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Glucocorticoid receptors and beta-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1.
Neuropharmacology. 2007 Jan; 52(1):244-52.N

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+Show Affiliations

Department of Psychology, Brain and Behavior Research Center, Haifa University, Israel. rm.vouimba@lnc.u-bordeaux1.frNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16890964

Citation

Vouimba, Rose-Marie, et al. "Glucocorticoid Receptors and Beta-adrenoceptors in Basolateral Amygdala Modulate Synaptic Plasticity in Hippocampal Dentate Gyrus, but Not in Area CA1." Neuropharmacology, vol. 52, no. 1, 2007, pp. 244-52.
Vouimba RM, Yaniv D, Richter-Levin G. Glucocorticoid receptors and beta-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1. Neuropharmacology. 2007;52(1):244-52.
Vouimba, R. M., Yaniv, D., & Richter-Levin, G. (2007). Glucocorticoid receptors and beta-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1. Neuropharmacology, 52(1), 244-52.
Vouimba RM, Yaniv D, Richter-Levin G. Glucocorticoid Receptors and Beta-adrenoceptors in Basolateral Amygdala Modulate Synaptic Plasticity in Hippocampal Dentate Gyrus, but Not in Area CA1. Neuropharmacology. 2007;52(1):244-52. PubMed PMID: 16890964.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucocorticoid receptors and beta-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1. AU - Vouimba,Rose-Marie, AU - Yaniv,Dan, AU - Richter-Levin,Gal, Y1 - 2006/08/07/ PY - 2006/04/26/received PY - 2006/07/05/revised PY - 2006/07/06/accepted PY - 2006/8/8/pubmed PY - 2007/3/3/medline PY - 2006/8/8/entrez SP - 244 EP - 52 JF - Neuropharmacology JO - Neuropharmacology VL - 52 IS - 1 N2 - 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. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/16890964/Glucocorticoid_receptors_and_beta_adrenoceptors_in_basolateral_amygdala_modulate_synaptic_plasticity_in_hippocampal_dentate_gyrus_but_not_in_area_CA1_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(06)00212-7 DB - PRIME DP - Unbound Medicine ER -