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1 Department of Physiology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan; Department of Oral and Maxillofacial Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
2 Department of Anatomy, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
3 Department of Biological Information Processing, Graduate School of Electronic Science and Technology, Shizuoka University, Hamamatsu, Shizuoka, Japan
4 Department of Physiology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
5 Department of Oral and Maxillofacial Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
6 Department of Physiology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan; Department of Biological Information Processing, Graduate School of Electronic Science and Technology, Shizuoka University, Hamamatsu, Shizuoka, Japan
* To whom correspondence should be addressed. E-mail: axfukuda{at}hama-med.ac.jp.
To clarify the changes that occur in 
-aminobutyric acid type A (GABAA) receptor-mediated effects and contribute to alterlations in the network activities after neuronal injury, we studied intracellular Ca2+ concentration ([Ca2+]i) dynamics in a rat facial-nerve-transection model. In facial motoneurons, an elevation of the resting [Ca2+]i, GABA-mediated [Ca2+]i transients, enhancement of the glutamate-evoked [Ca2+]i increases, and spontaneous [Ca2+]i oscillations were induced by axotomy. All these axotomy-induced modifications were abolished by the GABAA-receptor antagonist bicuculline and NMDA-receptor antagonist D-AP5. A downregulation of K+-Cl- cotransporter (KCC2) mRNA, an increase in intracellular Cl- concentration ([Cl-]i) and transformation of GABAergic hyperpolarization to depolarization were also induced by axotomy. We suggest that in axotomized neurons KCC2 downregulation impairs Cl- homeostasis and makes GABA act depolarizing, resulting in endogenous GABA inducing [Ca2+]i oscillations via facilitation of NMDA-receptor activation. Such GABAA-receptor-mediated [Ca2+]i oscillations may play a role in neural survival and regeneration.
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