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Related Experiment Videos

Decrease in alpha3*/alpha6* nicotinic receptors but not nicotine-evoked dopamine release in monkey brain after

Sarah E McCallum1, Neeraja Parameswaran, Tanuja Bordia

  • 1The Parkinson's Institute, 1170 Morse Ave, Sunnyvale, CA 94089-1605, USA.

Molecular Pharmacology
|June 4, 2005
PubMed
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Parkinson's disease (PD) models show reduced nicotinic acetylcholine receptors (nAChRs). However, alpha3*/alpha6* nAChR function is preserved in key brain areas, suggesting a potential mechanism for maintaining dopamine release despite nigrostriatal damage.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Parkinson's Disease Research

Background:

  • Nicotinic acetylcholine receptors (nAChRs) are diminished in Parkinson's disease (PD) striata and after nigrostriatal damage.
  • Presynaptic nAChRs on dopamine terminals regulate dopamine release, and their loss may contribute to PD-related behavioral deficits.

Purpose of the Study:

  • To investigate the impact of nigrostriatal damage on nAChR function in nonhuman primates, a model relevant to PD.
  • To determine if nAChR-mediated dopamine release is altered following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioning.

Main Methods:

  • Characterization of nicotine-evoked [3H]dopamine release from monkey striatal synaptosomes.
  • MPTP-induced lesioning in monkeys to assess dopamine transporter levels, nAChR binding, and nAChR-mediated dopamine release.

Related Experiment Videos

  • Differential use of selective nAChR antagonists, including alpha-conotoxinMII (alpha-CtxMII).

    • Main Results:

    • MPTP lesioning decreased dopamine transporter and alpha3*/alpha6* nAChRs in the caudate and putamen.
    • alpha3*/alpha6* nAChR-evoked dopamine release was reduced in the caudate but not the putamen, indicating a dissociation between receptor levels and function.
    • In the mesolimbic system, alpha3*/alpha6* nAChR sites declined, but receptor-evoked dopamine release remained intact.

    Conclusions:

    • A selective preservation of alpha3*/alpha6* nAChR-mediated dopamine release function occurs in nigrostriatal and mesolimbic systems after nigrostriatal damage.
    • The maintained function in the putamen, despite dopaminergic terminal loss, may be a crucial compensatory mechanism in Parkinson's disease.