Differential patterns of expression of neuropeptide Y throughout abstinence in outbred Swiss mice classified as susceptible or resistant to ethanol-induced locomotor sensitization

Pauli, Ricardo Fontão de; Coelhoso, Cássia Canha; Tesone-Coelho, Carolina; Linardi, Alessandra; Mello, Luiz E.; Silveira, Dartiu Xavier da; Santos-Junior, Jair Guilherme

doi:10.1016/j.alcohol.2013.11.004

Cited by 2 publications

(1 citation statement)

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“…Ethanol exposure can result in decreased NPY expression in some regions including the central nucleus of the amygdala (CeA), the hippocampus, and the motor cortex [13][14][15][16]. Ethanol withdrawal can produce an opposite effect, with elevated NPY levels reported in the amygdala, frontal cortex, dorsomedial striatum, and hippocampus during withdrawal in mice and rats [13][16][17]. The ethanol metabolite acetaldehyde has also been shown to produce decreases in NPY levels in the hippocampus and nucleus accumbens (NAc) following acute treatment, and increases in these same regions during withdrawal [18].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y response to alcohol is altered in nucleus accumbens of mice selectively bred for drinking to intoxication

Barkley-Levenson

Ryabinin

Crabbe

2016

Behavioural Brain Research

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The High Drinking in the Dark (HDID) mice have been selectively bred for drinking to intoxicating blood alcohol levels and represent a genetic model of risk for binge-like drinking. Presently, little is known about the specific genetic factors that promote excessive intake in these mice. Previous studies have identified neuropeptide Y (NPY) as a potential target for modulating alcohol intake. NPY expression differs in some rodent lines that have been selected for high and low alcohol drinking phenotypes, as well as inbred mouse strains that differ in alcohol preference. Alcohol drinking and alcohol withdrawal also produce differential effects on NPY expression in the brain. Here, we assessed brain NPY protein levels in HDID mice of two replicates of selection and control heterogeneous stock (HS) mice at baseline (water drinking) and after binge-like alcohol drinking to determine whether selection is associated with differences in NPY expression and its sensitivity to alcohol. NPY levels did not differ between HDID and HS mice in any brain region in the water-drinking animals. HS mice showed a reduction in NPY levels in the nucleus accumbens (NAc) – especially in the shell – in ethanol-drinking animals vs. water-drinking controls. However, HDID mice showed a blunted NPY response to alcohol in the NAc core and shell compared to HS mice. These findings suggest that the NPY response to alcohol has been altered by selection for drinking to intoxication in a region-specific manner. Thus, the NPY system may represent a potential target for altering binge-like alcohol drinking in these mice.

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