Role of calcium in inactivation of calcium/calmodulin dependent protein kinase II after cerebral ischemia

1992 ◽  
Vol 113 (1) ◽  
pp. 31-37 ◽  
Author(s):  
David M. Hiestand ◽  
Boyd E. Haley ◽  
Mark S. Kindy
Keyword(s):  
Cerebral Ischemia ◽  
Protein Kinase ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein

Role of Calcium-Calmodulin–Dependent Protein Kinase II in Modulation of Sensorimotor Synapses in Aplysia

1997 ◽  
Vol 78 (1) ◽  
pp. 409-416 ◽  
Author(s):  
Keiko Nakanishi ◽  
Fan Zhang ◽  
Douglas A. Baxter ◽  
Arnold Eskin ◽  
John H. Byrne
Keyword(s):  
Protein Kinase ◽  
Sensory Neuron ◽  
Action Potentials ◽  
Short Term ◽  
Dependent Protein Kinase ◽  
Duration Of Action ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein

Nakanishi, Keiko, Fan Zhang, Douglas A. Baxter, Arnold Eskin, and John H. Byrne. Role of calcium-calmodulin–dependent protein kinase II in modulation of sensorimotor synapses in Aplysia. J. Neurophysiol. 78: 409–416, 1997. The Ca2+-calmodulin–dependent protein kinase II (CaMKII) inhibitor, {1-[N,O - bis(5 - isoquinolinesulfonyl) - N - methyl - L - tyrosyl] - 4 - phenylpiper azine} (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 μM) 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.

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