Acute social defeat stress increases the conditioned rewarding effects of cocaine in adult but not in adolescent mice

Montagud‐Romero, Sandra; Aguilar, M.A.; Maldonado, Carmen; Manzanedo, Carmen; Miñarro, José; Rodrı́guez-Arias, Marta

doi:10.1016/j.pbb.2015.05.008

Cited by 50 publications

(27 citation statements)

References 116 publications

(119 reference statements)

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“…Defeat also inhibits the extinction of cocaine induced CPP (Montagud-Romero et al , 2015). Finally, social defeat facilitates the reinstatement of cocaine CPP after extinction (Land et al , 2009; Ribeiro Do Couto et al , 2009; Titomanlio et al , 2013; Montagud-Romero et al , 2015). These results indicate that intermittent defeat increases the reward value of cocaine and increases the likelihood that an individual will seek cocaine after a period of abstinence.…”

Section: Effects Of Social Defeat On Drug Seeking Behaviormentioning

confidence: 99%

Stress, sex, and motivated behaviors

Laman-Maharg

Trainor

2016

J of Neuroscience Research

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Stress is a major risk factor for the development of psychiatric disorders, such as depression, and the development of substance use disorder. Although there are important sex differences in the prevalence of these disorders, the majority of preclinical models used to study stress induced disorders use males only. Social defeat stress is a commonly used method to induce stress in an ethologically relevant way, but has only recently begun to be used in female rodents. Using these new female models, recent studies have examined how social defeat stress affects males and females differently at the behavioral, circuit, and molecular levels. This review discusses sex differences in the effects of social defeat stress on social behavior and drug seeking behavior, as well as its impact on the mesolimbic dopamine system and the highly connected region of the bed nucleus of the stria terminalis.

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Section: Effects Of Social Defeat On Drug Seeking Behaviormentioning

confidence: 99%

Stress, sex, and motivated behaviors

Laman-Maharg

Trainor

2016

J of Neuroscience Research

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“…We showed that CUS-ETOH adolescents also displayed lower cross-sensitization, compared to adults. Age-related differences were also observed for different behavioral parameters, such as higher sensitivity in alcohol intake after stress in adults versus adolescents (Spanagel, Noori, & Heilig, 2014) and lower cocaine-induced CPP and corticosterone levels in adolescent mice previously exposed to social defeat stress, in contrast to higher levels in adults (Montagud-Romero et al, 2015). The ontogeny in the HPA axis should be considered as a hypothetical reason for the observed age differences in drug sensitivity, behavioral sensitization, and cross-sensitization to ethanol in adolescents, as adolescent rats are less sensitive to negative feedback control of the HPA axis after stress than adults (Sapolsky, Meaney, & McEwen, 1985).…”

Section: Discussionmentioning

confidence: 88%

Involvement of neuronal nitric oxide synthase in cross-sensitization between chronic unpredictable stress and ethanol in adolescent and adult mice

Santos-Rocha

Rae

Teixeira

et al. 2018

Alcohol

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a b s t r a c tThe peculiar neurochemical profile of the adolescent brain renders it differently susceptible to several stimuli, including stress and/or drug exposure. Among several stress mediators, nitric oxide (NO) has a role in stress responses. We have demonstrated that adolescent mice are less sensitive to ethanolinduced sensitization than adult mice. The present study investigated whether chronic unpredictable stress (CUS) induces behavioral sensitization to ethanol in adolescent and adult Swiss mice, and investigated the influence of Ca 2þ -dependent nitric oxide synthase (NOS) activity in the phenomenon.Adolescent and adult mice were exposed to repeated 1.8 g/kg ethanol or CUS and challenged with saline or ethanol. A neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral sensitization. Both adolescent and adult mice displayed cross-sensitization between CUS and ethanol in adult mice, with adolescents showing a lower degree of sensitization than adults. nNOS inhibition by 7NI reduced both ethanol sensitization and crosssensitization. All age differences in the Ca 2þ -dependent NOS activity in the hippocampus and prefrontal cortex were in the direction of greater activity in adults than in adolescents. Adolescents showed lower sensitivity to cross-sensitization between CUS and ethanol, and the nitric oxide (NO) system seems to have a pivotal role in ethanol-induced behavioral sensitization and cross-sensitization in both adolescent and adult mice.

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“…Many stressors, including social defeat, heat, noise, electric foot shock, and restraint stress cause elevation of circulating CORT levels in mice (Hu et al, 2014; Ito et al, 2015; Jaroenporn et al, 2007; Montagud-Romero et al, 2015; Yamano et al, 2004). Acute stress leads to CRH releases into the pituitary portal circulation and a rapid increase in CRH mRNA and c-fos expression in the PVN (Alexander et al, 1994; Day et al, 2005; Girotti et al, 2006; Imaki et al, 1998; Plotsky, 1988).…”

Section: Discussionmentioning

confidence: 99%

Acute stress diminishes M-current contributing to elevated activity of hypothalamic-pituitary-adrenal axis

et al. 2017

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Acute stress stimulates corticotrophin-releasing hormone (CRH)-expressing neurons in the hypothalamic paraventricular nucleus (PVN), which is an essential component of hypothalamic-pituitary-adrenal (HPA) axis. However, the cellular and molecular mechanisms remain unclear. The M-channel is a voltage-dependent K+ channel involved in stabilizing the neuronal membrane potential and regulating neuronal excitability. In this study, we tested our hypothesis that acute stress suppresses expression of Kv7 channels to stimulate PVN-CRH neurons and the HPA axis. Rat PVN-CRH neurons were identified by expressing enhanced green fluorescent protein driven by Crh promoter. Acute restraint stress attenuated the excitatory effect of Kv7 blocker XE-991 on the firing activity of PVN-CRH neurons and blunted the increase in plasma corticosterone (CORT) levels induced by microinjection of XE-991 into the PVN. Furthermore, acute stress significantly decreased the M-currents in PVN-CRH neurons and reduced PVN expression of Kv7.3 subunit in the membrane. In addition, acute stress significantly increased phosphorylated AMP-activated protein kinase (AMPK) levels in the PVN tissue. Intracerebroventricular injection of the AMPK inhibitor dorsomorphin restored acute stress-induced elevation of CORT levels and reduction of membrane Kv7.3 protein level in the PVN. Dorsomorphin treatment increased the M-currents and reduced the firing activity of PVN-CRH neurons in acutely stressed rats. Collectively, these data suggest that acute stress diminishes Kv7 channels to stimulate PVN-CRH neurons and the HPA axis potentially via increased AMPK activity.

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Acute social defeat stress increases the conditioned rewarding effects of cocaine in adult but not in adolescent mice

Cited by 50 publications

References 116 publications

Stress, sex, and motivated behaviors

Stress, sex, and motivated behaviors

Involvement of neuronal nitric oxide synthase in cross-sensitization between chronic unpredictable stress and ethanol in adolescent and adult mice

Acute stress diminishes M-current contributing to elevated activity of hypothalamic-pituitary-adrenal axis

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