Abstract
In Aplysia, long-term sensitization (LTS) occurs concurrently with a suppression of feeding. At the cellular level, the suppression of feeding is accompanied by decreased excitability of decision-making neuron B51. We examined the contribution of voltage-gated Na(+) and K(+) channels to B51 decreased excitability. In a pharmacologically isolated Na(+) channels environment, LTS training significantly increased B51 firing threshold, compared with untrained controls. Conversely, in a pharmacologically isolated K(+) channels environment, no differences were observed between trained and untrained animals in either amplitude or area of B51 K(+)-dependent depolarizations. These findings suggest that Na(+) channels contribute to the decrease in B51 excitability induced by LTS training.