title: Involvement of protein kinase C in serotonin-induced spike broadening and synaptic facilitation in sensorimotor connections of Aplysia.
abstract: 1. Plasticity at the connections between sensory neurons and their follower cells in Aplysia has been used extensively as a model system to examine mechanisms of simple forms of learning. Earlier studies have concluded that serotonin (5-HT) is a key modulatory transmitter and that it exerts its short-term actions via cAMP-dependent activation of protein kinase A. Subsequently, it has become clear that other kinase systems such as protein kinase C (PKC) also may be involved in the actions of 5-HT. 2. Application of phorbol esters, which activate PKC, produced a slowly developing spike broadening but had little effect on excitability (a process known to be primarily cAMP dependent). Moreover, the effects of phorbol esters and 5-HT on spike duration were not additive, suggesting that they may share some common mechanisms. 3. The protein kinase inhibitor staurosporine suppressed both 5-HT-induced slowly developing spike broadening and, under certain conditions, facilitation of transmitter release. Staurosporine did not inhibit 5-HT-induced enhancement of excitability. The effectiveness of staurosporine on spike broadening was dependent on the time at which spike broadening was examined after application of 5-HT. Staurosporine appeared to have little effect on spike broadening 3 min after application of 5-HT, whereas it inhibited significantly 5-HT-induced spike broadening at later times. The staurosporine-insensitive component of 5-HT-induced spike broadening may be mediated by cAMP. 4. The results suggest that the activation of PKC plays a key role in components of both 5-HT-induced spike broadening and facilitation of synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225.
authors.forename: S
authors.initials: S
authors.lastname: Sugita
authors.forename: J R
authors.initials: JR
authors.lastname: Goldsmith
authors.forename: D A
authors.initials: DA
authors.lastname: Baxter
authors.forename: J H
authors.initials: JH
authors.lastname: Byrne
mesh_terms: D000470:Alkaloids / Q000494:pharmacology; D000818:Animals; D001048:Aplysia / Q000502:physiology*; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects*; D005724:Ganglia / Q000166:cytology / Q000187:drug effects; D009434:Neural Pathways / Q000187:drug effects; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D010703:Phorbol Esters / Q000494:pharmacology; D011493:Protein Kinase C / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology*; D013003:Somatosensory Cortex / Q000166:cytology / Q000502:physiology*; D019311:Staurosporine; D013569:Synapses / Q000187:drug effects*
chemical_list: D000470:Alkaloids; D010703:Phorbol Esters; D012701:Serotonin; D011493:Protein Kinase C; D019311:Staurosporine