Synaptic strength between motoneurons and terminals of the dorsolateral funiculus is regulated by GABA receptors in the turtle spinal cord

被引:18
作者
Delgado-Lezama, R [1 ]
Aguilar, J [1 ]
Cueva-Rolón, R [1 ]
机构
[1] Inst Politecn Nacl, Ctr Invest & Estudios Avanzados, Dept Fisiol Biofis & Neurociencias, Mexico City 07000, DF, Mexico
关键词
D O I
10.1152/jn.00569.2003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The role of GABA(A) and GABA(B) receptors in modulation of excitatory synaptic transmission between motoneurons and terminals from dorsolateral funiculus (DLF) was studied in in vitro spinal cord slices of adult turtles. Muscimol-a GABA(A) receptor agonist-depressed the monosynaptic excitatory postsynaptic potential (EPSP) induced by stimulation of the DLF and shortened its duration. The input resistance and the membrane time constant also were strongly reduced. The input membrane resistance, the amplitude, and the half-width of the EPSP were reduced at the same rate in the presence of muscimol. Bicuculline-a GABA(A) receptor antagonist-increased the EPSPs amplitude and the input membrane resistance. The EPSP amplitude ratio elicited by a paired-pulse protocol did not change significantly. Our results suggest that muscimol acts mainly by activation of postsynaptic GABA(A) receptors located on the motoneuron and the synaptic strength on motoneurons may be modulated by tonic activation of postsynaptic GABA(A) receptors. Baclofen-a GABA(B) receptor agonist-also depressed DLF-motoneuron synaptic transmission. However, it did not affect the falling phase of the EPSPs or the motoneuron membrane time constant but induced a small decrement in input resistance. In the presence of baclofen, the amplitude ratio produced by a paired-pulse protocol increased significantly. This suggests that baclofen decreased the synaptic strength by inhibition of neurotransmitter release from the DLF terminals via activation of presynaptic GABA(B) receptors.
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页码:40 / 47
页数:8
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