Characterization of buccal motor programs elicited by a cholinergic agonist applied to the cerebral ganglion of Aplysia californica

A. J. Susswein, S. C. Rosen, S. Gapon, I. Kupfermann

    Research output: Contribution to journalArticlepeer-review

    39 Scopus citations

    Abstract

    Applying the non-hydrolyzable cholinergic agonist carbachol (CCh) to the cerebral ganglion of Aplysia elicits sustained, regular bursts of activity in the buccal ganglia resembling those seen during biting. The threshold for bursting is ~ 10-4 M. Bursting begins after a 2 to 5 min delay. The burst frequency increases over the first 5 bursts, reaching a plateau value of ~ 3 per minute. Bursting is maintained for over 10 min. Some of the effects of CCh may be attributed to its ability to depolarize and life CBI-2, a command- like neuron in the cerebral ganglion that initiates biting. CBI-2 is also depolarized by ACh, and by stimulating peripheral sensory nerves. Excitation of CBI-2 caused by carbachol is partially blocked by the muscarinic antagonist 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-contingent with food, and training animals with an inedible food. No treatment consistently and repeatedly affected the latency, the peak burst period, the length of time that bursting was maintained, or the threshold CCh concentration for eliciting bursting. However, there was a decrease in the rate of the buildup of the buccal ganglion program in previously satiated animals.

    Original languageEnglish
    Pages (from-to)509-524
    Number of pages16
    JournalJournal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology
    Volume179
    Issue number4
    DOIs
    StatePublished - Oct 1996

    Keywords

    • Aplysia
    • Feeding
    • Learning
    • Modulation
    • Satiation

    Fingerprint

    Dive into the research topics of 'Characterization of buccal motor programs elicited by a cholinergic agonist applied to the cerebral ganglion of Aplysia californica'. Together they form a unique fingerprint.

    Cite this