The Journal of Neurophysiology Vol. 78 No. 1 July 1997, pp. 409-416
Copyright ©1997 The American Physiological Society

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

Keiko Nakanishi¹, Fan Zhang¹, Douglas A. Baxter¹, Arnold Eskin², and John H. Byrne¹

¹ Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, 77225; and ² Department of Biochemistry and Biophysical Sciences, University of Houston, Houston, Texas 77204

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.

This article has been cited by other articles:

				A. Khoutorsky and M. E. Spira Activity-dependent calpain activation plays a critical role in synaptic facilitation and post-tetanic potentiation Learn. Mem., January 29, 2009; 16(2): 129 - 141. [Abstract] [Full Text] [PDF]

				A. Y. Hung and N. S. Magoski Activity-Dependent Initiation of a Prolonged Depolarization in Aplysia Bag Cell Neurons: Role for a Cation Channel J Neurophysiol, March 1, 2007; 97(3): 2465 - 2479. [Abstract] [Full Text] [PDF]

				R. D. Hawkins, E. R. Kandel, and C. H. Bailey Molecular Mechanisms of Memory Storage in Aplysia Biol. Bull., June 1, 2006; 210(3): 174 - 191. [Abstract] [Full Text] [PDF]

				Q. Li, A. C. Roberts, and D. L. Glanzman Synaptic Facilitation and Behavioral Dishabituation in Aplysia: Dependence on Release of Ca2+ from Postsynaptic Intracellular Stores, Postsynaptic Exocytosis, and Modulation of Postsynaptic AMPA Receptor Efficacy J. Neurosci., June 8, 2005; 25(23): 5623 - 5637. [Abstract] [Full Text] [PDF]

				I. Jin and R. D. Hawkins Presynaptic and Postsynaptic Mechanisms of a Novel Form of Homosynaptic Potentiation at Aplysia Sensory-Motor Neuron Synapses J. Neurosci., August 13, 2003; 23(19): 7288 - 7297. [Abstract] [Full Text] [PDF]

				A. Angers, D. Fioravante, J. Chin, L. J. Cleary, A. J. Bean, and J. H. Byrne Serotonin Stimulates Phosphorylation of Aplysia Synapsin and Alters Its Subcellular Distribution in Sensory Neurons J. Neurosci., July 1, 2002; 22(13): 5412 - 5422. [Abstract] [Full Text] [PDF]

				S. Royer, R. L. Coulson, and M. Klein Switching Off and On of Synaptic Sites at Aplysia Sensorimotor Synapses J. Neurosci., January 15, 2000; 20(2): 626 - 638. [Abstract] [Full Text] [PDF]

				D. A. Baxter, C. C. Canavier, J. W. Clark Jr., and J. H. Byrne Computational Model of the Serotonergic Modulation of Sensory Neurons in Aplysia J Neurophysiol, December 1, 1999; 82(6): 2914 - 2935. [Abstract] [Full Text] [PDF]

				X.-Y. Jiang and T. W. Abrams Use-Dependent Decline of Paired-Pulse Facilitation at Aplysia Sensory Neuron Synapses Suggests a Distinct Vesicle Pool or Release Mechanism J. Neurosci., December 15, 1998; 18(24): 10310 - 10319. [Abstract] [Full Text] [PDF]

				R E Zwartjes, H West, S Hattar, X Ren, F Noel, M Nunez-Regueiro, K MacPhee, R Homayouni, M T Crow, J H Byrne, et al. Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia. Learn. Mem., January 1, 1998; 4(6): 478 - 495. [Abstract] [PDF]