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Upregulation of presynaptic mGluR2, but not mGluR3 in the epileptic medial perforant path

Judith Rohde1, Timo Kirschstein, Wiebke Wilkars

  • 1Oscar Langendorff Institute of Physiology, University of Rostock, Gertrudenstrasse 9, 18057 Rostock, Germany.

Neuropharmacology
|December 29, 2011
PubMed

Insights

Chronic epilepsy enhances group II metabotropic glutamate receptors (mGluRs) in the medial perforant path, increasing presynaptic inhibition. This contrasts with hippocampal downregulation, suggesting region-specific receptor changes in epilepsy.

Area of Science:

  • Neuroscience
  • Epilepsy Research
  • Synaptic Plasticity

Background:

  • Presynaptic metabotropic glutamate receptors (mGluRs) regulate neurotransmitter release.
  • Group III mGluRs are downregulated in the lateral perforant path in chronic epilepsy.
  • The role of medial perforant path mGluRs in chronic epilepsy remains unclear.

Purpose of the Study:

  • To investigate mGluR-dependent presynaptic inhibition at the medial perforant path-granule cell synapse in a rat model of chronic epilepsy.
  • To determine the expression levels of group II mGluRs in the epileptic medial perforant path.

Main Methods:

  • Electrophysiological recordings of medial perforant path-evoked responses in control and pilocarpine-treated epileptic rats.
  • Administration of a specific group II mGluR agonist (DCG-IV).
  • Quantitative real-time reverse transcriptase-PCR and immunohistochemistry to assess mGluR transcript and protein expression.

Main Results:

  • DCG-IV caused significantly greater depression of medial perforant path responses in epileptic rats compared to controls.
  • Increased paired-pulse ratio indicated a presynaptic mechanism for this enhanced depression.
  • Quantitative PCR revealed increased mGluR2 transcripts in the entorhinal cortex of epileptic rats.
  • Immunohistochemistry confirmed elevated group II mGluR expression in the epileptic medial molecular layer.

Conclusions:

  • Chronic epilepsy enhances group II mGluR-mediated presynaptic inhibition at the medial perforant path.
  • This enhancement is associated with increased expression of mGluR2 transcripts in the entorhinal cortex.
  • Epilepsy can induce region-specific alterations in mGluR expression, with potential increases in some pathways despite hippocampal downregulation.

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