Effects of 3,3-Dipyridylmethyl-1-Phenyl-2-Indolinone on γ-Aminobutyric Acid Elicited Chloride Current of Snail Central Neuron

The effects of (1) γ-aminobutyric acid (GABA) on the excitable membrane and (2) DPMPI (3,3-dipyridylmethyl-1-phenyl-2-indolinone) on the microperfused GABA elicited currents were investigated on central LP5 neuron of giant African snail, Achatina fulica Ferussac, with conventional voltage-clamp technique. GABA elicited an inward current of LP5 neuron by a concentration and voltage dependent manner. Muscimol, GABA A receptor agonist, did, while baclofen, GABA B receptor agonist, did not, elicit the membrane current on the neuron. The GABA elicited currents in LP5 neuron were blocked by picrotoxin, a GABA A receptor ion channel complex antagonist while the currents were not blocked by phaclofen, a GABA B receptor antagonist. The results suggested that the GABA elicited current in LP5 neuron was mainly due to activation of GABA A receptor. DPMPI increased the frequency of the spontaneously generated action potential of the neuron. In the voltage clamped neuron, DPMPI decreased the GABA elicited responses by a concentration dependent manner. DPMPI altered neither the reversal potential of GABA elicited current, nor the membrane resistance of the excitable membrane of central LP5 neuron. The results concluded that DPMPI altered the GABA A activated receptor ionic channel complex of the LP5 neuron.