Mediation of inking behavior in Aplysia californica by an identified neuron in the abdominal ganglion

Thomas Carew, E. R. Kandel

Research output: Contribution to journalArticle

Abstract

Noxious stimuli cause Aplysia to release ink from acinar vesicles of the purple gland, which is located in the mantle shelf. Inking behavior has a high threshold; mild or moderate tactile stimuli, sufficient to produce gill and siphon withdrawal, fail to produce inking. Once elicited, inking behavior often becomes refractory for many minutes, although the gland still contains ink. Most, if not all, of this behavior is mediated by identified cell L14. Intracellular firing of this cell produces massive inking. L14 sends axons to the purple gland via peripheral nerves. There is a good correspondance between L14's cellular properties and the characteristics of inking behavior. L14 is silent, has a high threshold and little spontaneous synaptic input. Weak or moderate stimuli that produce large suprathreshold EPSPs in gill and siphon motor neurons produce small subthreshold EPSPs in L14. But strong stimuli produce large EPSPs in L14 causing it to fire in an accelerating train of spikes. The effectiveness of stimuli in initiating inking is greatly reduced or abolished when L14 is prevented from firing by hyperpolarization. Repeated firing of L14 leads to refractoriness of inking, presumably because of neuroglandular or secretory failure. Although it is not certain that L14 is the only motor cell controlling inking, the effectiveness of this cell and its properties seem to account for the major features of inking behavior.

Original languageEnglish (US)
JournalFederation Proceedings
Volume32
Issue number3
StatePublished - 1973

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Aplysia
Ganglia
Excitatory Postsynaptic Potentials
Neurons
Ink
Touch
Motor Neurons
Peripheral Nerves
Axons

ASJC Scopus subject areas

  • Medicine(all)

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Mediation of inking behavior in Aplysia californica by an identified neuron in the abdominal ganglion. / Carew, Thomas; Kandel, E. R.

In: Federation Proceedings, Vol. 32, No. 3, 1973.

Research output: Contribution to journalArticle

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