Ethanol-Induced c-Fos Expression in Catecholamine- and Neuropeptide Y-Producing Neurons in Rat Brainstem

Thiele, Todd E.; Cubero, Inmaculada; Dijk, Gertjan van; Mediavilla, Cristina; Bernstein, Ilene L.

doi:10.1097/00000374-200006000-00009

Cited by 37 publications

(36 citation statements)

References 53 publications

(45 reference statements)

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“…Immunohistochemistry procedures were based on those routinely used in our laboratory (Thiele et al, 1996; Thiele et al, 1997; Thiele et al, 2000; Hayes et al, 2005). Mice were perfused transcardially with 0.1 mM phosphate-buffered saline (PBS; pH7.4) followed by 4% paraformaldehyde in phosphate buffer immediately following ethanol access on day 4 of the final DID cycle or 18-24 h following ethanol access on day 4 of the final DID cycle.…”

Section: Methodsmentioning

confidence: 99%

Corticotropin Releasing Factor Signaling in the Central Amygdala is Recruited during Binge-Like Ethanol Consumption in C57BL/6J Mice

Lowery-Gionta

Navarro²,

Li³

et al. 2012

J. Neurosci.

137

183

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A well-established body of work indicates a crucial role for corticotropin releasing factor (CRF) in neurobiological responses associated with excessive dependence-like ethanol drinking in ethanol vapor exposed rodents. Recent evidence demonstrates a role for CRF in the modulation of binge-like ethanol consumption by non-dependent mice, a behavior which can precede ethanol dependence. The CRF circuitry that is engaged by binge-like ethanol exposure, however, is unknown. Using converging approaches, we provide evidence that, similar to ethanol vapor-induced increases in ethanol intake, CRF signaling in the central nucleus of the amygdala (CeA) is engaged during binge-like ethanol consumption by C57BL/6J mice. Specifically, we found that binge-like consumption of an ethanol solution (20% ethanol v/v) was attenuated by pretreatment with the CRF1R antagonists antalarmin, (4-ethyl-[2,5,6-trimethyl-7-(2,4,6-trimethylphenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yl]amino-1-butanol (LWH-63), and NBI-27914 at doses (30 mg/kg, i.p.) that did not alter non-binge-like ethanol consumption. Binge-like ethanol consumption resulted in significant increases of CRF immunoreactivity in the CeA immediately following ethanol drinking and 18-24 h following ethanol removal and also blocked the ability of CRF to enhance GABAergic transmission in the CeA 18-24 h following ethanol removal. Pretreatment with bilateral injections of antalarmin (1 μg/ 0.5 μl per side) into the CeA, but not the adjacent basolateral amygdala (BLA), significantly attenuated binge-like ethanol consumption. These findings suggest that CRF signaling in the CeA is recruited during excessive ethanol intake, prior to the development of dependence. We hypothesize that plastic changes in CRF signaling develop with repeated binge-like drinking episodes, contributing to the transition to dependence.

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Section: Methodsmentioning

confidence: 99%

Corticotropin Releasing Factor Signaling in the Central Amygdala is Recruited during Binge-Like Ethanol Consumption in C57BL/6J Mice

Lowery-Gionta

Navarro²,

Li³

et al. 2012

J. Neurosci.

137

183

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“…We chose a 2 hour post-injection perfusion time because we have previously found treatment-induced differences in proteins at this time point (Cubero et al, 1999; Cubero et al, 2010; Thiele et al, 2000). Brains were removed and post-fixed in paraformaldehyde for 48 h at 4°C, at which point they were transferred to PBS.…”

Section: Methodsmentioning

confidence: 99%

Adolescent binge-like ethanol exposure reduces basal α-MSH expression in the hypothalamus and the amygdala of adult rats

Lerma-Cabrera

Carvajal

Alcaraz-Iborra

et al. 2013

Pharmacology Biochemistry and Behavior

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Melanocortins (MC) are central peptides that have been implicated in the modulation of ethanol consumption. There is experimental evidence that chronic ethanol exposure reduces α-MSH expression in limbic and hypothalamic brain regions and alters central pro-opiomelanocortin (POMC) mRNA activity in adult rats. Adolescence is a critical developmental period of high vulnerability in which ethanol exposure alters corticotropin releasing factor, neuropeptide Y, substance P and neurokinin neuropeptide activities, all of which have key roles in ethanol consumption. Given the involvement of MC and the endogenous inverse agonist AgRP in ethanol drinking, here we evaluate whether a binge-like pattern of ethanol treatment during adolescence has a relevant impact on basal and/or ethanol-stimulated α-MSH and AgRP activities during adulthood. To this end, adolescent Sprague-Dawley rats (beginning at PND25) were pre-treated with either saline (SP group) or binge-like ethanol exposure (BEP group; 3.0 g/kg given in intraperitoneal (i.p.) injections) of one injection per day over two consecutive days, followed by 2 days without injections, repeated for a total of 8 injections. Following 25 ethanol-free days, we evaluated α-MSH and AgRP immunoreactivity (IR) in the limbic and hypothalamic nuclei of adult rats (PND63) in response to ethanol (1.5 or 3.0 g/kg i.p.) and saline. We found that binge-like ethanol exposure during adolescence significantly reduced basal α-MSH IR in the central nucleus of the amygdala (CeA), the arcuate nucleus (Arc) and the paraventricular nucleus of the hypothalamus (PVN) during adulthood. Additionally, acute ethanol elicited AgRP IR in the Arc. Rats given the adolescent ethanol treatment required higher doses of ethanol than saline-treated rats to express AgRP. In light of previous evidence that endogenous MC and AgRP regulate ethanol intake through MC-receptor signaling, we speculate that the α-MSH and AgRP disturbances induced by binge-like ethanol exposure during adolescence may contribute to excessive ethanol consumption during adulthood.

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“…The whole brain was sliced into 40 mm sections using a Leica VT 1000S vibratome (Leica Microsystems, Nussloch, Germany) and stored in a cryopreserve solution until IR analysis. The sections were cut into three sets and processed with antibodies raised against NPY (Phoenix Pharmaceuticals; 1 : 1000; Thiele et al, 2000), Y1R (Antibody 96106 raised against NPY Y1R was provided by CURE/Digestive Disease Research Center, Antibody/RIA Core, NIH grant DK41301 (Los Angeles, CA); 1 : 25 000; Lyons and Thiele, 2010), or Y2R (Neuromics, Edina, MN; 1 : 4000). Tissues from all experimental groups were run through each assay at the same time for each antibody tested.…”

Section: Effects Of Binge-like Ethanol Drinking On Npy Y1r and Y2r Irmentioning

confidence: 99%

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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Ethanol-Induced c-Fos Expression in Catecholamine- and Neuropeptide Y-Producing Neurons in Rat Brainstem

Cited by 37 publications

References 53 publications

Corticotropin Releasing Factor Signaling in the Central Amygdala is Recruited during Binge-Like Ethanol Consumption in C57BL/6J Mice

Corticotropin Releasing Factor Signaling in the Central Amygdala is Recruited during Binge-Like Ethanol Consumption in C57BL/6J Mice

Adolescent binge-like ethanol exposure reduces basal α-MSH expression in the hypothalamus and the amygdala of adult rats

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

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