9-Phenanthrol modulates postinhibitory rebound and afterhyperpolarizing potentials in an excitatory motor neuron of the medicinal leech

Abstract

Postinhibitory rebound (PIR) responses in leech dorsal excitatory motor neurons (cell DE-3) are eliminated by Ca²⁺ channel blockers but also exhibit a strong dependence on extracellular Na⁺. These features could be explained by a voltage-gated Ca²⁺ current acting in concert with a Ca²⁺-activated nonspecific current (I_CAN). In vertebrates, I_CAN is associated with TRPM4 channels which are blocked selectively by 9-phenanthrol. Here, we show that 9-phenanthrol selectively inhibits a late phase of PIR and simultaneously enhances afterhyperpolarizing potentials (AHPs). Bath application of NNC 55-0396 or Cd²⁺ combined with ion substitution experiments indicate that a low-voltage-activated Ca²⁺ current plays a key role in generating PIR and that Ca²⁺ influx through low- or high-voltage-activated Ca²⁺ channels can trigger AHPs via activation of a Ca²⁺-dependent K⁺ current. We also demonstrate modulation of rebound responses by other I_CAN blockers such as gadolinium and flufenamic acid, as well as the calmodulin antagonist W-7. We discuss how these results provide additional insights into the specific types of ionic currents underlying rebound responses of motor neuron DE-3 in the medicinal leech.

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