The Alpha Subunit of Calcium/Calmodulin-Dependant Protein Kinase II
Enhances -Aminobutyric Acid and Inhibitory Synaptic Responses of Rat Neurons
In Vitro.
Wang, R.A., G. Cheng, M. Kolaj and M. Randi.
Department of Veterinary Physiology and Pharmacology and Neuroscience
Program, Iowa State University, Ames, Iowa 50011.
APStracts 2:0003N, 1995.
SUMMARY AND CONCLUSIONS
1. Here we report that in acutely isolated rat spinal dorsal horn (DH)
neurons, the [gamma]-aminobutyric acid type A receptor (GABAA) can be
regulated by calcium/calmodulin-dependent protein kinase II (CaM-KII).
Intracellularly applied, the [alpha]-subunit of CaM-KII enhanced GABAA
receptor-activated current recorded with the use of the whole-cell patch-
clamp technique. This effect was associated with reduced desensitization of
GABA responses. 2. GABA- induced currents are also potentiated by calyculin
A, an inhibitor of protein phosphatases 1 and 2A. 3. Conventional
intracellular recordings were made from hippocampal CA1 neurons in slices to
determine the effect of intracellular application of CaM-KII on inhibitory
synaptic potentials evoked by electrical stimulation of the stratum
oriens/alveus. The inhibitory synaptic potential was enhanced by CaM-KII; this
mechanism may contribute to long-term enhancement of inhibitory synaptic
transmission and may also play a role in other forms of plasticity in the
mammalian brain.
Received 2 January 1995; accepted in final form 23 February 1995.
APS Manuscript Number J002-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 3 April 1995.