title: Basolateral amygdala noradrenergic activity mediates corticosterone-induced enhancement of auditory fear conditioning.
abstract: The present experiment examined whether posttraining noradrenergic activity within the basolateral complex of the amygdala (BLA) is required for mediating the facilitating effects of acutely administered glucocorticoids on memory for auditory-cue classical fear conditioning. Male Sprague-Dawley rats received five pairings of a single-frequency auditory stimulus and footshock, followed immediately by bilateral infusions of the beta1-adrenoceptor antagonist atenolol (0.5 microg in 0.2 microl) or saline into the BLA together with a subcutaneous injection of either corticosterone (3.0 mg/kg) or vehicle. Retention was tested 24 h later in a novel test chamber and suppression of ongoing motor behavior served as the measure of conditioned fear. Corticosterone facilitated memory as assessed by suppression of motor activity during the 10-s presentation of the auditory stimulus and intra-BLA administration of atenolol selectively blocked this corticosterone-induced memory enhancement. These findings provide evidence that, as found with other emotionally arousing tasks, the enhancing effects of corticosterone on memory consolidation of auditory-cue fear conditioning require posttraining noradrenergic activity within the BLA.
authors.affiliation: Center for the Neurobiology of Learning and Memory, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-3800, USA.
authors.forename: Benno
authors.initials: B
authors.lastname: Roozendaal
authors.forename: Gabriel K
authors.initials: GK
authors.lastname: Hui
authors.forename: Isabel R
authors.initials: IR
authors.lastname: Hui
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Berlau
authors.forename: James L
authors.initials: JL
authors.lastname: McGaugh
authors.forename: Norman M
authors.initials: NM
authors.lastname: Weinberger
mesh_terms: D000161:Acoustic Stimulation; D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage; D000679:Amygdala / Q000187:drug effects / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D001245:Association Learning / Q000187:drug effects / Q000502:physiology; D001262:Atenolol / Q000008:administration & dosage; D003214:Conditioning, Classical / Q000187:drug effects / Q000502:physiology*; D003345:Corticosterone / Q000008:administration & dosage / Q000494:pharmacology*; D005239:Fear / Q000187:drug effects / Q000502:physiology*; D007279:Injections, Subcutaneous; D008297:Male; D008845:Microinjections; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018342:Receptors, Adrenergic, beta-1 / Q000378:metabolism*; D012153:Retention, Psychology / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D018342:Receptors, Adrenergic, beta-1; D001262:Atenolol; D003345:Corticosterone; D009638:Norepinephrine