β1-Adrenoceptor or α1-adrenoceptor activation initiates early odor preference learning in rat pups: Support for the mitral cell/cAMP model of odor preference learning
Author(s) -
Carolyn W. Harley,
Andrea DarbyKing,
Jennifer McCann,
John H. McLean
Publication year - 2006
Publication title -
learning and memory
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 136
eISSN - 1549-5485
pISSN - 1072-0502
DOI - 10.1101/lm.62006
Subject(s) - agonist , phenylephrine , propranolol , odor , endocrinology , medicine , adrenergic receptor , chemistry , preference learning , adrenergic agent , receptor , psychology , preference , neuroscience , adrenergic , blood pressure , economics , microeconomics
We proposed that mitral cell beta1-adrenoceptor activation mediates rat pup odor preference learning. Here we evaluate beta1-, beta2-, alpha1-, and alpha2-adrenoceptor agonists in such learning. The beta1-adrenoceptor agonist, dobutamine, and the alpha1-adrenoceptor agonist, phenylephrine, induced learning, and both exhibited an inverted U-curve dose-response relationship to odor preference learning. Phenylephrine-induced learning occurred in the presence of propranolol to prevent indirect activation of beta-adrenoceptors. Alpha1-adrenoceptor mediation may represent a novel mechanism inducing learning or may increase cAMP in mitral cells via indirect activation of GABA(B) receptors. Neither the beta2-adrenoceptor agonist, salbutamol, nor the alpha2-adrenoceptor agonist, clonidine, induced learning.
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