Noradrenaline triggers multivesicular release at glutamatergic synapses in the hypothalamus

J Neurosci. 2005 Dec 7;25(49):11385-95. doi: 10.1523/JNEUROSCI.2378-05.2005.

Abstract

The origin of large-amplitude miniature EPSCs (mEPSCs) at central synapses remains to be firmly established. Here, we show that at excitatory synapses onto magnocellular neurosecretory cells in the hypothalamus, noradrenaline induces a rapid and robust increase in mEPSC amplitude that requires alpha1-adrenoceptor activation but is impervious to postsynaptic manipulations that block the putative insertion of AMPA receptors. In response to noradrenaline, mEPSCs exhibit a putative multimodal amplitude histogram distribution that is not attributable to random temporal summation, the unveiling of a quiescent synapse, or the release of large vesicles. Large-amplitude mEPSCs are sensitive to a high dose of ryanodine and are associated with an enhanced glutamate cleft concentration. Together, these data are consistent with the hypothesis that large-amplitude mEPSCs result from the synchronous release of multiple vesicles via rapid presynaptic calcium expulsion from intracellular stores.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Excitatory Postsynaptic Potentials / drug effects
  • Excitatory Postsynaptic Potentials / physiology
  • Glutamic Acid / metabolism*
  • Hypothalamus / drug effects
  • Hypothalamus / metabolism*
  • In Vitro Techniques
  • Male
  • Norepinephrine / pharmacology*
  • Norepinephrine / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, AMPA / agonists
  • Receptors, AMPA / metabolism*
  • Synapses / drug effects
  • Synapses / metabolism
  • Synaptic Vesicles / drug effects
  • Synaptic Vesicles / metabolism*

Substances

  • Receptors, AMPA
  • Glutamic Acid
  • Norepinephrine