012
-
Ingår i: Behavioural brain research. - : Elsevier BV. - 1872-7549 .- 0166-4328. ; 228:1, s. 232-5
-
Tidskriftsartikel (refereegranskat)abstract
- Matrix metalloproteinases (MMPs) are enzymes involved in degradation of proteins in the extracellular matrix and have been shown to contribute to neuroinflammation by several mechanisms such as blood-brain barrier breakdown. Among the MMPs, MMP-9 (gelatinase B) has been suggested to be of relevance also for synaptic and behavioural plasticity. In order to explore the role of MMP-9 for mental functions a polymorphism in MMP-9 was analysed with respect to personality traits. The two studied populations consisted of women and men, respectively, both recruited from the population registry and assessed by means of the Karolinska Scales of Personality. The non-synonymous single nucleotide polymorphism (R668Q, rs17577) studied is located in the coding region of MMP-9 and is believed to affect the activity of the enzyme. The present study found that an amino acid change from arginine (R) to glutamine (Q) was associated with higher scores of the personality trait inhibition of aggression in the female population whilst this substitution was associated with higher scores of verbal aggression and irritability in men. These findings give support for an influence of MMP-9 on mental functions.
|
|
| 24. |
- Tabansky, Inna, et al.
(författare)
-
Temporally-patterned deep brain stimulation in a mouse model of multiple traumatic brain injury
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier. - 0166-4328 .- 1872-7549. ; 273, s. 123-132
-
Tidskriftsartikel (refereegranskat)abstract
- We report that mice with closed-head multiple traumatic brain injury (TBI) show a decrease in the motoric aspects of generalized arousal, as measured by automated, quantitative behavioral assays. Further, we found that temporally-patterned deep brain stimulation (DBS) can increase generalized arousal and spontaneous motor activity in this mouse model of TBI. This arousal increase is input-pattern-dependent, as changing the temporal pattern of DBS can modulate its effect on motor activity. Finally, an extensive examination of mouse behavioral capacities, looking for deficits in this model of TBI, suggest that the strongest effects of TBI in this model are found in the initiation of any kind of movement.
|
|
| 25. |
- Teles, Magda C, et al.
(författare)
-
Social modulation of brain monoamine levels in zebrafish
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328 .- 1872-7549. ; 253, s. 17-24
-
Tidskriftsartikel (refereegranskat)abstract
- In social species animals tend to adjust their social behaviour according to the available social information in the group, in order to optimize and improve their one social status. This changing environment requires for rapid and transient behavioural changes that relies primarily on biochemical switching of existing neural networks. Monoamines and neuropeptides are the two major candidates to mediate these changes in brain states underlying socially behavioural flexibility. In the current study we used zebrafish (Danio rerio) males to study the effects of acute social interactions on rapid regional changes in brain levels of monoamines (serotonin and dopamine). A behavioural paradigm under which male zebrafish consistently express fighting behaviour was used to investigate the effects of different social experiences: winning the interaction, losing the interaction, or fighting an unsolved interaction (mirror image). We found that serotonergic activity is significantly higher in the telencephalon of winners and in the optic tectum of losers, and no significant changes were observed in mirror fighters suggesting that serotonergic activity is differentially regulated in different brain regions by social interactions. Dopaminergic activity it was also significantly higher in the telencephalon of winners which may be representative of social reward. Together our data suggests that acute social interactions elicit rapid and differential changes in serotonergic and dopaminergic activity across different brain regions.
|
|
| 26. |
|
|
| 27. |
|
|
| 28. |
- Bay-Richter, Cecilie, et al.
(författare)
-
Changes in behaviour and cytokine expression upon a peripheral immune challenge
- 2011
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328. ; 222:1, s. 193-199
-
Tidskriftsartikel (refereegranskat)abstract
- Depression is frequently associated with inflammation. Animal studies have shown that peripheral inflammation induces depressive-like behaviour, but the underlying mechanisms remain unclear. A distinction between sickness- and depressive-like behaviour has been proposed. We hypothesize that the behavioural distinction is due to changes in the central production of immune mediators. As a model of peripheral inflammation, we administered lipopolysaccharide (LPS) intraperitoneally daily for 4 days in rats. The effect of LPS on sickness- and depressive-like behaviour was assessed. We examined protein levels and mRNA expression of cytokines and cyclooxygenase (COX) enzymes in serum, cerebrospinal fluid (CSF) and specific brain regions. Two hours post-LPS, the rats displayed sickness behaviour and cytokine levels were elevated in both serum and CSF. This was paralleled by specific alterations of mRNA transcription of IL-1β, IL-6 and TNF-α in frontal cortex, hippocampus and striatum. Twenty-four hours post-LPS the rats showed depressive-like behaviour and peripheral cytokine levels were back close to baseline. In contrast, the central transcription of IL-1β mRNA had increased even further, as well as IL-1β CSF levels. IL-6 and TNF-α transcription was unaltered compared to controls. COX enzymes were downregulated in the hippocampus during sickness behaviour and unaltered during depressive-like behaviour. Our results show for the first time that a peripheral immune challenge induces a region specific transcription of cytokines and COX-enzymes in the brain, at time-points corresponding to behavioural sickness and depression. When the peripheral inflammation and sickness behaviour had ceased, a production of proinflammatory cytokines remained within the brain parenchyma.
|
|
| 29. |
- Lindgren, Hanna, et al.
(författare)
-
Nigral 6-hydroxydopamine lesion impairs performance in a lateralised choice reaction time task-Impact of training and task parameters
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328. ; 266, s. 207-215
-
Tidskriftsartikel (refereegranskat)abstract
- Unilateral intrastriatal and intra-medial forebrain bundle injections of 6-OHDA impair the performance in a lateralised choice reaction time task. However, the extent and pattern of deficits after nigral 6-OHDA injections is less well studied, as well as the impact of training regime or the modification of various task parameters. The nigral 6-OHDA lesion resulted in impaired response accuracy and an increased time to react to and execute the response on the side contralateral to the lesion as compared to sham-lesioned controls. Pre-training of the rats on the task prior to the lesion resulted in slightly faster reaction times as well as a reduced number of preservative panel presses compared to when rats were trained after the 6-OHDA injection. When the rat had to perform a longer sustained nose poke before responding to the lateralised stimuli, the number of useable trials was reduced in both controls and 6-OHDA rats as a result of an increased number of premature withdrawals from the centre hole. This study demonstrates that rats with a nigral 6-OHDA lesion display several distinct deficits in this operant task, which are similar to those seen after striatal and bundle 6-OHDA injections. In addition, by combining pre-training with the use of a short set of holds, improved sensitivity of this task can be achieved. This improvement in sensitivity may be of advantage when exploring new therapeutic interventions for PD, where subtle but relevant changes in performance may arise. (C) 2014 Elsevier B.V. All rights reserved.
|
|
| 30. |
- Madinier, Alexandre, et al.
(författare)
-
Impact of estrogen receptor beta activation on functional recovery after experimental stroke.
- 2014
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328. ; 261, s. 282-288
-
Tidskriftsartikel (refereegranskat)abstract
- Acute treatment with 17β-estradiol provides effective neuroprotection during the first days after acute brain injury, however, effects of chronic activation of estrogen receptor beta (ERβ) on recovery of function after experimental stroke have not been investigated. The present study, therefore, was conducted to test if delayed treatment with the specific ERβ ligand 4-(1-phenyl-cyclohexyl)-phenol (AC-131) improves recovery of lost neurological function after permanent focal stroke induced by photothrombosis in adult Sprague-Dawley rats. Treatment was initiated on day 2 after photothrombosis and AC-131 (1, 10, and 50mg/kg) was administered by daily subcutaneous injections for 14 days. On day 2, 4, 6, 8, 11, 14, and 17 after photothrombosis, functional deficits were assessed by the paw placement test, a standardized grip strength test and an adhesive removal test. Daily treatment with AC-131 significantly improved test scores in all three behavioral tests. Importantly, improved function was not associated with a decrease in infarct volume on day 17 after stroke onset. Our results suggest that increased activity of the ERβ is involved in mechanisms of stroke recovery.
|
|
| 31. |
- Mulcahy, Padraig, et al.
(författare)
-
The behavioural and neuropathological impact of intranigral AAV-alpha-synuclein is exacerbated by systemic infusion of the Parkinson's disease-associated pesticide, rotenone, in rats
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328. ; 243, s. 6-15
-
Tidskriftsartikel (refereegranskat)abstract
- Despite the widely held belief that Parkinson's disease is caused by both underlying genetics and exposure to environmental risk factors, it is still widely modelled in preclinical models using a single genetic or neurotoxic insult. This single-insult approach has resulted in a variety of models that are limited with respect to their aetiological, construct, face and/or predictive validity. Thus, the aim of the current study was to investigate the interplay between genes and the environment as an alternative approach to modelling Parkinson's disease. To do so, rats underwent stereotaxic surgery for unilateral delivery of the Parkinson's disease-associated gene, alpha-synuclein, into the substantia nigra (using AAV vectors). This was followed 13 weeks later by subcutaneous implantation of an osmotic minipump delivering the Parkinson's disease-associated pesticide, rotenone (2.5 mg kg(-1) day(-1) for 4 weeks): The effect of the genetic and environmental insults alone or in combination on lateralised motor performance (Corridor, Stepping and Whisker Tests), nigrostriatal integrity (tyrosine hydroxylase immunohistochemistry) and alpha-synucleinopathy (alpha-synuclein immunohistochemistry) was assessed. We found that exposing AAV-alpha-synuclein-treated rats to rotenone led to a model in which the classical Parkinson's disease triad of progressive motor dysfunction, nigrostriatal neurodegeneration and alpha-synucleinopathy was evident. However, delivering rotenone systemically was also associated with bilateral motor dysfunction and loss of body weight. Thus, although we have shown that Parkinson's disease can be modelled in experimental animals by combined exposure to both genetic and environmental risk factors, this approach is limited by systemic toxicity of the pesticide rotenone. Direct intracerebral delivery of rotenone may be more useful in longer-term studies as we have previously shown that it overcomes this limitation. (C) 2013 Elsevier B.V. All rights reserved.
|
|
| 32. |
- Tönnesen, Jan
(författare)
-
Optogenetic cell control in experimental models of neurological disorders
- 2013
-
Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328. ; 255, s. 35-43
-
Forskningsöversikt (refereegranskat)abstract
- The complexity of the brain, in which different neuronal cell types are interspersed and complexly interconnected, has posed a major obstacle in identifying pathophysiological mechanisms underlying prevalent neurological disorders. This is largely based in the inability of classical experimental approaches to target defined neural populations at sufficient temporal and spatial resolution. As a consequence, effective clinical therapies for prevalent neurological disorders are largely lacking. Recently developed optogenetic probes are genetically expressed photosensitive ion channels and pumps that in principal overcome these limitations. Optogenetic probes allow millisecond resolution functional control over selected optogenetically transduced neuronal populations targeted based on promoter activity. This optical cell control scheme has already been applied to answer fundamental questions pertaining to neurological disorders by allowing researchers to experimentally intercept, or induce, pathophysiological neuronal signaling activity in a highly controlled manner. Offering high temporal resolution control over neural activity at high cellular specificity, optogenetic tools constitute a game changer in research aiming at understanding pathophysiological signaling mechanisms in neurological disorders and in developing therapeutic strategies to correct these. In this regard, recent experimental work has provided new insights in underlying mechanisms, as well as preliminary proof-of-principle for optogenetic therapies, of several neurological disorders, including Parkinson's disease, epilepsy and progressive blindness. This review synthesizes experimental work where optogenetic tools have been applied to explore pathologic neural network activity in models of neurological disorders. (C) 2013 Elsevier B.V. All rights reserved.
|
|
