Su C K, Chai C Y
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, China.
Neurosci Lett. 1998 Jun 5;248(3):191-4. doi: 10.1016/s0304-3940(98)00361-9.
Phrenic motoneurons (PMNs) receive intermittently glutaminergic inspiratory drives and GABAergic inhibition in adult mammals. Since gamma-amino-butyric acid (GABA) might act as an excitatory amino acid in early stages of development, we here investigated if GABA(A) receptors inhibit PMNs in neonates. Using in vitro neonatal rat brainstem-spinal cord preparation, local application of GABA and muscimol (a GABA(A) receptor agonist) to the vicinity of PMNs consistently reduced the inspiratory activity of C4 ventral roots. Under whole-cell patch-clamp conditions and in the presence of 0.5 microM TTX to block synaptic transmission, muscimol (10 microM) decreased whole-cell input resistance, and surprisingly, when PMNs were voltage-clamped at their resting membrane potential, muscimol induced depolarizing-inward, rather than hyperpolarizing-outward membrane current. Our findings indicate that GABA(A) receptors mediate a depolarizing blockade of the glutaminergic excitatory inputs to neonatal rat PMNs.
在成年哺乳动物中,膈运动神经元(PMNs)间歇性地接受谷氨酰胺能吸气驱动和GABA能抑制。由于γ-氨基丁酸(GABA)在发育早期可能作为兴奋性氨基酸起作用,我们在此研究了GABA(A)受体是否在新生儿中抑制PMNs。使用新生大鼠脑桥-脊髓的体外制备,将GABA和蝇蕈醇(一种GABA(A)受体激动剂)局部应用于PMNs附近,持续降低C4腹根的吸气活动。在全细胞膜片钳条件下,且存在0.5微摩尔TTX以阻断突触传递时,蝇蕈醇(10微摩尔)降低了全细胞输入电阻,令人惊讶的是,当将PMNs钳制在其静息膜电位时,蝇蕈醇诱导内向去极化而非外向超极化膜电流。我们的研究结果表明,GABA(A)受体介导对新生大鼠PMNs谷氨酰胺能兴奋性输入的去极化阻断。