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Selective metabolic activation by apomorphine in striosomes of denervated striatum in MPTP-induced hemiparkinsonian

F E Pontieri1, J J Viola, L Sokoloff

  • 1Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, MD, USA.

Neuroreport
|June 19, 1995
PubMed

Insights

Apomorphine boosts glucose metabolism in the denervated striatum of MPTP-lesioned monkeys. This effect is stronger in striosomes than matrix, indicating distinct regulation in parkinsonian syndromes.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Metabolic studies

Background:

  • Previous studies suggest differing regulatory mechanisms in striatal striosomes and matrix after dopaminergic input loss.
  • Parkinsonian syndromes involve the degeneration of dopaminergic neurons, impacting striatal function.

Purpose of the Study:

  • To investigate if apomorphine differentially affects glucose metabolism in striatal striosomes and matrix.
  • To explore functional and metabolic regulation differences in striatal compartments during parkinsonian syndromes.

Main Methods:

  • Utilized MPTP-lesioning in monkeys to create a parkinsonian model.
  • Administered apomorphine to stimulate dopamine receptors.
  • Measured and compared glucose utilization rates in striatal striosomes and matrix between hemispheres.

Main Results:

  • Apomorphine treatment increased glucose utilization in the denervated striatum compared to the intact hemisphere.
  • The increase in glucose utilization was more pronounced in the striosomes than in the matrix.
  • These findings suggest differential metabolic responses within striatal compartments.

Conclusions:

  • Apomorphine differentially modulates glucose metabolism in striatal striosomes and matrix in a parkinsonian model.
  • Provides evidence for distinct functional and/or metabolic regulation in these striatal compartments during parkinsonian syndromes.
  • Highlights the potential for compartment-specific therapeutic strategies in Parkinson's disease.

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