scholarly journals Adolescent male rats exposed to social defeat exhibit altered anxiety behavior and limbic monoamines as adults.

2009 ◽  
Vol 123 (3) ◽  
pp. 564-576 ◽  
Author(s):  
Michael J. Watt ◽  
Andrew R. Burke ◽  
Kenneth J. Renner ◽  
Gina L. Forster
2021 ◽  
Vol 13 ◽  
Author(s):  
Danna Ellner ◽  
Bryana Hallam ◽  
Jude A. Frie ◽  
Hayley H. A. Thorpe ◽  
Muhammad Shoaib ◽  
...  

The endocannabinoid system is responsible for regulating a spectrum of physiological activities and plays a critical role in the developing brain. During adolescence, the endocannabinoid system is particularly sensitive to external insults that may change the brain’s developmental trajectory. Cannabinoid receptor type 2 (CB2R) was initially thought to predominantly function in the peripheral nervous system, but more recent studies have implicated its role in the mesolimbic pathway, a network largely attributed to reward circuitry and reward motivated behavior, which undergoes extensive changes during adolescence. It is therefore important to understand how CB2R modulation during adolescence can impact reward-related behaviors in adulthood. In this study, adolescent male rats (postnatal days 28–41) were exposed to a low or high dose of the CB2R antagonist/inverse agonist SR144528 and Pavlovian autoshaping and instrumental conditional behavioral outcomes were measured in adulthood. SR144528-treated rats had significantly slower acquisition of the autoshaping task, seen by less lever pressing behavior over time [F(2, 19) = 5.964, p = 0.010]. Conversely, there was no effect of adolescent SR144528 exposure on instrumental conditioning. These results suggest that modulation of the CB2R in adolescence differentially impacts reward-learning behaviors in adulthood.


eNeuro ◽  
2021 ◽  
pp. ENEURO.0045-21.2021
Author(s):  
Philip Vassilev ◽  
Andrea Haree Pantoja-Urban ◽  
Michel Giroux ◽  
Dominique Nouel ◽  
Giovanni Hernandez ◽  
...  

2021 ◽  
Vol 15 ◽  
Author(s):  
Omar K. Sial ◽  
Tamara Gnecco ◽  
Astrid M. Cardona-Acosta ◽  
Emily Vieregg ◽  
Ernesto A. Cardoso ◽  
...  

A dramatic increase in the prevalence of major depression and diet-related disorders in adolescents has been observed over several decades, yet the mechanisms underlying this comorbidity have only recently begun to be elucidated. Exposure to western-style diet (WSD), high in both fats (45% kcal) and carbohydrates (35% kcal): e.g., high fat diet (HFD), has been linked to the development of metabolic syndrome-like symptoms and behavioral dysregulation in rodents, as similarly observed in the human condition. Because adolescence is a developmental period highlighted by vulnerability to both stress and poor diet, understanding the mechanism(s) underlying the combined negative effects of WSDs and stress on mood and reward regulation is critical. To this end, adolescent male C57 mice were exposed to vicarious social defeat stress (VSDS), a stress paradigm capable of separating physical (PS) versus psychological/emotional (ES) stress, followed by normal chow (NC), HFD, or a separate control diet high in carbohydrates (same sucrose content as HFD) and low in fat (LFD), while measuring body weight and food intake. Non-stressed control mice exposed to 5 weeks of NC or HFD showed no significant differences in body weight or social interaction. Mice exposed to VSDS (both ES and PS) gain weight rapidly 1 week after initiation of HFD, with the ES-exposed mice showing significantly higher weight gain as compared to the HFD-exposed control mice. These mice also exhibited a reduction in saccharin preference, indicative of anhedonic-like behavior. To further delineate whether high fat was the major contributing factor to these deficits, LFD was introduced. The mice in the VSDS + HFD gained weight more rapidly than the VSDS + LFD group, and though the LFD-exposed mice did not gain weight as rapidly as the HFD-exposed mice, both the VSDS + LFD- and VSDS + HFD-exposed mice exhibited attenuated response to the antidepressant fluoxetine. These data show that diets high in both fats and carbohydrates are responsible for rapid weight gain and reduced reward sensitivity; and that while consumption of diet high in carbohydrate and low in fat does not lead to rapid weight gain, both HFD and LFD exposure after stress leads to reduced responsiveness to antidepressant treatment.


2013 ◽  
Vol 33 (2) ◽  
pp. 203-213 ◽  
Author(s):  
G Han ◽  
L An ◽  
B Yang ◽  
L Si ◽  
T Zhang

The aim of the present study was to investigate whether cognitive behavioral impairment, induced by nicotine in offspring rats, was associated with the alteration of hippocampal short-term potentiation (STP) and long-term potentiation (LTP) and to discuss the potential underlying mechanism. Young adult offspring rats were randomly divided into three groups. The groups include: control group (CC), nicotine group 1 (NC), in which their mothers received nicotine from gestational day 3 (GD3) to GD18, and nicotine group 2 (CN), in which young adult offspring rats received nicotine from postnatal day 42 (PD42) to PD56. Morris water maze (MWM) test was performed and then field excitatory postsynaptic potentials elicited by the stimulation of perforant pathway were recorded in the hippocampal dentate gyrus region. The results of the MWM test showed that learning and memory were impaired by either prenatal or postnatal nicotine exposure. In addition, it was found that there was no statistical difference of the MWM data between both nicotine treatments. In the electrophysiological test, LTP and STP were significantly inhibited in both NC and CN groups in comparison with the CC group. Notably, STP in CN group was also lower than that in the NC group. These findings suggested that both prenatal and postnatal exposure to nicotine induced learning and memory deficits, while the potential mechanism might be different from each other due to their dissimilar impairments of synaptic plasticity.


Author(s):  
Sarieh Shahraki ◽  
Khadijeh Esmaeilpour ◽  
Mohammad Shabani ◽  
Gholamreza Sepehri ◽  
Mohammad Amin Rajizadeh ◽  
...  

Andrologia ◽  
2019 ◽  
Vol 51 (6) ◽  
pp. e13268 ◽  
Author(s):  
Ahmet Yardimci ◽  
Nazife Ulker ◽  
Ozgur Bulmus ◽  
Nalan Kaya ◽  
Neriman Colakoglu ◽  
...  

2011 ◽  
Vol 32 (4) ◽  
pp. 355-361 ◽  
Author(s):  
Wen-Qiang Chen ◽  
Li Yuan ◽  
Rui Xue ◽  
Yun-Feng Li ◽  
Rui-Bin Su ◽  
...  

2018 ◽  
Vol 34 (3) ◽  
pp. 525-537 ◽  
Author(s):  
Katarzyna Kamińska ◽  
Karolina Noworyta-Sokołowska ◽  
Anna Górska ◽  
Joanna Rzemieniec ◽  
Agnieszka Wnuk ◽  
...  

Abstract According to the European Drug Report (2016), the use of synthetic cathinones, such as mephedrone, among young people has rapidly increased in the last years. Studies in humans indicate that psychostimulant drug use in adolescence increases risk of drug abuse in adulthood. Mephedrone by its interaction with transporters for dopamine (DAT) and serotonin (SERT) stimulates their release to the synaptic cleft. In animal studies, high repeated doses of mephedrone given to adolescent but not adult mice or rats induced toxic changes in 5-hydroxytryptamine (5-HT) neurons. The aim of our study was to investigate the effects of mephedrone given in adolescence on brain neurotransmission and possible neuronal injury in adult rats. Adolescent male rats were given mephedrone (5 mg/kg) for 8 days. In vivo microdialysis in adult rats showed an increase in dopamine (DA), 5-HT, and glutamate release in the nucleus accumbens and frontal cortex but not in the striatum in response to challenge dose in animals pretreated with mephedrone in adolescence. The 5-HT and 5-hydroxyindoleacetic acid contents decreased in the striatum and nucleus accumbens while DA turnover rates were decreased in the striatum and nucleus accumbens. The oxidative damage of DNA assessed with the alkaline comet assay was found in the cortex of adult rats. Therefore, the administration of repeated low doses of mephedrone during adolescence does not seem to induce injury to 5-HT and DA neurons. The oxidative stress seems to be responsible for possible damage of cortical cell bodies which causes maladaptive changes in serotonergic and dopaminergic neurons.


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