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Interaction of sigma-1 receptor modulators with seizure development in pentylenetetrazole-induced kindled mice

Masoumeh Emamghoreishi1, Marzieh Shahpari2, Mojtaba Keshavarz3

  • 1Research Center for Psychiatry and Behavior Sciences, Shiraz University of Medical Sciences, Shiraz, Iran; Department of Pharmacology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran; Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.

Epilepsy Research
|May 12, 2019
PubMed

Insights

Opipramol, a sigma receptor modulator, appears to worsen epilepsy development (epileptogenesis) in a mouse model. However, blocking sigma-1 receptors with BD-1063 prevented this pro-convulsant effect, suggesting a role for sigma-1 receptors in epilepsy.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Epilepsy Research

Background:

  • Epileptogenesis, the process by which epilepsy develops, is a complex neurological phenomenon.
  • Sigma receptors, particularly the sigma-1 subtype, are implicated in various neurological functions and disorders.
  • Understanding modulators of sigma receptors may offer new therapeutic targets for epilepsy.

Purpose of the Study:

  • To investigate the influence of opipramol and BD-1063 on the development of epilepsy.
  • To explore the role of sigma-1 receptors in the pentylenetetrazole (PTZ)-kindling model of epilepsy.

Main Methods:

  • Utilized the pentylenetetrazole (PTZ)-kindling model in mice to study epileptogenesis.
  • Administered PTZ with varying doses of opipramol and the selective sigma-1 receptor antagonist BD-1063.
  • Monitored seizure scores and the development of full kindling over a 15-day period.

Main Results:

  • Opipramol administration (5 and 10 mg/kg) alongside PTZ resulted in fully kindled mice with elevated seizure scores.
  • Mice treated with PTZ plus BD-1063, or PTZ plus opipramol and BD-1063, did not achieve full kindling.
  • BD-1063 administration counteracted the pro-convulsant effects of opipramol in the PTZ-kindling model.

Conclusions:

  • Opipramol exhibits a pro-convulsant effect, potentially exacerbating epileptogenesis.
  • The pro-convulsant action of opipramol appears to be mediated through the activation of sigma-1 receptors.
  • Selective antagonism of sigma-1 receptors may offer a protective strategy against PTZ-induced epileptogenesis.
Keywords:
MiceOpipramolPentylenetetrazoleSeizureSigma-1 receptors

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