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Modulation of M-current by intracellular Ca2+

N V Marrion1, R S Zucker, S J Marsh

  • 1Howard Hughes Medical Institute, State University of New York, Stony Brook 11794.

Neuron
|April 1, 1991
PubMed

Insights

This study reveals that the ion current IM, suppressed by muscarinic receptors, is modulated by intracellular calcium ([Ca2+]i). Small calcium increases enhance IM, while large or prolonged increases inhibit it, impacting cell excitability.

Area of Science:

  • Neuroscience
  • Electrophysiology
  • Ion Channel Physiology

Background:

  • The M-current (IM) is a voltage- and time-dependent potassium current.
  • Muscarinic receptor activation suppresses IM.
  • The precise role of intracellular calcium ([Ca2+]i) in IM regulation is not fully understood.

Purpose of the Study:

  • To investigate the modulatory role of intracellular calcium ([Ca2+]i) on the M-current (IM).
  • To determine how varying levels and durations of [Ca2+]i affect IM function and its response to muscarinic receptor agonists.

Main Methods:

  • Voltage-clamp electrophysiology in neurons.
  • Photolysis of caged calcium compounds (nitr-5) to induce controlled intracellular calcium transients.
  • Evoking action potentials to study calcium dynamics.
  • Heavy buffering of intracellular calcium using BAPTA.

Main Results:

  • IM augmentation after agonist washout was prevented by heavy intracellular calcium buffering (BAPTA).
  • Small increases in [Ca2+]i (via nitr-5 photolysis or action potentials) augmented IM.
  • Larger or prolonged increases in [Ca2+]i inhibited IM and reduced its sensitivity to muscarinic agonists.

Conclusions:

  • Intracellular calcium ([Ca2+]i) dynamically regulates the M-current (IM).
  • Physiologically relevant changes in [Ca2+]i can modulate IM, influencing neuronal excitability.
  • IM's sensitivity to calcium suggests a role in integrating electrical activity and receptor signaling.

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