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Multiple actions of Bay K 8644 on high-threshold Ca channels in adult rat sensory neurons

E Carbone1, A Formenti, A Pollo

  • 1Dip Anatomia e Fisiologia Umana, Turin, Italy.

Neuroscience Letters
|April 6, 1990
PubMed

Insights

Omega-conotoxin (omega-CgTx) partially blocked high-voltage activated (HVA) barium currents in rat sensory neurons. The dihydropyridine Bay K 8644 further modulated these omega-CgTx-resistant currents.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Ion Channel Physiology

Background:

  • Neuronal calcium channels are crucial for neurotransmitter release and neuronal excitability.
  • Omega-conotoxins (omega-CgTx) are peptide toxins that selectively block certain types of voltage-gated calcium channels.
  • Dihydropyridines (DHPs) like Bay K 8644 are known modulators of high-voltage activated (HVA) calcium channels.

Purpose of the Study:

  • To investigate the effects of omega-conotoxin (omega-CgTx) on high-threshold (HVA) and low-voltage activated (LVA) barium currents in adult rat sensory neurons.
  • To determine if the dihydropyridine Bay K 8644 can modulate omega-CgTx-resistant HVA currents.

Main Methods:

  • Electrophysiological recordings (whole-cell patch-clamp) were used to measure barium currents in adult rat sensory neurons.
  • Neurons were treated with omega-conotoxin (omega-CgTx) to assess its blocking effects.
  • The effects of Bay K 8644 on residual currents were then examined.

Main Results:

  • Omega-conotoxin (omega-CgTx) did not fully block HVA barium currents (L,N types) and had minimal effect on LVA,T currents.
  • The residual HVA current in omega-CgTx-treated neurons was significantly potentiated (3-4 fold) by Bay K 8644.
  • Bay K 8644 also altered the deactivation kinetics and accelerated inactivation of the omega-CgTx-resistant HVA current.

Conclusions:

  • Omega-conotoxin (omega-CgTx) is not a complete blocker of all neuronal HVA calcium channel subtypes.
  • Bay K 8644 exhibits complex modulatory actions on neuronal HVA calcium channels, including potentiation and altered gating kinetics.
  • These findings suggest multiple functional states or subtypes of neuronal HVA calcium channels that can be differentially affected by toxins and pharmacological agents.

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