Activation of Protein Kinase A Contributes to the Expression But Not the Induction of Long-Term Hyperexcitability Caused by Axotomy ofAplysiaSensory Neurons

摘要: Nociceptive sensory neurons (SNs) in Aplysia provide useful models to study both memory and adaptive responses nerve injury. Induction of long-term many species, including , is thought depend on activation cAMP-dependent protein kinase (PKA). Because SNs display similar alterations after injury, a plausible hypothesis that axotomy triggers memory-like modifications by activating PKA damaged axons. The present disproves this hypothesis. SN was produced (1) dissociation somata from the ganglion [which shown induce hyperexcitability (LTH)], (2) transection neurites dissociated growing vitro or (3) peripheral crush. Application competitive inhibitor Rp-8-CPT-cAMPS at time failed alter induction LTH each form axotomy, although antagonized 5-HT application. Strong coapplication membrane-permeant analog cAMP phosphodiesterase not sufficient either Furthermore, crush activate axonal stimulate its retrograde transport. Therefore, plays little if any role axotomy. However, expression reduced intracellular injection highly specific PKI several days This suggests long-lasting near soma contributes maintenance