Involvement of protein kinase C in serotonin-induced spike broadening and synaptic facilitation in sensorimotor connections of Aplysia

J Neurophysiol. 1992 Aug;68(2):643-51. doi: 10.1152/jn.1992.68.2.643.


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)

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alkaloids / pharmacology
  • Animals
  • Aplysia / physiology*
  • Evoked Potentials, Somatosensory / drug effects*
  • Ganglia / cytology
  • Ganglia / drug effects
  • Neural Pathways / drug effects
  • Neurons, Afferent / drug effects
  • Neurons, Afferent / physiology
  • Phorbol Esters / pharmacology
  • Protein Kinase C / physiology*
  • Serotonin / pharmacology*
  • Somatosensory Cortex / cytology
  • Somatosensory Cortex / physiology*
  • Staurosporine
  • Synapses / drug effects*


  • Alkaloids
  • Phorbol Esters
  • Serotonin
  • Protein Kinase C
  • Staurosporine