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The vertebrate neurohypophysial peptide arginine vasotocin (AVT), which may be endogenous to the Aplysia central nervous system, was tested for its effect on sensory to motor neurone synaptic transmission. In the semi-intact preparation, superfusion of AVT (10(−6) moll-1) over the abdominal ganglion decreased the amplitude of both the gill withdrawal reflex and the short-latency excitatory postsynaptic potentials (EPSPs) evoked in gill and siphon motor neurones by single action potentials elicited in sensory neurones. AVT slowed the rate of rise of the EPSP, enhanced the rate of homosynaptic depression, and reversibly decreased the duration of the action potential of mechanosensory neurones in isolated, perfused abdominal and pleural ganglia. Frequency-dependent prolongation of action potentials of pleural sensory cells was also decreased by application of AVT. Because this peptide has been shown to modulate the gill withdrawal reflex and its subsequent habituation, the hypothesis that AVT plays a physiological role in the expression of the suppressed behavioural state is proposed. In addition, it is proposed that modulation of the reflex by AVT occurs in part by shortening the duration of the sensory neurone action potential.

journal of experimental biology

Suppression of sensory to motor synaptic transmission and narrowing of the sensory neurone action potential by arginine vasotocin in <i>Aplysia californica</i>

Suppression of sensory to motor synaptic transmission and narrowing of the sensory neurone action potential by arginine vasotocin in Aplysia californica