L-type voltage-dependent Ca(2+) channels mediate expression of presynaptic LTP in amygdala

Nat Neurosci. 2009 Sep;12(9):1093-5. doi: 10.1038/nn.2378. Epub 2009 Aug 2.

Abstract

The molecular mechanisms underlying the expression of postsynaptic long-term potentiation (LTP) at glutamatergic synapses are well understood. However, little is known about those that mediate the expression of presynaptic LTP. We found that presynaptic LTP at cortical inputs to the mouse lateral amygdala was blocked and reversed by L-type voltage-dependent Ca(2+) channel (L-VDCC) blockers. Thus, a persistent increase in L-VDCC-mediated glutamate release underlies the expression of presynaptic LTP in the amygdala.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amygdala / drug effects
  • Amygdala / physiology*
  • Animals
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels, L-Type / metabolism*
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / physiology
  • Conotoxins / pharmacology
  • Excitatory Postsynaptic Potentials / drug effects
  • Excitatory Postsynaptic Potentials / physiology
  • In Vitro Techniques
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neural Pathways / drug effects
  • Neural Pathways / physiology
  • Neuronal Plasticity / drug effects
  • Neuronal Plasticity / physiology
  • Nickel / pharmacology
  • Nimodipine / pharmacology
  • Presynaptic Terminals / drug effects
  • Presynaptic Terminals / physiology*
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology
  • Verapamil / pharmacology

Substances

  • Calcium Channel Blockers
  • Calcium Channels, L-Type
  • Conotoxins
  • Nimodipine
  • Nickel
  • Verapamil