Abstract
Neuromodulators can have long-lasting effects on neural circuits by changing the intrinsic membrane properties of neurons as well as the synaptic connections between them. Over recent years, many neuromodulatory substances have been identified in the stomatogastric ganglion (STG) of different crustacean species. The majority of them are now known to be released onto the STG as either descending or ascending inputs from projection neurons, and some have been shown to circulate as hormones. \r One neurotransmitter agonist that has not been characterized thoroughly in the STG is nicotine. Previous studies have found however, that some neurons in the STG do exhibit nicotinic-like responses when their receptors are bound by other cholinergic agonists. Considering that nicotine’s modulatory actions are mostly unknown, the exogenous application of nicotine to the STG can be an insightful method for the detection of large-scale changes to motor rhythm output. Results from nicotine-application experiments show that nicotine can activate or terminate the gastric-mill rhythm in Cancer borealis, and increase the rate of action potentials fired by the lateral gastric neuron (LG). Wider implications of nicotine’s effects are that there are nicotinic acetylcholine receptors in the STG network, and that nicotine can be a state-dependent modulator of the gastric-mill rhythm.