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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Henderson, Angela N. Czachowski, Cristine L.
Description	Country affiliation: United States Author Affiliation: Henderson AN ( Department of Psychology, Purdue School of Science, Indiana University-Purdue University Indianapolis: 402 North Blackford Street, LD 124, Indianapolis, IN 46202, United States.)
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 (0.25µg, 0.50µg, or 1.00µg/.5µL). Subjects in the Ethanol Group were consuming an average of 1.2g/kg of ethanol (yielding BELs of ~90mg%) during the 20min 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.
File Format	HTM / HTML
ISSN	00913057
e-ISSN	18735177
DOI	10.1016/j.pbb.2011.11.008
Journal	Pharmacology Biochemistry and Behavior
Issue Number	1
Volume Number	101
Language	English
Publisher	Elsevier
Publisher Date	2012-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Behavioral Sciences Discipline Biochemistry Discipline Pharmacology Alcohol Drinking Psychology Amygdala Physiology Appetite Stimulants Pharmacology Central Nervous System Depressants Ethanol Neuropeptide Y Genetics Anatomy & Histology Animals Administration & Dosage Blood Conditioning, Operant Drug Effects Microinjections Rats, Long-evans Reinforcement Schedule Stereotaxic Techniques Sucrose Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Biological Psychiatry Behavioral Neuroscience Biochemistry Clinical Biochemistry Toxicology Pharmacology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

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

Neuropeptide Y in the central nucleus of the amygdala suppresses dependence-induced increases in alcohol drinking.

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

A 3-day exposure to 10% ethanol with 10% sucrose successfully initiates ethanol self-administration.

Relationship between ethanol and sucrose self-administration and schedule-induced polydipsia.

Ethanol-mediated operant learning in the infant rat leads to increased ethanol intake during adolescence.

Diethylpropion produces psychostimulant and reward effects.

Intermittent exposure to a social stimulus enhances ethanol drinking in rats.

Adolescent rats are resistant to the development of ethanol-induced chronic tolerance and ethanol-induced conditioned aversion.

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

Similar Documents

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

Neuropeptide Y in the central nucleus of the amygdala suppresses dependence-induced increases in alcohol drinking.

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

A 3-day exposure to 10% ethanol with 10% sucrose successfully initiates ethanol self-administration.

Relationship between ethanol and sucrose self-administration and schedule-induced polydipsia.

Ethanol-mediated operant learning in the infant rat leads to increased ethanol intake during adolescence.

Diethylpropion produces psychostimulant and reward effects.

Intermittent exposure to a social stimulus enhances ethanol drinking in rats.

Adolescent rats are resistant to the development of ethanol-induced chronic tolerance and ethanol-induced conditioned aversion.

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