Increases in Sucrose Consumption, But Not Ethanol Consumption, Following ICV NPY Administration

Slawecki, Craig J.; Betancourt, Michelle; Walpole, T.; Ehlers, C. L.

doi:10.1016/s0091-3057(00)00215-x

Cited by 64 publications

(41 citation statements)

References 35 publications

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“…Previous studies also support the relationship between decreased CREB and NPY levels and anxiety and alcohol-drinking behaviors (15,16,(36)(37)(38)(39)(40)(41). It has been shown that icv infusions of NPY significantly attenuate the alcohol intake in P rats (53), but not in an unselected stock of rats (54). We reported earlier that CREB-haplodeficient mice have lower levels of NPY throughout the brain, display higher anxiety-like behaviors, and also have higher preference for alcohol (31).…”

Section: Figuresupporting

confidence: 62%

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Pandey¹,

Zhang²,

Roy³

et al. 2005

J. Clin. Invest.

185

178

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We investigated the role of cAMP-responsive element-binding protein (CREB) in genetic predisposition to anxiety and alcohol-drinking behaviors using alcohol-preferring (P) and -nonpreferring (NP) rats. The levels of CREB, phosphorylated CREB, and neuropeptide Y (NPY) were innately lower in the central amygdala (CeA) and medial amygdala (MeA), but not in the basolateral amygdala (BLA), of P rats compared with NP rats. P rats displayed higher baseline anxiety-like behaviors and consumed higher amounts of alcohol compared with NP rats. Ethanol injection or voluntary intake reduced the higher anxiety levels in P rats. Ethanol also increased CREB function in the CeA and MeA, but not in the BLA, of P rats. Infusion of the PKA activator Sp-cAMP or NPY into the CeA decreased the alcohol intake and anxiety-like behaviors of P rats. PKA activator infusion also increased CREB function in the CeA of P rats. On the other hand, ethanol injection or voluntary intake did not produce any changes either in anxiety levels or on CREB function in the amygdaloid structures of NP rats. Interestingly, infusion of the PKA inhibitor Rp-cAMP into the CeA provoked anxiety-like behaviors and increased alcohol intake in NP rats. PKA inhibitor decreased CREB function in the CeA of NP rats. These novel results provide the first evidence to our knowledge that decreased CREB function in the CeA may be operative in maintaining the high anxiety and excessive alcohol-drinking behaviors of P rats.

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Section: Figuresupporting

confidence: 62%

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Pandey¹,

Zhang²,

Roy³

et al. 2005

J. Clin. Invest.

185

178

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“…When access to ethanol is limited to a brief (e.g., 2 hr) period each day, intracerebroventricular (ICV) administration of NPY decreases ethanol intake in P and HAD1 rats (Badia-Elder et al 2001, but does not alter ethanol intake in selectively bred alcoholnonpreferring (NP), low alcohol drinking (LAD1), or unselected Wistar rats (Badia-Elder et al, 2001Katner et al, 2002a;Slawecki et al, 2000). However, ICV-administered NPY does effectively reduce limited-access ethanol intake in Wistar rats if they have a history of chronic intermittent exposure to ethanol vapor (Thorsell et al, 2005a(Thorsell et al, , 2005b.…”

mentioning

confidence: 99%

Neuropeptide Y administration into the amygdala suppresses ethanol drinking in alcohol-preferring (P) rats following multiple deprivations

Gilpin

Stewart

Badia-Elder

2008

Pharmacology Biochemistry and Behavior

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The present experiment examines the effects of NPY administered into the amygdala on ethanol drinking by alcohol-preferring P rats following long-term continuous ethanol access, with and without multiple periods of imposed ethanol abstinence. P rats had access to 15% (v/v) ethanol and water for 11 weeks followed by 2 weeks of ethanol abstinence, re-exposure to ethanol for 2 weeks, 2 more weeks of ethanol abstinence, and a final ethanol re-exposure. Immediately prior to the second ethanol re-exposure, 4 groups of rats received bilateral infusions NPY (0.25, 0.5, 1.0 μg) or artificial cerebrospinal fluid (aCSF) into the amygdala. Two additional groups were given uninterrupted ethanol access and were infused with a single NPY dose (1.0 μg) or aCSF. The highest NPY dose (1.0 μg) suppressed ethanol intake for 24 hrs in rats with a history of ethanol abstinence (i.e. deprivation) periods, but had no effect in rats with a history of continuous ethanol access. Water and food intakes were not altered. These results suggest that the amygdala mediates the suppressive effects of centrally administered NPY on ethanol drinking, and that NPY may block relapse-like drinking by opposing the anxiogenic effects of ethanol abstinence. KeywordsAlcohol-preferring rats; neuropeptide Y; abstinence; deprivation; anxiety; amygdala; allostasis Dysregulation of brain neuropeptide Y (NPY) systems involved in emotionality may mediate both the negative affective state that defines ethanol abstinence and the negative reinforcing effects of ethanol during relapse drinking (Valdez & Koob, 2004). NPY decreases anxiety-like behavior in rats in multiple behavioral assays (Heilig et al., 1989;1992;Broqua et al., 1995;Britton et al., 1997;Sajdyk et al., 1999Sajdyk et al., , 2008. The anxiolytic effects of NPY appear to be mediated by the central nucleus of the amygdala (CeA; Heilig et al., 1993), although a role has also been suggested for the basolateral nucleus of the amygdala (Sajdyk et al., 1999(Sajdyk et al., , 2008. Since there is a body of evidence suggesting that the CeA is involved in the regulation of both Corresponding Author: Nancy E. Badia-Elder, Department of Psychology, IUPUI, 402 N. Blackford Street, LD 124, Indianapolis, IN 46202, Phone:317-278-1815, Fax:317-274-6756, Email: nbadiael@iupui.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Davis, 1992) and ethanol drinking (McBride, 2002), the focus of this investigation was to examine the effects of NPY infusions into the CeA on ethanol intake. NIH Public AccessThe alcohol-preferring (P) and high alcohol drinking (HAD1) lines of r...

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“…Additionally, the effects of NPY on sucrose and food intake were assessed in order to examine the selectivity of NPY on feeding and drinking behaviors. Previous studies have found no effect of lateral ventricle NPY infusion on ethanol intake in Wistar rats (Slawecki et al 2000a;Badia-Elder et al 2001), perhaps due to the widespread diffusion of NPY following lateral ventricle infusion. Therefore, in the present study it was postulated that the injection of NPY into the third ventricle would allow for more selective activation of the PVN.…”

Section: Introductionmentioning

confidence: 81%

“…Previous studies have demonstrated that NPY can increase sucrose consumption (Lynch et al 1993;Slawecki et al 2000a;BadiaElder et al 2001). To determine if NPY would differentially effect sucrose versus ethanol consumption, all rats were given access to 2% sucrose during 25-min drinking sessions.…”

Section: Phase 2: Effects Of Npy On 2% Sucrose Consumptionmentioning

confidence: 94%

Neuropeptide Y administration into the third ventricle does not increase sucrose or ethanol self-administration but does affect the cortical EEG and increases food intake

2002

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These data suggest that NPY administration into the third ventricle preferentially regulates feeding compared to ethanol or sucrose drinking. In addition, since NPY significantly altered the cortical EEG in the absence of effects on ethanol and sucrose consumption, these data may indicate that NPY's cortical EEG effects are more related to its sedative or anxiolytic properties, rather than any effect on consumption.

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Increases in Sucrose Consumption, But Not Ethanol Consumption, Following ICV NPY Administration

Cited by 64 publications

References 35 publications

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Neuropeptide Y administration into the amygdala suppresses ethanol drinking in alcohol-preferring (P) rats following multiple deprivations

Neuropeptide Y administration into the third ventricle does not increase sucrose or ethanol self-administration but does affect the cortical EEG and increases food intake

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