ANALYSIS OF SYNAPTIC DEPRESSION CONTRIBUTING TO HABITUATION OF GILL-WITHDRAWAL REFLEX IN APLYSIA-CALIFORNICA
ANALYSIS OF SYNAPTIC DEPRESSION CONTRIBUTING TO HABITUATION OF GILL-WITHDRAWAL REFLEX IN APLYSIA-CALIFORNICA
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DOI:
10.1152/jn.1982.48.2.431
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发表时间:
1982-01-01
影响因子:
2.5
通讯作者:
BYRNE, JH
中科院分区:
文献类型:
--
作者:
BYRNE, JH
Repeated stimulation of the siphon skin results in short-term habituation of the reflex contractions of the gill. The habituation, in turn, is correlated with a depression of the excitatory postsynaptic potentials (EPSP) in motor neurons from mechanoreceptor sensory neurons (SN). This study examined the parametric features of the synaptic depression to gain insights into the mechanisms underlying the reduced transmitter release. Single sensory neuron action potentials were repeatedly elicited with depolarizing current pulses while the amplitude of the resultant EPSP in the motor neuron was monitored. Synaptic depression varies as a complex function of interstimulus interval (ISI). At an ISI of 1 s, depression is rapid and reaches a plateau at 36% of control. The depression at an ISI of 100 s is less pronounced, showing a gradual decay to 65% of control with the 10th EPSP. There are no significant differences in time course or magnitude of depression across a broad range of intermediate ISI (3, 10 and 30 s), although depression at these ISI is intermediate between the 1-100 s ISI. There is also a complex relationship between spike interval and the depression of the 2nd of 2 EPSP. Depression of the 2nd of EPSP or depression of a train of EPSP is not a monotonic function of spike interval. There may be a slight underlying facilitatory process with short spike intervals. The recovery of synaptic depression following a train of 10 stimuli is not constant; shorter spike intervals produce more rapid recovery. These data are inconsistent with a classical depletion model for synaptic depression and indicate that either a single complex function of time and ISI or multiple functions underlie synaptic depression and its recovery at the sensory neuron synapse.