Alpha-subunit of calcium/calmodulin-dependent protein kinase II enhances gamma-aminobutyric acid and inhibitory synaptic responses of rat neurons in vitro

• Published in: Journal of neurophysiology Vol. 73; no. 5; p. 2099
• Main Authors: Wang, R A, Cheng, G, Kolaj, M, Randić, M
• Format: Journal Article
• Language: English
• Published: United States 01.05.1995
• Subjects: Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases - pharmacology; Evoked Potentials - drug effects; gamma-Aminobutyric Acid - pharmacology; In Vitro Techniques; Neurons - drug effects; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Receptors, GABA-A - drug effects; Receptors, GABA-A - physiology; Spinal Cord - cytology; Spinal Cord - physiology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology
• ISSN: 0022-3077
• DOI: 10.1152/jn.1995.73.5.2099

1. Here we report that in acutely isolated rat spinal dorsal horn neurons, the gamma-aminobutyric acid-A (GABAA) receptor 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.