TY - JOUR
T1 - Reversal of relative thresholds for synaptic facilitation and increased excitability induced by serotonin and tail nerve stimulation in Aplysia sensory neurons
AU - Bunge, Silvia A.
AU - Mauelshagen, Juliane
AU - Carew, Thomas J.
N1 - Funding Information:
1We thank Laura Stark for helpful comments on the manuscript. This work was supported by a DFG grant to J.M. and NSF Grant BNS831130 and NIH Grant R01-14-1083 to T.J.C. We also acknowledge here the loss of a coauthor of this paper, Juliane Mauleshagen, a valued friend and colleague, who died in a climbing accident on October 4, 1996.
PY - 1997/5
Y1 - 1997/5
N2 - Tail shock induces reflex sensitization in Aplysia and, in parallel, induces a number of modulatory effects in central neurons, such as increased excitability in tail sensory neurons (SNs) and facilitation of synaptic transmission from SNs to motor neurons. Both of these modulatory effects are mimicked by exogenous application of serotonin (5HT) or electrical stimulation of the tail nerve P9. In the present study we examined the activation thresholds for increased excitability and synaptic facilitation induced by either 5HT or P9 stimulation. We found that the concentration of SHT sufficient to produce a significant increase in excitability produced no significant synaptic facilitation and, conversely, that the intensity of nerve stimulation sufficient to produce significant synaptic facilitation produced no excitability changes. This reversal of relative thresh-olds for these modulatory effects may reflect the differential access of exogenous 5HT and endogenous 5HT (released by tail nerve stimulation) to the SN cell body and synaptic terminals, respectively.
AB - Tail shock induces reflex sensitization in Aplysia and, in parallel, induces a number of modulatory effects in central neurons, such as increased excitability in tail sensory neurons (SNs) and facilitation of synaptic transmission from SNs to motor neurons. Both of these modulatory effects are mimicked by exogenous application of serotonin (5HT) or electrical stimulation of the tail nerve P9. In the present study we examined the activation thresholds for increased excitability and synaptic facilitation induced by either 5HT or P9 stimulation. We found that the concentration of SHT sufficient to produce a significant increase in excitability produced no significant synaptic facilitation and, conversely, that the intensity of nerve stimulation sufficient to produce significant synaptic facilitation produced no excitability changes. This reversal of relative thresh-olds for these modulatory effects may reflect the differential access of exogenous 5HT and endogenous 5HT (released by tail nerve stimulation) to the SN cell body and synaptic terminals, respectively.
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U2 - 10.1006/nlme.1996.3764
DO - 10.1006/nlme.1996.3764
M3 - Article
C2 - 9159764
AN - SCOPUS:0031148397
SN - 1074-7427
VL - 67
SP - 259
EP - 263
JO - Neurobiology of Learning and Memory
JF - Neurobiology of Learning and Memory
IS - 3
ER -