title: Control of gill reflex habituation and the rate of EPSP decrement of L7 by a common source in the CNS of Aplysia.
abstract: It was found in older Aplysia that the rate of decrement of the EPSP evoked in L7 by repreated tactile stimulation of the gill was dependent on the strength of the applied stimulus and that the rate of decrement paralleled the rate of gill reflex habituation. As the stimulus intensity was increased both rates slowed. In contrast, it was found in young Aplysia that the rate of EPSP decrement and the rate of gill reflex habituation were independent of the strength of the stimulus applied to the gill. Neither rate changes as the stimulus intensity was changed. Moreover, L7's of young animals are more responsive to tactile stimuli applied to the gill than are L7's of older animals, and the difference in excitability is not due to any differences in passive membrane properties between the L7's in young and older Aplysia. These findings are fully consistent with and supportive of the proposal that a common neuronal source in the parieto-visceral ganglion of Aplysia controls the rate of gill reflex habituation, the synaptic input to L7, and the rate of decrement of this input, evoked by repeated tactile stimulation of the gill. Additionally, it was proposed that this common source is developed incompletely in the young. As a consequence of this incomplete development, young Aplysia exhibit less adaptability to changing stimulus conditions and, in general, less ability to suppress their behavior. It may thus be possible to study directly developmental changes in the nervous system which act to transform juvenile behavior to adult behavior.
mesh_terms: D000375:Aging; D000818:Animals; D001048:Aplysia / Q000502:physiology*; D005724:Ganglia / Q000254:growth & development / Q000502:physiology; D005880:Gills / Q000502:physiology*; D006185:Habituation, Psychophysiologic / Q000502:physiology; D008564:Membrane Potentials; D010812:Physical Stimulation; D012018:Reflex / Q000502:physiology; D013569:Synapses / Q000502:physiology