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Related Experiment Videos

Group I mGluRs modulate calcium currents in rat GP: functional implications

A Stefani1, F Spadoni, G Bernardi

  • 1IRCCS Ospedale S. Lucia, Italy. Stefani@uniroma2.it

Synapse (New York, N.Y.)
|November 24, 1998
PubMed
Summary

Metabotropic glutamate receptors (mGluRs) modulate calcium currents in globus pallidus neurons, potentially impacting movement disorders. This G-protein-mediated inhibition involves group I mGluRs and N- and P-type calcium channels.

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Area of Science:

  • Neuroscience
  • Cellular Physiology
  • Neuropharmacology

Background:

  • Changes in mammalian globus pallidus cell firing patterns are linked to movement disorders.
  • Pallidal neurons receive excitatory input from the subthalamus, activating glutamate receptors.
  • Metabotropic glutamate receptor activation influences dopamine-mediated motor behaviors in the basal ganglia.

Purpose of the Study:

  • To investigate if metabotropic glutamate receptor agonists modulate high-threshold calcium currents in pallidal neurons.
  • To elucidate the specific group and channel types involved in this modulation.

Main Methods:

  • Electrophysiological recordings of high-threshold calcium currents in pallidal neurons.
  • Application of metabotropic glutamate receptor agonists (1S,3R-ACPD, DHPG) and antagonists (MCPG).

Related Experiment Videos

  • Assessment of voltage-dependence, G-protein mediation (NEM), and channel subtype involvement (omega-conotoxin-GVIA, omega-agatoxin-IVA).

    • Main Results:

    • The broad agonist 1S,3R-ACPD and group I agonist DHPG reduced calcium currents by 22%, with non-additive effects.
    • Inhibition was prevented by MCPG, suggesting group I metabotropic glutamate receptor (mGluR) involvement.
    • Modulation was rapid, G-protein-mediated, partially voltage-dependent, and involved N- and P-type calcium channels.

    Conclusions:

    • Group I mGluRs inhibit high-threshold calcium currents in globus pallidus neurons via G-proteins and N-/P-type channels.
    • This modulation may influence pallidal excitability and counterbalance subthalamic nucleus excitation.
    • In parkinsonism, this inhibition could potentially counteract excessive excitatory drive but may also lead to disinhibition of basal ganglia output.