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J Neurophysiol (March 1, 2003). 10.1152/jn.00721.2002
Submitted on Submitted 22 August 2002; accepted in final form 31 October 2002
Departments of 1Physiology, 2Anatomy, and 3Oral and Maxillofacial Surgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192; and 4Department of Biological Information Processing, Graduate School of Electronic Science and Technology, Shizuoka University, Hamamatsu, Shizuoka 432-8011, Japan
Toyoda, Hiroki,
Koji Ohno,
Junko Yamada,
Masahiko Ikeda,
Akihito Okabe,
Kohji Sato,
Kenji Hashimoto, and
Atsuo Fukuda.
Induction of NMDA and GABAA Receptor-Mediated
Ca2+ Oscillations With KCC2 mRNA Downregulation in
Injured Facial Motoneurons. J. Neurophysiol. 89: 1353-1362, 2003. To clarify
the changes that occur in 
-aminobutyric acid type A
(GABAA) receptor-mediated effects and contribute
to alterations 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
N-methyl-D-aspartate (NMDA)-receptor antagonist D(
)-2-amino-5-phosphonopentanoic acid. 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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