title: Glucocorticoid receptors and beta-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1.
abstract: The basolateral amygdala (BLA) is a key structure in a memory-modulatory system that regulates stress and stress hormones (glucocorticoid and noradrenaline) effects on hippocampal functioning. We have shown previously that priming the amygdala differentially affects plasticity in the hippocampal dentate gyrus (DG) and CA1, and mimicked acute stress effect on plasticity in these two subregions. In the present study, we investigated the mechanisms that mobilize the BLA to differentially alter plasticity in DG and CA1. Glucocorticoid receptors antagonist RU 38486 or beta-adrenoceptor antagonist propranolol were microinfused in the BLA, 10 min prior to BLA activation-induced modulation of long-term potentiation (LTP) in DG and CA1. The results showed that neither glucocorticoid nor noradrenergic transmissions in the BLA are necessary for LTP induction and for the impairing effect of amygdala activation on CA1 LTP. In contrast, blockade of glucocorticoid or noradrenergic transmission in BLA, increased baseline synaptic transmission in the DG, but suppressed the enhancing effect of BLA activation on DG LTP. These findings provide further evidence for a differential amygdala control of hippocampal subregions as well as for differential memory processes involving CA1 and DG. They also provide insight into how stress hormones exert their actions on the circuits involved in these processes.
authors.affiliation: Department of Psychology, Brain and Behavior Research Center, Haifa University, Israel. rm.vouimba@lnc.u-bordeaux1.fr
authors.forename: Rose-Marie
authors.initials: RM
authors.lastname: Vouimba
authors.forename: Dan
authors.initials: D
authors.lastname: Yaniv
authors.forename: Gal
authors.initials: G
authors.lastname: Richter-Levin
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000679:Amygdala / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D000704:Analysis of Variance; D000818:Animals; D003345:Corticosterone / Q000097:blood; D004307:Dose-Response Relationship, Radiation; D004558:Electric Stimulation / Q000379:methods; D006624:Hippocampus / Q000033:anatomy & histology / Q000502:physiology*; D006727:Hormone Antagonists / Q000494:pharmacology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D011965:Receptors, Glucocorticoid / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D013997:Time Factors
chemical_list: D000319:Adrenergic beta-Antagonists; D006727:Hormone Antagonists; D011943:Receptors, Adrenergic, beta; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D011433:Propranolol; D003345:Corticosterone