Glucocorticoids interact with the basolateral amygdala beta-adrenoceptor--cAMP/cAMP/PKA system in influencing memory consolidation

Eur J Neurosci. 2002 Feb;15(3):553-60. doi: 10.1046/j.0953-816x.2001.01876.x.


Infusion of a beta-adrenoceptor antagonist into the basolateral nucleus of the amygdala (BLA) blocks memory enhancement induced by systemic or intra-BLA administration of a glucocorticoid receptor (GR) agonist. As there is evidence that glucocorticoids interact with the noradrenergic signalling pathway in activating adenosine 3prime prime or minute,5prime prime or minute-cyclic monophosphate (cAMP), the present experiments examined whether glucocorticoids influence the beta-adrenoceptor--cAMP system in the BLA in modulating memory consolidation. Male, Sprague--Dawley rats received bilateral infusions of atenolol (a beta-adrenoceptor antagonist), prazosin (an alpha1-adrenoceptor antagonist) or Rp-cAMPS (a protein kinase A inhibitor) into the BLA 10 min before inhibitory avoidance training and immediate post-training intra-BLA infusions of the GR agonist, RU 28362. Atenolol and Rp-cAMPS, but not prazosin, blocked 48-h retention enhancement induced by RU 28362. A second series of experiments investigated whether a GR antagonist alters the effect of noradrenergic activation in the BLA on memory consolidation. Bilateral intra-BLA infusions of the GR antagonist, RU 38486, administered 10 min before inhibitory avoidance training completely blocked retention enhancement induced by alpha1-adrenoceptor activation and attenuated the dose--response effects of post-training intra-BLA infusions of clenbuterol (a beta-adrenoceptor agonist). However, the GR antagonist did not alter retention enhancement induced by post-training intra-BLA infusions of 8-Br-cAMP (a synthetic cAMP analogue). These findings suggest that glucocorticoids influence the efficacy of noradrenergic stimulation in the BLA on memory consolidation via an interaction with the beta-adrenoceptor--cAMP cascade, at a locus between the membrane-bound beta-adrenoceptor and the intracellular cAMP formation site.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 8-Bromo Cyclic Adenosine Monophosphate / pharmacology
  • Adrenergic alpha-1 Receptor Antagonists
  • Adrenergic alpha-Agonists / pharmacology
  • Adrenergic beta-Agonists / pharmacology
  • Adrenergic beta-Antagonists / pharmacology
  • Amygdala / cytology
  • Amygdala / drug effects
  • Amygdala / metabolism*
  • Animals
  • Avoidance Learning / drug effects
  • Avoidance Learning / physiology
  • Cyclic AMP / metabolism*
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Glucocorticoids / metabolism*
  • Glucocorticoids / pharmacology
  • Male
  • Memory / drug effects
  • Memory / physiology*
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Reaction Time / drug effects
  • Reaction Time / physiology
  • Receptors, Adrenergic, alpha-1 / metabolism
  • Receptors, Adrenergic, beta / drug effects
  • Receptors, Adrenergic, beta / metabolism*
  • Receptors, Glucocorticoid / agonists
  • Receptors, Glucocorticoid / antagonists & inhibitors
  • Receptors, Glucocorticoid / metabolism
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology


  • Adrenergic alpha-1 Receptor Antagonists
  • Adrenergic alpha-Agonists
  • Adrenergic beta-Agonists
  • Adrenergic beta-Antagonists
  • Enzyme Inhibitors
  • Glucocorticoids
  • Receptors, Adrenergic, alpha-1
  • Receptors, Adrenergic, beta
  • Receptors, Glucocorticoid
  • 8-Bromo Cyclic Adenosine Monophosphate
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases