Nigral GABAergic inhibition upon cholinergic neurons in the rat pedunculopontine tegmental nucleus

被引:43
作者
Saitoh, K
Hattori, S
Song, WJ
Isa, T
Takakusaki, K
机构
[1] Asahikawa Med Coll, Dept Physiol, Asahikawa, Hokkaido 0788510, Japan
[2] Osaka Univ, Grad Sch Engn, Dept Elect Engn, Osaka, Japan
[3] Natl Inst Physiol Sci, Dept Integrat Physiol, Okazaki, Aichi 444, Japan
关键词
basal ganglia; GABA receptor; single-cell reverse transcription-PCR; substantia nigra pars reticulata; whole-cell patch-clamp recording;
D O I
10.1046/j.1460-9568.2003.02825.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated, in a midbrain parasagittal slice preparation of Wistar rats (postnatal day 9-17), the synaptic inhibition of neurons in the pedunculopontine tegmental nucleus (PPN), which was mediated by gamma (gamma)-amino-butyric acid (GABA). Whole-cell patch-clamp recording was used, in combination with a single-cell reverse transcription-polymerise chain reaction amplification technique, to record synaptic potentials and to identify the phenotype of the recorded PPN neuron. In the presence of the ionotropic glutamate receptor antagonists, 6-cyano-2, 3-dihydroxy-7-nitro-quinoxaline-2, 3, dione, and DL-2-amino-5-phosphonovaleric acid, single electrical stimuli were applied to the substantia nigra pars reticulata (SNr), one of the basal ganglia output nuclei. Stimulation of the SNr evoked inhibitory postsynaptic potentials (IPSPs) in 73 of the 104 neurons in the PPN. The IPSPs were abolished with a GABA(A) receptor antagonist, bicuculline. Inhibitory postsynaptic currents of the neurons were reversed in polarity at approximately -93.5 mV, which was close to the value of the equilibrium potential for chloride ions of -88.4 mV Single-cell reverse transcription-polymerise chain reactions revealed that approximately 30% (9/32) of the PPN neurons that received inhibition from the SNr expressed detectable levels of choline acetyltransferase mRNA. These findings show that output from the SNr regulates the activity of cholinergic PPN neurons through GABA(A) receptors.
引用
收藏
页码:879 / 886
页数:8
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