Effects of scheduled access on ethanol intake by the alcohol-preferring (P) line of rats

Murphy, James M.; Gatto, Gregory J.; Waller, M.B.; McBride, William J.; Lumeng, Lawrence; Li, T.-K.

doi:10.1016/0741-8329(86)90010-8

Cited by 170 publications

(109 citation statements)

References 17 publications

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“…Voluntary consumption by P rats of amounts of ethanol similar to those in the present study produce pharmacologically significant blood ethanol levels, ranging from 50 to 200 mg% (Li et al, 1979;Murphy et al, 1986), and these levels of consumption by P rats produce tolerance to the effects of ethanol (Gatto et al, 1987; and perhaps even dependence (Kampov-Polevoy et al, 2000;Waller et al, 1982). Ethanoldependent animals exhibit a long-lasting negative affective state defined partly by elevated anxiety-like behavior (Valdez et al, 2002;Koob and LeMoal, 1997) that may be attributable to decreased NPY levels in the amygdala during ethanol abstinence (Roy & Pandey, 2002).…”

Section: Discussionsupporting

confidence: 59%

“…More specifically, the orexigenic effects of NPY are mediated by the PVN (Stanley et al, 1985), the sedative effects by the posterior hypothalamic nucleus (Naveilhan et al, 2001), and the CeA mediates the suppressive effects of NPY on anxiety-like behavior (Heilig et al, 1993) and possibly ethanol drinking (Pandey et al, 2005); the effects of NPY on most, if not all, of these behaviors is augmented following periods of ethanol abstinence (Gilpin et al, 2005;Rimondini et al, 2005). Therefore, Voluntary consumption by P rats of amounts of ethanol similar to those in the present study produce pharmacologically significant blood ethanol levels, ranging from 50 to 200 mg% (Li et al, 1979;Murphy et al, 1986), and these levels of consumption by P rats produce tolerance to the effects of ethanol (Gatto et al, 1987; and perhaps even dependence (Kampov-Polevoy et al, 2000;Waller et al, 1982). Ethanoldependent animals exhibit a long-lasting negative affective state defined partly by elevated anxiety-like behavior (Valdez et al, 2002;Koob and LeMoal, 1997) that may be attributable to decreased NPY levels in the amygdala during ethanol abstinence (Roy & Pandey, 2002).…”

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confidence: 56%

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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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Section: Discussionsupporting

confidence: 59%

supporting

confidence: 56%

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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“…Following the third deprivation period, rats initially deprived for 5 weeks consumed 15.3 ml, which resulted in an average ETOH intake of 3.8 g/kg. ETOH intakes by P rats under 1-h limited access conditions were 1.3 g/kg and equivalent to the amount consumed by P rats in the present operant studies; this intake produced blood alcohol concentrations of 76 7 13 mg% (Murphy et al, 1986). Therefore, blood alcohol concentrations following the third deprivation could be approaching 200 mg%.…”

Section: Discussionmentioning

confidence: 44%

Effects of Repeated Alcohol Deprivations on Operant Ethanol Self-Administration by Alcohol-Preferring (P) Rats

Rodd

Bell

Kuc

et al. 2003

Neuropsychopharmacol

100

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We reported that repeated alcohol deprivations prolonged the expression of an alcohol-deprivation effect (ADE) under 24-h freechoice alcohol-drinking access and that the duration of the initial deprivation period had a positive effect of prolonging the duration of the ADE. In the present study, operant techniques (including progressive ratio measures) were used to examine the effects of initial deprivation length and number of deprivation cycles on the magnitude and duration of the ADE in alcohol-preferring (P) rats to test the hypothesis that repeated deprivations can increase the reinforcing effects of ethanol (ETOH). Adult male P rats were trained in two-lever operant chambers to self-administer 15% ETOH (v/v) on a fixed-ratio 5 (FR-5) and water on a FR-1 schedule of reinforcement in daily 1-h sessions. Following 6 weeks of daily 1-h sessions, the P rats were randomly assigned to one of four groups (n ¼ 10/group): nondeprived or deprived of alcohol for 2, 5, or 8 weeks. Following this initial period, the deprived groups were given 15% ETOH again in the operant chambers for a 2-week period, following which they were deprived again for 2 weeks (all three deprived groups). Following the fourth deprivation, the rats underwent a progressive ratio test to determine the breakpoints (FR values) for the nondeprived and the deprived groups. Repeated deprivations increased both the magnitude and duration of the ADE as indicated by increased responding on the ETOH lever. However, the length of the initial deprivation had little effect on expression of the ADE except following the first deprivation, where an ADE was not observed for the 8-week group. Breakpoint values for responding on the ETOH lever for all three deprived groups were two-fold higher than the value for the nondeprived group. The results suggest that repeated cycles of alcohol deprivation and alcohol access increased the reinforcing effects of ETOH in the P rats.

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“…In vitro studies indicated that 45-225 mg% EtOH could generate up to 4 nmol/mg tissue wet wt/h of ACD (approximately 4 mM ACD). These brain EtOH concentrations could be attained by P rats under a variety of self-administration conditions (Murphy et al, 1986;Rodd-Henricks et al, 2001;Waller et al, 1984), and produce brain levels of ACD that are within a range that is reinforcing ( Figure 2). P rats learn to discriminate the active from the inactive lever by the second acquisition session for either EtOH, at concentrations greater than 50 mg%, or ACD, at concentrations greater than 3 mM (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

Regional Heterogeneity for the Intracranial Self-Administration of Ethanol and Acetaldehyde within the Ventral Tegmental Area of Alcohol-Preferring (P) Rats: Involvement of Dopamine and Serotonin

Rodd

Bell

Zhang

et al. 2004

Neuropsychopharmacol

138

175

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The meso-limbic dopamine (DA) system has an important role in regulating alcohol drinking. Previous findings from our laboratory indicated that Wistar rats self-administered ethanol (EtOH) directly into the posterior, but not anterior, ventral tegmental area (VTA), and that coadministration of a DA D 2,3 receptor agonist or a serotonin-3 (5-HT 3 ) receptor antagonist blocked EtOH self-administration. In addition, we reported that alcohol-preferring (P) rats self-administered acetaldehyde (ACD), the first metabolite of EtOH, into the posterior VTA. The objectives of this study were to compare the reinforcing effects of EtOH and ACD within the VTA of P rats to examine the possibility that the reinforcing effects of EtOH within the VTA may be mediated by its conversion to ACD. Adult female P rats were stereotaxically implanted with guide cannulae aimed at either the posterior or anterior VTA. At 1 week after surgery, rats were placed in standard two-lever (active and inactive) experimental chambers for a total of seven to eight sessions. The 4-h sessions were conducted every other day. The results indicated that (a) 75-300 mg% (17-66 mM) EtOH and 6-90 mM ACD were self-administered into the posterior, but not anterior, VTA; (b) the self-administration of 150 mg% EtOH was not altered by coinfusion of a catalase inhibitor; (c) coadministration of the D 2/3 agonist quinpirole (100 mM) blocked the self-infusions of 150 mg% EtOH and 23 mM ACD into the posterior VTA; and (d) coadministration of 200 mM ICS205,930 (5-HT 3 receptor antagonist) prevented the self-infusion of 150 mg% EtOH, whereas concentrations of ICS 205,930 up to 400 mM had no effect on the self-infusion of 23 mM ACD into the posterior VTA. Overall, the results of this study indicate that EtOH and ACD can independently produce reinforcing effects within the posterior VTA, and that activation of DA neurons mediates these effects. Furthermore, activation of 5-HT 3 receptors within the posterior VTA is involved in the self-infusion of EtOH, but not ACD.

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Effects of scheduled access on ethanol intake by the alcohol-preferring (P) line of rats

Cited by 170 publications

References 17 publications

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

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

Effects of Repeated Alcohol Deprivations on Operant Ethanol Self-Administration by Alcohol-Preferring (P) Rats

Regional Heterogeneity for the Intracranial Self-Administration of Ethanol and Acetaldehyde within the Ventral Tegmental Area of Alcohol-Preferring (P) Rats: Involvement of Dopamine and Serotonin

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