scholarly journals Clozapine impact on FosB/ΔFosB expression in stress preconditioned rats: response to a novel stressor

2019 ◽  
Vol 53 (2) ◽  
pp. 83-92
Author(s):  
Jana Osacka ◽  
Lubica Horvathova ◽  
Alena Cernackova ◽  
Alexander Kiss
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Medial Prefrontal Cortex ◽  
Acute Stress ◽  
Chronic Mild Stress ◽  
Brain Regions ◽  
Prolonged Treatment ◽  
Mild Stress ◽  
Nucleus Accumbens Shell ◽  
The Individual

AbstractObjective. Prolonged treatment with neuroleptics has been shown to induce FosB/ΔFosB expression in several brain regions including the medial prefrontal cortex, dorsomedial and dorsolateral striatum, ventrolateral and dorsolateral septum, nucleus accumbens shell and core, and the hypothalamic paraventricular nucleus (PVN). Some of these regions are known to be also stress responsive. This study was designed to determine whether repeated clozapine (CLZ) administration for 7 consecutive days to Wistar rats may modify FosB/ΔFosB expression in the above-mentioned brain areas induced by acute stress or novel stressor that followed 13-day chronic mild stress preconditioning.Methods. Following experimental groups were used: unstressed animals treated with vehicle/ CLZ for 7 days; 7-day vehicle/CLZ-treated animals on the last day exposed to acute stress – forced swimming (FSW); and animals preconditioned with stress for 13 days treated from the 8th day with vehicle/CLZ and on the 14th day exposed to novel stress – FSW.Results. In the unstressed animals CLZ markedly increased FosB/ΔFosB immunoreactivity in the ventrolateral septum and PVN. FSW elevated FosB/ΔFosB expression in the medial prefrontal cortex, striatum, and septum. CLZ markedly potentiated the effect of the FSW on FosB/ΔFosB expression in the PVN, but suppressed it in the dorsomedial striatum. Novel stress with stress preconditioning increased FosB/ΔFosB immunoreactivity in the prefrontal cortex, striatum, ventrolateral septum, and the PVN. In the nucleus accumbens the effect of the novel stressor was potentiated by CLZ.Conclusion. Our data indicate that CLZ may modulate the acute as well as novel stress effects on FosB/ΔFosB expression but its effect differs within the individual brain regions.

Circadian disruption in mice through chronic jetlag-like conditions modulates molecular profiles of cancer in nucleus accumbens and prefrontal cortex

2021 ◽  
Author(s):  
Suliman Khan ◽  
V Wee Yong ◽  
Mengzhou Xue
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Pet Imaging ◽  
Biological Rhythms ◽  
Brain Regions ◽  
Molecular Signature ◽  
Environmental Light ◽  
Positron Emission ◽  
The Individual ◽  
Risk Of Cancer

Abstract Biological rhythms regulate physiological activities. Shiftwork disrupts normal circadian rhythms and may increase the risk of cancer through unknown mechanisms. To mimic environmental light/dark changes encountered by shift workers, a protocol called “chronic jet lag (CJL)” induced by repeatedly shifting light-dark cycles has been used. Here, we subjected mice to CJL by advancing light–dark cycle by 6 hours every 2 days, and conducted RNA sequencing to analyze the expression profile and molecular signature in the brain areas of prefrontal cortex and nucleus accumbens. We also performed positron emission tomography (PET) imaging to monitor changes related to glucose metabolism in brain. Our results reveal systematic reprogramming of gene expression associated with cancer related pathways and metabolic pathways in prefrontal cortex and nucleus accumbens. PET imaging indicates that glucose uptake level was significantly reduced in whole brain as well as the individual brain regions. Moreover, qPCR analysis describes that the expression levels of cancer related genes were altered in prefrontal cortex and nucleus accumbens. Overall, these results suggest a molecular and metabolic link with CJL mediated cancer risk, and generate hypotheses on how CJL increases the susceptibility to cancer.

The galanin receptor-3 antagonist, SNAP 37889, inhibits cue-induced reinstatement of alcohol-seeking and increases c-Fos expression in the nucleus accumbens shell of alcohol-preferring rats

2018 ◽  
Vol 32 (8) ◽  
pp. 911-921 ◽  
Author(s):  
Kira-Elise Wilson ◽  
Sigrid Limburg ◽  
Melissa K Duggan ◽  
Adam J Lawther ◽  
Spencer J Williams ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Medial Prefrontal Cortex ◽  
Dopamine Neurons ◽  
Nucleus Accumbens Shell ◽  
Nucleus Accumbens Core ◽  
Fos Protein ◽  
Fos Expression ◽  
Dual Label ◽  
Alcohol Seeking

Introduction: This study aimed to investigate the effects of the galanin-3 receptor antagonist, SNAP 37889, on c-Fos protein expression after cue-induced reinstatement of alcohol-seeking in the brains of alcohol-preferring rats. Methods: Eighteen alcohol-preferring rats were trained to self-administer 10% v/v ethanol in the presence of response-contingent cues, which was followed by extinction. Rats were then treated with SNAP 37889 (30 mg/kg, i.p.) or vehicle, before being tested for cue-induced reinstatement. Administration of SNAP 37889 reduced cue-induced reinstatement of ethanol-seeking behaviour. To examine the effect of SNAP 37889 and cue-induced reinstatement on neuronal activation, c-Fos expression was measured in subregions of the medial prefrontal cortex and nucleus accumbens. Results: SNAP 37889 administration increased c-Fos immunoreactivity in the nucleus accumbens shell, but was without effect in the nucleus accumbens core and the medial prefrontal cortex. Dual-label Fos/tyrosine hydroxylase immunohistochemistry was used to examine the effects of SNAP 37889 on dopamine neurons in the ventral tegmental area; however, no differences between SNAP 37889 and vehicle-treated rats were found. Conclusions: These data support previous findings of galanin-3 receptor involvement in cue-induced reinstatement of alcohol-seeking behaviour, and provide novel evidence that the ability of galanin-3 receptor antagonism to attenuate cue-induced reinstatement relates to activation of the nucleus accumbens shell.

scholarly journals Identification of a stress-sensitive anorexigenic neurocircuit from medial prefrontal cortex to lateral hypothalamus in humans and mice

2021 ◽  
Author(s):  
Rachel E Clarke ◽  
Katharina Voigt ◽  
Romana Stark ◽  
Urvi Bharania ◽  
Harry Dempsey ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Food Intake ◽  
Medial Prefrontal Cortex ◽  
Lateral Hypothalamus ◽  
Acute Stress ◽  
Mild Stress ◽  
Potential Threat ◽  
Reward Seeking ◽  
Neural Network Dynamics ◽  
Predictive Assessment

AbstractAnimal models that examine neural circuits controlling food intake often lack translational relevance. To address this limitation, we identified neural network dynamics related to homeostatic state and BMI in humans. This approach predicted a novel pathway projecting from the medial prefrontal cortex (mPFC) to the lateral hypothalamus (LH) in humans. We then dissected the mechanistic underpinnings of this human-relevant mPFC-LH circuit in mice. Chemogenetic or optogenetic activation of the mPFC-LH pathway in mice suppressed food intake and motivated sucrose-seeking. Fibre photometry demonstrated this pathway was active in response to acute stress or prior to novel environment or object exposure, suggesting a role in the predictive assessment of potential threat. Food consumption suppressed mPFC-LH neuronal activity, independent of metabolic state or palatability. Finally, inhibition of this circuit increased feeding and motivated behaviour under mild stress and chronic ablation caused weight gain. These studies identify the mPFC-LH as a novel stress-sensitive anorexigenic neural pathway involved in the cortical control of food intake and motivated reward-seeking.

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