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

  1. Rick E. Bernardi1,4,
  2. Andrey E. Ryabinin1,
  3. S. Paul Berger1,2,3 and
  4. K. Matthew Lattal1
  1. 1Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon 97239, USA;
  2. 2Department of Psychiatry, Oregon Health and Science University, Portland, Oregon 97239, USA;
  3. 3Department of Psychiatry, Portland Veterans' Affairs Medical Center, Portland, Oregon 97239, USA

    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 preference 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.

    Footnotes

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