Blockade of the Corticotropin Releasing Factor Type 1 Receptor Attenuates Elevated Ethanol Drinking Associated With Drinking in the Dark Procedures

Sparta, Dennis R.; Sparrow, Angela M.; Lowery, Emily G.; Fee, Jon R.; Knapp, Darin J.; Thiele, Todd E.

doi:10.1111/j.1530-0277.2007.00575.x

Cited by 93 publications

(130 citation statements)

References 39 publications

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“…We have recently found that corticotropin-releasing factor (CRF) type-1 receptor (CRF1R) antagonists reduce binge-like ethanol intake in C57BL/6J mice but fail to alter nonbinge-like (low level) ethanol intake (Lowery et al, 2010;Sparta et al, 2008). These observations are strikingly similar to evidence showing that CRF1R antagonists protect against excessive dependence-like ethanol drinking in ethanol vapor-exposed rats but fail to alter normal ethanol drinking in nondependent animals (Finn et al, 2007;Funk et al, 2006;Gehlert et al, 2007;Valdez et al, 2002).…”

Section: Introductionsupporting

confidence: 70%

Central Neuropeptide Y Modulates Binge-Like Ethanol Drinking in C57BL/6J Mice via Y1 and Y2 Receptors

Sparrow

Lowery-Gionta

Pleil

et al. 2012

Neuropsychopharmacol

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Frequent binge drinking has been linked to heart disease, high blood pressure, type 2 diabetes, and the development of ethanol dependence. Thus, identifying pharmaceutical targets to treat binge drinking is of paramount importance. Here we employed a mouse model of binge-like ethanol drinking to study the role of neuropeptide Y (NPY). To this end, the present set of studies utilized pharmacological manipulation of NPY signaling, immunoreactivity (IR) mapping of NPY and NPY receptors, and electrophysiological recordings from slice preparations of the amygdala. The results indicated that central infusion of NPY, a NPY Y1 receptor (Y1R) agonist, and a Y2R antagonist significantly blunted binge-like ethanol drinking in C57BL/6J mice (that achieved blood ethanol levels >80 mg/dl in control conditions). Binge-like ethanol drinking reduced NPY and Y1R IR in the central nucleus of the amygdala (CeA), and 24 h of ethanol abstinence after a history of binge-like drinking promoted increases of Y1R and Y2R IR. Electrophysiological recordings of slice preparations from the CeA showed that binge-like ethanol drinking augmented the ability of NPY to inhibit GABAergic transmission. Thus, binge-like ethanol drinking in C57BL/6J mice promoted alterations of NPY signaling in the CeA, and administration of exogenous NPY compounds protected against binge-like drinking. The current data suggest that Y1R agonists and Y2R antagonists may be useful for curbing and/or preventing binge drinking, protecting vulnerable individuals from progressing to the point of ethanol dependence.

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Section: Introductionsupporting

confidence: 70%

Central Neuropeptide Y Modulates Binge-Like Ethanol Drinking in C57BL/6J Mice via Y1 and Y2 Receptors

Sparrow

Lowery-Gionta

Pleil

et al. 2012

Neuropsychopharmacol

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“…After repeated and chronic exposure to alcohol, rats show hyperactive extrahypothalamic CRF activity, as indicated by increases in CRF levels and its receptors in the extended amygdala (Merlo Pich et al, 1995;Olive et al, 2002;Sommer et al, 2008). Systemic or intra-amygdaloid blockade of CRF-R1 attenuates increased alcohol seeking and intake in alcohol-dependent animals (Funk et al, 2006;Gehlert et al, 2007;Sommer et al, 2008;Heilig and Koob, 2007) or in high-alcohol-consuming mice (Sparta et al, 2008). We also recently observed that CP-154,526 microinjected in the DRN reduced alcohol drinking CRF-R1 and 5-HT on alcohol-heightened aggression IM Quadros et al in rats and mice that drank excessively, but not in those animals that showed low-level or moderate alcohol drinking (Hwa et al, 2013).…”

Section: Blockade Of Crf-r1: Systemic Vs Drn Effects On Alcohol-relatmentioning

confidence: 99%

Prevention of Alcohol-Heightened Aggression by CRF-R1 Antagonists in Mice: Critical Role for DRN-PFC Serotonin Pathway

Quadros

Hwa

Shimamoto

et al. 2014

Neuropsychopharmacol

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Alcohol can escalate aggressive behavior in a significant subgroup of rodents, humans, and nonhuman primates. The present study investigated whether blockade of corticotropin-releasing factor receptor type 1 (CRF-R1) could prevent the emergence of alcoholheightened aggression in mice. The serotonin (5-HT) pathway from the dorsal raphe nucleus (DRN) to the medial prefrontal cortex (mPFC) by CRF-R1 was investigated as a possible target for the prevention of alcohol-heightened aggressive behavior. Male CFW mice that reliably exhibited aggressive behaviors after consuming 1 g/kg of alcohol received systemic or intra-DRN administration of CRF-R1 antagonists, CP-154,526 or MTIP, before a confrontation with a male conspecific. Blockade of DRN CRF-R1 receptors with both antagonists significantly reduced only alcohol-heightened aggression, whereas systemic administration reduced both alcohol-heightened and species-typical aggression. Next, a 5-HT1A agonist, 8-OH-DPAT, was coadministered with CP-154,526 into the DRN to temporarily disrupt 5-HT activity. This manipulation abolished the antiaggressive effects of intra-DRN CP-154,526. In the mPFC, in vivo microdialysis revealed that extracellular 5-HT levels were increased in mice that consumed alcohol and were then injected with CP-154,526, both systemically or intra-DRN. Neither alcohol nor CP-154,526 alone affected 5-HT release in the mPFC. The present results suggest the DRN as a critical site for CRF-R1 to modulate alcohol-heightened aggression via action on the serotonergic DRN-PFC pathway.

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“…Ongoing electrophysiological studies reveal that the increased sensitivity of the CeA GABAergic synapses to exogenous application of CRF still persist after one and two weeks of withdrawal from alcohol-vapor exposure (unpublished observations from our lab), suggesting that the neuroadaptive changes associated with chronic alcohol are long lasting. Recent data suggest binge-like alcohol drinking increases CRF 1 signaling in the CeA of C57BL/6J mice , and CRF 1 antagonists reduce binge-like alcohol drinking in non-dependent rodents without affecting non-binge-like alcohol intake (Cippitelli et al, 2012;Lowery et al, 2010;Sparta et al, 2008). The ability of CRF to increase GABAergic transmission in the CeA is blunted in mice with a history of binge-like alcohol drinking , in contrast to the upregulated CRF 1 /CRF signaling observed in the CeA of alcohol-dependent rats (Roberto, Cruz, Gilpin, et al, 2010;Lowery-Gionta et al, 2012) it is suggested that binge alcohol drinking may abolish CRF effects on GABAergic transmission in the CeA via functional downregulation or desensitization of CRF 1 , as seen in the dorsal raphe following stress (Waselus, Nazzaro, Valentino, & Van Bockstaele, 2009).…”

Section: Crf Effects On Synaptic Transmission In the Cea And Alcohol-mentioning

confidence: 99%

Central Amygdala Neuroplasticity in Alcohol Dependence

Roberto

Gilpin

2014

Neurobiology of Alcohol Dependence

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Blockade of the Corticotropin Releasing Factor Type 1 Receptor Attenuates Elevated Ethanol Drinking Associated With Drinking in the Dark Procedures

Cited by 93 publications

References 39 publications

Central Neuropeptide Y Modulates Binge-Like Ethanol Drinking in C57BL/6J Mice via Y1 and Y2 Receptors

Central Neuropeptide Y Modulates Binge-Like Ethanol Drinking in C57BL/6J Mice via Y1 and Y2 Receptors

Prevention of Alcohol-Heightened Aggression by CRF-R1 Antagonists in Mice: Critical Role for DRN-PFC Serotonin Pathway

Central Amygdala Neuroplasticity in Alcohol Dependence

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