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Related Experiment Videos

Frontal cortex lesion prior to hyperglycemic ischemia: no decrease in ensuing substantia nigra pars reticulata damage

J Lundgren1, M Ingvar, M L Smith

  • 1Department of Neurobiology, University of Lund, Sweden.

Experimental Brain Research
|January 1, 1992
PubMed
Summary

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Preischemic hyperglycemia worsens brain damage, causing seizures and substantia nigra pars reticulata (SNPR) lesions. Reducing frontal cortex input did not prevent these effects, suggesting other mechanisms are involved in SNPR damage.

Area of Science:

  • Neuroscience
  • Pathology
  • Ischemic Stroke Research

Background:

  • Preischemic hyperglycemia exacerbates brain damage following ischemic events.
  • Hyperglycemia is linked to post-ischemic seizures and necrotic lesions in the substantia nigra pars reticulata (SNPR).
  • Excitatory input to the SNPR is hypothesized to contribute to this observed damage.

Purpose of the Study:

  • To investigate if reducing excitatory input to the SNPR by creating a unilateral frontal cortex lesion ameliorates post-ischemic seizures.
  • To determine if a prior frontal cortex lesion alters the light microscopical damage in the SNPR after ischemia in hyperglycemic subjects.

Main Methods:

  • Unilateral frontal cortex lesions were performed 6-19 days before inducing ischemia.
  • Hyperglycemic subjects underwent 10 minutes of ischemia followed by 15 hours of recovery.

Related Experiment Videos

  • Post-ischemic seizures and SNPR damage were evaluated between lesioned and non-lesioned sides.

    • Main Results:

    • Unilateral frontal cortex lesions did not prevent fatal post-ischemic seizures in hyperglycemic subjects (7/8 developed seizures and died within 20 hours).
    • No significant difference in post-ischemic SNPR damage was observed between the lesioned and contralateral sides.
    • No side differences in damage were noted in other evaluated brain regions.

    Conclusions:

    • Excessive excitatory input from the frontal cortex is unlikely to be the primary cause of SNPR pan-necrotic lesions in hyperglycemic ischemia.
    • Reduced GABA-ergic inhibitory input from the caudoputamen to the SNPR may be a more critical factor in excitotoxic SNPR damage and seizure development.