Arginine vasotocin, an endogenous neuropeptide of Aplysia, suppresses the gill withdrawal reflex and reduces the evoked synaptic input to central gill motor neurons.
The superfusion (15 min) of arginine vasotocin (AVT; 10(-9)--10(-12) M) over the abdominal ganglion of Aplysia californica suppressed the amplitude of the gill withdrawal reflex evoked by tactile stimulation of the siphon, increased the rate of gill reflex habituation, and decreased the evoked synaptic activity to central gill motor neurons. The suppressive effects of AVT on gill reflex behaviors were not due to toxic effects of the hormone since the effects were completely reversible following washout and 3 h rest. The results obtained with AVT were similar to those previously found using the mammalian neuropeptide arginine vasopressin. AVT may act by increasing the activity of central neurons which exert suppressive control over both gill reflex behaviors and evoked activity to central gill motor neurons.
D000818:Animals; D001048:Aplysia / Q000502:physiology*; D004553:Electric Conductivity; D005724:Ganglia / Q000187:drug effects / Q000502:physiology; D005880:Gills / Q000294:innervation*; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D012018:Reflex / Q000187:drug effects*; D014668:Vasotocin / Q000494:pharmacology*
D014668:Vasotocin