Corticotropin-releasing factor mediates the dysphoria-like state associated with alcohol withdrawal in rats

Bruijnzeel, Adrie W.; Small, Elysia; Pasek, Tim M.; Yamada, Hidetaka

doi:10.1016/j.bbr.2010.02.043

Cited by 30 publications

(17 citation statements)

References 25 publications

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“…CRF is critically involved in the anhedonia associated with acute ethanol intoxication and ethanol withdrawal (Valdez et al, 2002). Specifically, CRF administration induces ICSS threshold elevations (Macey et al, 2000) and threshold elevations during ethanol withdrawal are reduced by a CRF antagonist (Bruijnzeel et al, 2010). Notably, adolescent ethanol exposure attenuates the adult CRF response to ethanol (Allen et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Boutros

Semenova

Markou

2014

European Neuropsychopharmacology

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Adolescent alcohol use may interfere with neurodevelopment, increasing the likelihood of adult alcohol use disorders (AUDs). We investigated whether adolescent intermittent ethanol (AIE) exposure alters the adult reward response to ethanol. Adolescent rats were administered ethanol once (moderate exposure; Cohort 1) or three times per day (severe exposure; Cohort 2) in a 2 days on/2 days off pattern. In adulthood, subjects responded for electrical stimulation directed at the posterior lateral hypothalamus in a discrete-trials intracranial self-stimulation (ICSS) procedure that provides current-intensity thresholds as a measure of brain reward function. The effects of ethanol administration and withdrawal were assessed. Control rats showed dose-dependent threshold elevations after acute ethanol, indicating reward deficits. A majority of moderately AIE-exposed rats (Cohort 1) showed threshold lowering after ethanol, suggesting ethanol-induced reward enhancement in this sub-set of rats. Rats exposed to severe AIE (Cohort 2) showed no threshold elevation or lowering, suggesting blunted affective ethanol response. Daily ethanol induced threshold elevations 24 h after administration in control but not in either group of AIE-exposed rats, suggesting decreased sensitivity to the negative affective state of ethanol withdrawal. Withdrawal from a 4-day ethanol binge produced robust and enduring threshold elevations in all rats, although threshold elevations were diminished in rats exposed to severe AIE. These results indicate that AIE exposure diminished reward deficits associated with ethanol intoxication and withdrawal and may have increased ethanol-induced reward enhancement in a sub-set of rats. In humans, enhanced ethanol reward accompanied by reduced withdrawal severity may contribute to the development of AUDs.

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Section: Discussionmentioning

confidence: 99%

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Boutros

Semenova

Markou

2014

European Neuropsychopharmacology

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“…CRF exaggerates ethanol self-administration, withdrawal-induced dysphoria, and reinstatement (Bruijnzeel et al, 2010; Eisenhardt et al, 2015; Finn et al, 2007; Le et al, 2000; Sarnyai et al, 2001; Sparta et al, 2009; Valdez et al, 2002; Zorrilla et al, 2014; Zorrilla et al, 2001). The CRF system can alter mitochondrial function, thus stress-induced alcohol intake may be mediated by CRF at mitochondria (Manoli et al, 2007).…”

Section: Sudmentioning

confidence: 99%

Sex-dependent mental illnesses and mitochondria

Shimamoto

Rappeneau

2017

Schizophrenia Research

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The prevalence of some mental illnesses, including major depression, anxiety-, trauma-, and stress-related disorders, some substance use disorders, and later onset of schizophrenia, is higher in women than men. While the higher prevalence in women could simply be explained by socioeconomic determinants, such as income, social status, or cultural background, extensive studies show sex differences in biological, pharmacokinetic, and pharmacological factors contribute to females’ vulnerability to these mental illnesses. In this review, we focus on estrogens, chronic stress, and neurotoxicity from behavioral, pharmacological, biological, and molecular perspectives to delineate the sex differences in these mental illnesses. Particularly, we investigate a possible role of mitochondrial function, including biosynthesis, bioenergetics, and signaling, on mediating the sex differences in psychiatric disorders.

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“…Furthermore, the aversive state of opiate withdrawal and the decreased brain reward function associated with nicotine withdrawal are both CRF 1 receptor-dependent (Contarino and Papaleo, 2005;Stinus et al, 2005;Bruijnzeel et al, 2007;Bruijnzeel et al, 2009;Bruijnzeel et al, 2012;Garcia-Carmona et al, 2012). Likewise, intracerebroventricular administration of a nonselective CRF 1/2 antagonist ameliorated the decreased brain reward function resulting from ethanol withdrawal (Bruijnzeel et al, 2010). Supporting the motivational significance of these effects for addiction, systemic injections of small-molecule CRF 1 antagonists reduced the increased alcohol intake of dependent or postdependent rodents (Sabino et al, 2006;Chu et al, 2007;Funk et al, 2007;Gehlert et al, 2007;Gilpin et al, 2008;Richardson et al, 2008) as well as the increased intravenous self-administration of cocaine (Specio et al, 2008), nicotine (George et al, 2007), and heroin (Greenwell et al, 2009) in rats with a history of extended access to the drug of abuse.…”

Section: Introductionmentioning

confidence: 99%

Corticotropin releasing factor: A key role in the neurobiology of addiction

Zorrilla

Logrip

Koob

2014

Frontiers in Neuroendocrinology

219

130

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Drug addiction is a chronically relapsing disorder characterized by loss of control over intake and dysregulation of stress-related brain emotional systems. Since the discovery by Wylie Vale and his colleagues of corticotropin-releasing factor (CRF) and the structurally-related urocortins, CRF systems have emerged as mediators of the body’s response to stress. Relatedly, CRF systems have a prominent role in driving addiction via actions in the central extended amygdala, producing anxiety-like behavior, reward deficits, excessive, compulsive-like drug self-administration and stress-induced reinstatement of drug seeking. CRF neuron activation in the medial prefrontal cortex may also contribute to the loss of control. Polymorphisms in CRF system molecules are associated with drug use phenotypes in humans, often in interaction with stress history. Drug discovery efforts have yielded brain-penetrant CRF1 antagonists with activity in preclinical models of addiction.. The results support the hypothesis that brain CRF-CRF1 systems contribute to the etiology and maintenance of addiction.

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Corticotropin-releasing factor mediates the dysphoria-like state associated with alcohol withdrawal in rats

Cited by 30 publications

References 25 publications

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Sex-dependent mental illnesses and mitochondria

Corticotropin releasing factor: A key role in the neurobiology of addiction

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