Meeting Abstract

P3.95  Thursday, Jan. 6  The effects of cholinesterase toxins on buccal ganglia of Tritonia diomedea CHA, DJ; MURRAY, JA*; U. Washington, Friday Harbor Labs; Cal. State. U. East Bay, Friday Harbor Labs james.murray@csueastbay.edu

Cholinesterase inhibition was investigated in the buccal ganglia of Tritonia diomedea, by intracellular recording of an identified neuron, B5, with and without inhibitor treatment. The anti-cholinergic agents used were reversible BW284C51, specific to acetylcholinesterase, and irreversible iso-OMPA, a non-specific cholinesterase blocker. Whereas treatment with BW284C51 initiated spiking followed by a large hyperpolarization, iso-OMPA caused hyperpolarization to precede spiking. Both anti-cholinergic agents: (a) initiated inhibitory and excitatory postsynaptic potentials after application; and (b) significantly increased the maximal amplitude (MA) and width at 50% MA of hyperpolarizations. BW-treatment group exhibited partial recovery <15 minutes after its removal. Histochemical localization of cholinesterase activity was performed using acetylthiocholine as the substrate in isolated buccal ganglia and brain. Highest cholinesterase labeling occurred in: (a) cells near the posteromedial border of buccal ganglia; (b) pleural ganglia; and (c) posterolateral regions of the pedal ganglia. In both buccal ganglia and brain, individual cells displayed cholinesterase in regions around the somata. B5 exhibited moderate staining, providing further evidence that it is a cholinergic neuron.