Beta-adrenergic agonist-induced long-lasting synaptic modifications in hippocampal dentate gyrus require activation of NMDA receptors, but not electrical activation of afferents

Brain Res. 1990 Sep 3;526(2):347-50. doi: 10.1016/0006-8993(90)91245-c.

Abstract

Isoproterenol induced long-lasting potentiation (LLP) of the medial perforant path-evoked excitatory post-synaptic potential (EPSP) and long-lasting depression (LLD) of the lateral perforant path-evoked EPSP in the absence of perforant path activation. The NMDA receptor antagonist D-(-)-2-amino-5-phosphonovaleric acid [D(-)APV] blocked the induction of LLP and LLD. After wash, a subsequent exposure to isoproterenol induced only LLP of medial perforant path EPSPs; LLD of lateral perforant path-evoked EPSPs did not occur. Our results are consistent with the hypothesis that beta-adrenergic agonist-induced synaptic modifications in the dentate gyrus arise from pre- and postsynaptic events.

Publication types

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

MeSH terms

  • 2-Amino-5-phosphonovalerate / pharmacology
  • Adrenergic beta-Agonists / pharmacology*
  • Afferent Pathways / physiology
  • Animals
  • Electric Stimulation
  • Evoked Potentials / drug effects
  • Hippocampus / drug effects*
  • In Vitro Techniques
  • Isoproterenol / antagonists & inhibitors
  • Isoproterenol / pharmacology
  • Male
  • Rats
  • Rats, Inbred Strains
  • Receptors, N-Methyl-D-Aspartate / drug effects*
  • Synapses / drug effects*
  • Time Factors

Substances

  • Adrenergic beta-Agonists
  • Receptors, N-Methyl-D-Aspartate
  • 2-Amino-5-phosphonovalerate
  • Isoproterenol