Differential ontogenesis of presynaptic and postsynaptic GABAB inhibition in rat somatosensory cortex.
Differential ontogenesis of presynaptic and postsynaptic GABAB inhibition in rat somatosensory cortex.
复制标题
大鼠体感皮层突触前和突触后 GABAB 抑制的差异个体发生。
DOI：
10.1152/jn.1993.70.1.448
复制
发表时间：
1993
影响因子：
2.5
通讯作者：
Prince,DA
中科院分区：
文献类型：
--
作者：
Fukuda,A;Mody,I;Prince,DA
1.在体外培养的大鼠大脑皮层脑片上研究了γ-氨基丁酸（GABA）B受体介导的突触前抑制的生后成熟。膜片钳技术用于记录出生后第7-24天（P）动物中第II-III层神经元的全细胞抑制性突触后电流。在N-甲基-D-天冬氨酸（NMDA）和非NMDA型谷氨酸受体分别被D-氨基-膦酰基戊酸（D-AP 5，20 μ M）和6-氰基-7-硝基喹喔啉-2，3-二酮（CNQX，10 μ M）阻断后，诱发单突触抑制性突触后电流（IPSC）。这些IPSC仅由突触后GABAA受体介导，因为它们被荷包牡丹碱（10 μ M）消除，在氯平衡电位附近反转极性，并用含有Cs+的电极记录以阻断突触后GABAB反应。2.当成对的刺激分开的间隔为0.1-10秒被用来唤起IPSC，第二个反应被压抑，在300毫秒的效果是最大的。诱发IPSC也被巴氯芬（10 μ M）抑制。2-OH-萨氯芬（200 μ M）可降低或消除单突触IPSC的成对脉冲抑制（PPD）。这些结果表明，PPD的单突触IPSCs是由于突触前GABAB受体介导的抑制GABA的释放。3.不同年龄组（P7-10、P12-17、P22-24）神经元在任何刺激间期（0.1-10 s）的PPD含量均无显著性差异。（250字处删节）
1. The postnatal maturation of gamma-aminobutyric acid (GABA)B receptor-mediated presynaptic inhibition was studied in brain slices of rat somatosensory cortex maintained in vitro. Patchclamp techniques were used to record whole-cell inhibitory post-synaptic currents from layer II-III neurons in animals from postnatal days (P) 7-24. Monosynaptic inhibitory postsynaptic currents (IPSCs) were evoked after N-methyl-D-aspartate (NMDA) and non-NMDA type glutamate receptors had been blocked by D-amino-phosphonovaleric acid (D-AP5, 20 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), respectively. These IPSCs were solely mediated by postsynaptic GABAA receptors because they were abolished by bicuculline (10 microM), reversed polarity near the chloride equilibrium potential, and were recorded with electrodes that contained Cs+ to block postsynaptic GABAB responses. 2. When pairs of stimuli separated by intervals of 0.1-10 s were used to evoke IPSCs, the second response was depressed, an effect that was maximal at 300 ms. Evoked IPSCs were also depressed by baclofen (10 microM). The paired pulse depression (PPD) of monosynaptic IPSCs was decreased or eliminated by 2-OH-saclofen (200 microM). These findings indicate that PPD of monosynaptic IPSCs was due to presynaptic GABAB receptor-mediated inhibition of GABA release. 3. There were no significant differences in the amounts of PPD in neurons from different age groups (P7-10, P12-17, P22-24) at any interstimulus interval tested (0.1-10 s).(ABSTRACT TRUNCATED AT 250 WORDS)