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Related Experiment Videos

Deep prepiriform cortex modulates neuronal cell death in global ischemia

K Kawaguchi1, R P Simon

  • 1Department of Neurology, University of Pittsburgh, Pennsylvania 15213, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|March 1, 1997
PubMed
Summary

Blocking non-N-methyl-D-aspartate (NMDA) receptors in the deep prepiriform cortex protected hippocampal neurons from ischemic injury. This suggests excitatory pathways from this region modulate seizure-induced brain damage.

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Area of Science:

  • Neuroscience
  • Neurobiology
  • Neuropharmacology

Background:

  • The deep prepiriform cortex plays a role in neurotransmission modulation during limbic seizures.
  • Excitatory circuitry from the deep prepiriform cortex to the hippocampus is implicated in neuronal injury during global ischemia.

Purpose of the Study:

  • To investigate the role of excitatory amino acid-mediated circuitry from the deep prepiriform cortex in modulating hippocampal neuronal injury during global ischemia.
  • To determine the effect of non-N-methyl-D-aspartate (NMDA) receptor blockade on neuronal survival in the hippocampus following ischemic insult.

Main Methods:

  • Rats underwent global ischemia for 10 minutes.
  • NBQX, a non-NMDA glutamate receptor antagonist, was stereotactically microinjected into the deep prepiriform cortex.

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  • Neuronal cell death in the hippocampus (CA1 sector) was quantitatively assessed 72 hours post-ischemia.
  • Control groups included saline injections and misplaced NBQX injections.

    • Main Results:

    • Rats receiving NBQX injections in the deep prepiriform cortex exhibited significantly higher neuronal survival in the hippocampal CA1 sector compared to controls.
    • Saline-injected controls and rats with misplaced NBQX injections showed greater neuronal cell death.
    • These findings highlight the neuroprotective effect of non-NMDA receptor blockade in this specific brain circuit.

    Conclusions:

    • Excitatory amino acid-mediated circuitry originating from the deep prepiriform cortex significantly modulates ischemic neuronal injury in the hippocampus.
    • Pharmacological blockade of non-NMDA receptors in the deep prepiriform cortex confers neuroprotection against global ischemia-induced hippocampal damage.
    • Targeting specific excitatory pathways may represent a therapeutic strategy for mitigating seizure-related brain injury.