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The Modulatory Effect of Acetylcholinesterase On Neuronal Activity Is Dependent On Age in Aplysia

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image of Netherlands Journal of Zoology
For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

In the adult nervous system maintenance of function is poorly understood. A possible means to maintain ncuronal function is the level of excitatory input impinging on a neuron. In Aplysia gill motor neuron L7 mediates the gill withdrawal reflex and it exhibits reduced function with increased age, resulting from infrequent excitatory inputs (PERFTZ et al., 1984). This reduction is most pronounced with ageing from mature to old Aplysia, who are about 100 days older. Paralleling L7's reduced function is reduced hemolymph acetylcholinesterase (AChE) activity in old Aplysia (SRIVATSAN et al., 1992). By increased excitatory input on L7, using stimulation of the reflex pathway in old Aplysia, ZOLMAN & PERETZ (1987) found that L7'S function improved. Chronic stimulation of the reflex pathway also produced increased levels of AChE activity in old Aplysia (PERETZ & SRIVATSAN, 1993). This parallel between the level of hemolymph AChE activity and changes of L7 function led me to investigate the physiological effects of AChE on gill motor neurons: AChE was superfused over the gill motor neurons in the abdominal ganglion, and it induced increased excitability as expressed by membrane depolarization, increased spike rate and spike width, and it produced a change in the IV curve; most pronounced was a lessening of a presumed inward rectification during current clamping of L7' L7s from old Aplysia exhibited minimal inward rectification, no appreciable increase in spike rate, and little if any, increase in spike width, yet AChE did elicit membrane depolarization. These results show that AChE modulates neuronal properties, and age-related changes of these properties render L7 less responsive to AChE.

Affiliations: 1: Dept. of Physiology, Univ. of Kentucky Medical Center, Lexington KY 40536-0084, U.S.A


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