Intracellular and voltage clamp studies of capsaicin induced effects on a sensory neuron model.

The acute effects of capsaicin (CAP) were studied on membrane properties, the action potential (AP) and the membrane ionic currents in the giant serotoninergic neuron of the cerebral ganglion (MCC) in the snail of Helix pomatia L. CAP (30-300 microM) depolarized the MCC, decreased the amplitude, the rate of rise and the rate of fall of the action potential. CAP prolonged the AP-duration, increased the membrane slope resistance, decreased the hyperpolarizing afterpotential and the posttetanic hyperpolarization both in normal and Na-free media. All the effects were reversible and could be evoked repeatedly. CAP attenuated the outward membrane currents with decreasing potency in the sequence of the transient potassium (IA) voltage-dependent potassium (IK), Ca-dependent potassium (IC) and leakage currents (IL). CAP decreased or increased the peak amplitude of the Ca-current (ICa), depending on the extracellular Ca concentration. CAP increased the inactivation of the ICa, decreased the Ca-conductance (GCa) in normal and high Ca solutions and shifted the Ca-equilibrium potential (VCa) to more positive voltage in 30 mM Ca-solution. CAP decreased the electrically activated Na-current and blocked the acetylcholine (ACh) activated increase in Na-K conductances. It is concluded that CAP profoundly affects the electrically and some transmitter-activated cationic conductances. Further studies are needed to clarify the significance of these changes with respect to the mechanism of the selective neurotoxic effects of CAP.