Neuropeptide y (NPY) in the central nucleus of the amygdala (CeA) does not affect ethanol-reinforced responding in binge-drinking, nondependent rats

Angela N. Henderson, Cristine L. Czachowski

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The central nucleus of the amygdala (CeA) has been implicated as having a significant role in mediating alcohol-drinking behavior. Neuropeptide Y (NPY) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate ethanol intake, particularly when administered into the CeA. Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of NPY is contingent upon genetic background and/or prior history of ethanol dependence in rats. However, studies looking at the effects of NPY in nonselected animals lacking a history of ethanol dependence have two factors that could impact the interpretation of the results: ethanol history/selection AND relatively low baseline ethanol intakes as compared to ethanol-dependent and/or genetically selected controls. The purpose of the present study was to generate higher baseline ethanol intakes upon which to examine the effects of NPY on ethanol and sucrose drinking in nonselected rats using a binge drinking model. Long Evans rats were trained to complete a single response requirement resulting in access to either 2% sucrose (Sucrose Group) or 2% sucrose/10% ethanol (Ethanol Group) for a 20-min drinking session. On treatment days, rats were bilaterally microinjected into the CeA with aCSF or one of three doses of NPY (0.25 μg, 0.50 μg, or 1.00 μg/.5 μL). Subjects in the Ethanol Group were consuming an average of 1.2 g/kg of ethanol (yielding BELs of ~ 90 mg%) during the 20 min access period following aCSF treatments. The results revealed that NPY had no effect on either sucrose or ethanol consumption or on appetitive responding (latency to respond). Overall, the findings indicate that even a history of binge-like ethanol consumption is not sufficient to recruit CeA NPY activity, and are consistent with previous studies showing that the role of NPY in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol dependence.

Original languageEnglish
Pages (from-to)8-13
Number of pages6
JournalPharmacology Biochemistry and Behavior
Volume101
Issue number1
DOIs
StatePublished - Mar 2012

Fingerprint

Binge Drinking
Neuropeptides
Rats
Ethanol
Sucrose
Central Amygdaloid Nucleus
Drinking
Drinking Behavior
Long Evans Rats
Aptitude
Neuropeptide Y

Keywords

  • Central nucleus of the amygdala
  • Ethanol consumption
  • Neuropeptide Y
  • Sipper-tube model

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Pharmacology
  • Toxicology
  • Behavioral Neuroscience
  • Biological Psychiatry

Cite this

Neuropeptide y (NPY) in the central nucleus of the amygdala (CeA) does not affect ethanol-reinforced responding in binge-drinking, nondependent rats. / Henderson, Angela N.; Czachowski, Cristine L.

In: Pharmacology Biochemistry and Behavior, Vol. 101, No. 1, 03.2012, p. 8-13.

Research output: Contribution to journalArticle

@article{8432a0facc4f4995a58fbbbd6472be34,
title = "Neuropeptide y (NPY) in the central nucleus of the amygdala (CeA) does not affect ethanol-reinforced responding in binge-drinking, nondependent rats",
abstract = "The central nucleus of the amygdala (CeA) has been implicated as having a significant role in mediating alcohol-drinking behavior. Neuropeptide Y (NPY) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate ethanol intake, particularly when administered into the CeA. Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of NPY is contingent upon genetic background and/or prior history of ethanol dependence in rats. However, studies looking at the effects of NPY in nonselected animals lacking a history of ethanol dependence have two factors that could impact the interpretation of the results: ethanol history/selection AND relatively low baseline ethanol intakes as compared to ethanol-dependent and/or genetically selected controls. The purpose of the present study was to generate higher baseline ethanol intakes upon which to examine the effects of NPY on ethanol and sucrose drinking in nonselected rats using a binge drinking model. Long Evans rats were trained to complete a single response requirement resulting in access to either 2{\%} sucrose (Sucrose Group) or 2{\%} sucrose/10{\%} ethanol (Ethanol Group) for a 20-min drinking session. On treatment days, rats were bilaterally microinjected into the CeA with aCSF or one of three doses of NPY (0.25 μg, 0.50 μg, or 1.00 μg/.5 μL). Subjects in the Ethanol Group were consuming an average of 1.2 g/kg of ethanol (yielding BELs of ~ 90 mg{\%}) during the 20 min access period following aCSF treatments. The results revealed that NPY had no effect on either sucrose or ethanol consumption or on appetitive responding (latency to respond). Overall, the findings indicate that even a history of binge-like ethanol consumption is not sufficient to recruit CeA NPY activity, and are consistent with previous studies showing that the role of NPY in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol dependence.",
keywords = "Central nucleus of the amygdala, Ethanol consumption, Neuropeptide Y, Sipper-tube model",
author = "Henderson, {Angela N.} and Czachowski, {Cristine L.}",
year = "2012",
month = "3",
doi = "10.1016/j.pbb.2011.11.008",
language = "English",
volume = "101",
pages = "8--13",
journal = "Pharmacology, Biochemistry and Behavior",
issn = "0091-3057",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Neuropeptide y (NPY) in the central nucleus of the amygdala (CeA) does not affect ethanol-reinforced responding in binge-drinking, nondependent rats

AU - Henderson, Angela N.

AU - Czachowski, Cristine L.

PY - 2012/3

Y1 - 2012/3

N2 - The central nucleus of the amygdala (CeA) has been implicated as having a significant role in mediating alcohol-drinking behavior. Neuropeptide Y (NPY) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate ethanol intake, particularly when administered into the CeA. Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of NPY is contingent upon genetic background and/or prior history of ethanol dependence in rats. However, studies looking at the effects of NPY in nonselected animals lacking a history of ethanol dependence have two factors that could impact the interpretation of the results: ethanol history/selection AND relatively low baseline ethanol intakes as compared to ethanol-dependent and/or genetically selected controls. The purpose of the present study was to generate higher baseline ethanol intakes upon which to examine the effects of NPY on ethanol and sucrose drinking in nonselected rats using a binge drinking model. Long Evans rats were trained to complete a single response requirement resulting in access to either 2% sucrose (Sucrose Group) or 2% sucrose/10% ethanol (Ethanol Group) for a 20-min drinking session. On treatment days, rats were bilaterally microinjected into the CeA with aCSF or one of three doses of NPY (0.25 μg, 0.50 μg, or 1.00 μg/.5 μL). Subjects in the Ethanol Group were consuming an average of 1.2 g/kg of ethanol (yielding BELs of ~ 90 mg%) during the 20 min access period following aCSF treatments. The results revealed that NPY had no effect on either sucrose or ethanol consumption or on appetitive responding (latency to respond). Overall, the findings indicate that even a history of binge-like ethanol consumption is not sufficient to recruit CeA NPY activity, and are consistent with previous studies showing that the role of NPY in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol dependence.

AB - The central nucleus of the amygdala (CeA) has been implicated as having a significant role in mediating alcohol-drinking behavior. Neuropeptide Y (NPY) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate ethanol intake, particularly when administered into the CeA. Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of NPY is contingent upon genetic background and/or prior history of ethanol dependence in rats. However, studies looking at the effects of NPY in nonselected animals lacking a history of ethanol dependence have two factors that could impact the interpretation of the results: ethanol history/selection AND relatively low baseline ethanol intakes as compared to ethanol-dependent and/or genetically selected controls. The purpose of the present study was to generate higher baseline ethanol intakes upon which to examine the effects of NPY on ethanol and sucrose drinking in nonselected rats using a binge drinking model. Long Evans rats were trained to complete a single response requirement resulting in access to either 2% sucrose (Sucrose Group) or 2% sucrose/10% ethanol (Ethanol Group) for a 20-min drinking session. On treatment days, rats were bilaterally microinjected into the CeA with aCSF or one of three doses of NPY (0.25 μg, 0.50 μg, or 1.00 μg/.5 μL). Subjects in the Ethanol Group were consuming an average of 1.2 g/kg of ethanol (yielding BELs of ~ 90 mg%) during the 20 min access period following aCSF treatments. The results revealed that NPY had no effect on either sucrose or ethanol consumption or on appetitive responding (latency to respond). Overall, the findings indicate that even a history of binge-like ethanol consumption is not sufficient to recruit CeA NPY activity, and are consistent with previous studies showing that the role of NPY in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol dependence.

KW - Central nucleus of the amygdala

KW - Ethanol consumption

KW - Neuropeptide Y

KW - Sipper-tube model

UR - http://www.scopus.com/inward/record.url?scp=83255173851&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=83255173851&partnerID=8YFLogxK

U2 - 10.1016/j.pbb.2011.11.008

DO - 10.1016/j.pbb.2011.11.008

M3 - Article

VL - 101

SP - 8

EP - 13

JO - Pharmacology, Biochemistry and Behavior

JF - Pharmacology, Biochemistry and Behavior

SN - 0091-3057

IS - 1

ER -