Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β2- and α1-adrenergic antagonists

Rick E. Bernardi, Andrey Ryabinin, S. Paul Berger, Kennon (Matt) Lattal

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated by drugs of abuse, using nonspecific β-adrenergic receptor (β-AR) antagonists. Remarkably little is known about the role of the specific β-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of β1 and β2, as well as α1- adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the β2 antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the α1 antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated reference during a subsequent test, while the β1 antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Furthermore, post-test microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for α1- and β2-specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.

Original languageEnglish (US)
Pages (from-to)777-789
Number of pages13
JournalLearning and Memory
Volume16
Issue number12
DOIs
StatePublished - Dec 2009

Fingerprint

Adrenergic Antagonists
Prazosin
Amygdala
Cocaine
Adrenergic Receptors
Betaxolol
Street Drugs
Adrenergic Agents
Learning
Injections
Basolateral Nuclear Complex
ICI 118551
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience
  • Neuropsychology and Physiological Psychology

Cite this

@article{563552f2ed5f4cfe95a48ed0993f695f,
title = "Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β2- and α1-adrenergic antagonists",
abstract = "Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated by drugs of abuse, using nonspecific β-adrenergic receptor (β-AR) antagonists. Remarkably little is known about the role of the specific β-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of β1 and β2, as well as α1- adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the β2 antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the α1 antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated reference during a subsequent test, while the β1 antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Furthermore, post-test microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for α1- and β2-specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.",
author = "Bernardi, {Rick E.} and Andrey Ryabinin and Berger, {S. Paul} and Lattal, {Kennon (Matt)}",
year = "2009",
month = "12",
doi = "10.1101/lm.1648509",
language = "English (US)",
volume = "16",
pages = "777--789",
journal = "Learning and Memory",
issn = "1072-0502",
publisher = "Cold Spring Harbor Laboratory Press",
number = "12",

}

TY - JOUR

T1 - Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β2- and α1-adrenergic antagonists

AU - Bernardi, Rick E.

AU - Ryabinin, Andrey

AU - Berger, S. Paul

AU - Lattal, Kennon (Matt)

PY - 2009/12

Y1 - 2009/12

N2 - Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated by drugs of abuse, using nonspecific β-adrenergic receptor (β-AR) antagonists. Remarkably little is known about the role of the specific β-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of β1 and β2, as well as α1- adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the β2 antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the α1 antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated reference during a subsequent test, while the β1 antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Furthermore, post-test microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for α1- and β2-specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.

AB - Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated by drugs of abuse, using nonspecific β-adrenergic receptor (β-AR) antagonists. Remarkably little is known about the role of the specific β-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of β1 and β2, as well as α1- adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the β2 antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the α1 antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated reference during a subsequent test, while the β1 antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Furthermore, post-test microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for α1- and β2-specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.

UR - http://www.scopus.com/inward/record.url?scp=73349118739&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=73349118739&partnerID=8YFLogxK

U2 - 10.1101/lm.1648509

DO - 10.1101/lm.1648509

M3 - Article

C2 - 19940038

AN - SCOPUS:73349118739

VL - 16

SP - 777

EP - 789

JO - Learning and Memory

JF - Learning and Memory

SN - 1072-0502

IS - 12

ER -