Computer model of clonazepam's effect in thalamic slice

Neuroreport. 1997 Oct 20;8(15):3339-43. doi: 10.1097/00001756-199710200-00029.

Abstract

In the thalamus, paradoxical changes in response to augmentation of inhibition can occur as a result of either cellular or network effects. Clonazepam, a GABA(A) agonist, produces a paradoxical reduction in evoked thalamocortical neuron inhibitory postsynaptic potential (IPSP) in thalamic slice. This has been hypothesized to be a result of augmentation in inhibitory to inhibitory connections. In a computer model, orthodromic simulation produced an increase in initial IPSP, a result contrary to that found experimentally. This failure was traced to the inability of orthodromic activation to produce fast enough recurrent inhibition to alter initial reticularis neuron firing. Simulated antidromic stimulation was able to reduce this initial spike train and reproduced the experimental finding.

Publication types

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

MeSH terms

  • Animals
  • Clonazepam / pharmacology*
  • Electric Stimulation
  • GABA Modulators / pharmacology*
  • Models, Neurological
  • Neural Pathways / drug effects
  • Neural Pathways / physiology
  • Rats
  • Receptors, GABA-A / drug effects
  • Receptors, GABA-B / drug effects
  • Synapses / physiology
  • Thalamus / drug effects*

Substances

  • GABA Modulators
  • Receptors, GABA-A
  • Receptors, GABA-B
  • Clonazepam