CHARACTERIZATION OF BUCCAL MOTOR PROGRAMS ELICITED BY A CHOLINERGIC AGONIST APPLIED TO THE CEREBRAL GANGLION OF APLYSIA-CALIFORNICA

Applying the non-hydrolyzable cholinergic agonist carbachol (CCh) to t he cerebral ganglion of Aplysia elicits sustained, regular bursts of a ctivity in the buccal ganglia resembling those seen during biting, The threshold for bursting is similar to 10(-4) M. Bursting begins after a 2 to 5 min delay. The burst frequency increases over the first 5 bur sts, reaching a plateau value of similar to 3 per minute. Bursting is maintained for over 10 min. Some of the effects of CCh may be attribut ed to its ability to depolarize and fire CBI-2, a command-like neuron in the cerebral ganglion that initiates biting, CBI-2 is also depolari zed by ACh, and by stimulating peripheral sensory nerves, Excitation o f CBI-2 caused by carbachol is partially blocked by the muscarinic ant agonist atropine. We examined whether CCh-induced bursting is modified in ganglia taken from Aplysia that previously experienced treatments inhibiting feeding, such as satiation, head shock contingent or non-co ntingent with food, and training animals with an inedible food. No tre atment consistently and repeatedly affected the latency, the peak burs t period, the length of time that bursting was maintained, or the thre shold CCh concentration for eliciting bursting. However, there was a d ecrease in the rate of the build-up of the buccal ganglion program in previously satiated animals.