Aj. Susswein et al., CHARACTERIZATION OF BUCCAL MOTOR PROGRAMS ELICITED BY A CHOLINERGIC AGONIST APPLIED TO THE CEREBRAL GANGLION OF APLYSIA-CALIFORNICA, Journal of comparative physiology. A, Sensory, neural, and behavioral physiology, 179(4), 1996, pp. 509-524
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.