Role of calcium-calmodulin-dependent protein kinase II in modulation of sensorimotor synapses in Aplysia. Academic Article uri icon

abstract

  • The Ca2+-calmodulin-dependent protein kinase II (CaMKII) inhibitor, [1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazi ne) (KN-62), was used to investigate the role of CaMKII in synaptic transmission and serotonin (5-HT)-induced facilitation in Aplysia. Application of KN-62 (10 microM) by itself increased the amplitude of excitatory postsynaptic potentials (EPSPs) at sensorimotor synapses in pleural-pedal ganglia. Moreover, in the presence of KN-62, 5-HT-induced short-term facilitation was attenuated. Application of KN-62 by itself slightly increased the duration of action potentials in isolated sensory neuron somata but did not block spike broadening produced by 5-HT. KN-62 had no effect on excitability of isolated sensory neuron somata nor did it block 5-HT-induced enhancement of excitability. These results indicate that the attenuation of short-term facilitation by KN-62 is not due to modulation of the membrane currents contributing to 5-HT-induced spike broadening or enhancement of excitability. Rather, these data are consistent with the hypothesis that CaMKII contributes to the regulation of sensorimotor connections and that it has a role in spike-duration-independent processes contributing to short-term facilitation.

published proceedings

  • J Neurophysiol

altmetric score

  • 0.25

author list (cited authors)

  • Nakanishi, K., Zhang, F., Baxter, D. A., Eskin, A., & Byrne, J. H.

citation count

  • 23

complete list of authors

  • Nakanishi, K||Zhang, F||Baxter, DA||Eskin, A||Byrne, JH

publication date

  • July 1997