J Neurophysiol (January 1, 2003). 10.1152/jn.00384.2002
Submitted on Submitted 23 May 2002; accepted in final form 29 August 2002.
GABA-Mediated Inhibition of Glutamate Release During Ischemia
in Substantia Gelatinosa of the Adult Rat
Noriaki
Matsumoto,1,2
Eiichi
Kumamoto,1
Hidemasa
Furue,1 and
Megumu
Yoshimura1
1Department of Physiology and
2Department of Thoracic and Cardiovascular
Surgery, Saga Medical School, Saga 849-8501, Japan
Matsumoto, Noriaki,
Eiichi Kumamoto,
Hidemasa Furue, and
Megumu Yoshimura.
GABA-Mediated Inhibition of Glutamate Release During Ischemia
in Substantia Gelatinosa of the Adult Rat. J. Neurophysiol. 89: 257-264, 2003. An ischemia-induced
change in glutamatergic transmission was investigated in substantia
gelatinosa (SG) neurons of adult rat spinal cord slices by use of the
whole cell patch-clamp technique; the ischemia was simulated by
superfusing an oxygen- and glucose-free medium (ISM). Following ISM
superfusion, 21 of 37 SG neurons tested produced an outward current
(23 ± 4 pA at a holding potential of 
70 mV), which was followed
by a slow and subsequent rapid inward current; the remaining neurons
had only inward currents. During such a change in holding currents,
spontaneous excitatory postsynaptic currents (EPSCs) were
remarkably decreased in a frequency with time (half-decay time of the
frequency: about 65 s). The frequency of spontaneous EPSCs was
reduced to 28 ± 13% (n = 37) of the control
level during the generation of the slow inward current (about 4 min
after the beginning of ISM superfusion) without a change in the
amplitude of spontaneous EPSCs. When ISM was superfused together with
either bicuculline (10 µM) or CGP35348 (20 µM;
GABAA and GABAB receptor
antagonists, respectively), spontaneous EPSC frequency reduced by ISM
recovered to the control level and then the frequency markedly
increased [by 325 ± 120% (n = 22) and 326 ± 91% (n = 17), respectively, 4 min after ISM
superfusion]; this alteration in the frequency was not accompanied by
a change in spontaneous EPSC amplitude. Superfusing TTX (1 µM)-containing ISM resulted in a similar recovery of spontaneous EPSC
frequency and following increase (by 328 ± 26%,
n = 12) in the frequency; strychnine (1 µM) did not
affect ISM-induced changes in spontaneous EPSC frequency
(n = 5). It is concluded that the ischemic simulation inhibits excitatory transmission to SG neurons, whose action is in part
mediated by the activation of presynaptic GABAA
and GABAB receptors, probably due to GABA
released from interneurons as a result of an ischemia-induced increase
in neuronal activities. This action might protect SG neurons from an
excessive excitation mediated by L-glutamate during ischemia.
