Primary afferent‐evoked glycine‐ and GABA‐mediated IPSPs in substantia gelatinosa neurones in the rat spinal cord in vitro.
Primary afferent‐evoked glycine‐ and GABA‐mediated IPSPs in substantia gelatinosa neurones in the rat spinal cord in vitro.
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DOI：
10.1113/jphysiol.1995.sp020497
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发表时间：
1995
期刊：
影响因子：
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通讯作者：
Mokoto Yoshimura;S. Nishi
中科院分区：
文献类型：
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作者：
Mokoto Yoshimura;S. Nishi
1.通过保留附着的背根的成年大鼠脊髓横切片中的胶质质（SG）神经元的细胞内记录，研究了甘氨酸和γ-氨基丁酸（GABA）作为脊髓背角抑制性递质的可能作用。 2.初级传入A δ纤维的刺激引起初始兴奋性突触后电位（快EPSP），随后是短和/或长抑制性突触后电位（短和长IPSP）。在接受抑制性输入的 29 个 SG 神经元 (37%) 中观察到的短 IPSP，平均潜伏期为 3.6 ms，半衰变时间为 11 ms，而在 37 个 SG 神经元 (47%) 中观察到的长 IPSP，平均潜伏期为 3.7 ms，半衰变时间为 42 ms。其余 12 个神经元 (16%) 表现出短 IPSP 和长 IPSP。两个 IPSP 在膜电位为 ‐70 +/- 4 mV 时都反转了极性。短IPSP被甘氨酸受体拮抗剂士的宁(0.5-2μM)可逆性阻断，而长IPSP被GABAA受体拮抗剂荷包牡丹碱(10-20μM)可逆性阻断。 3. 在大多数 SG 神经元中，短 IPSP 和长 IPSP 似乎是非突触的，并被非 N-甲基-D-天冬氨酸（非 NMDA）受体拮抗剂 6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX；5-10 microM）阻断。两种 IPSP 对 NMDA 受体拮抗剂 DL-2-氨基-5-磷酸戊酸 (APV；50-100 microM) 的敏感性较低（降低不到 30%）。 4. 在 10 个 SG 神经元 (13%) 中，应用谷氨酸盐 (0.5-2 mM) 增加了 IPSP 的幅度和频率，其时间进程与传入 A δ 纤维诱发的短 IPSP 的时间进程相似。谷氨酸诱导的短 IPSP 被河豚毒素 (0.5 µM) 或士的宁 (0.5-1 µM) 阻断。在 12 个神经元 (16%) 中，谷氨酸使膜超极化或增加了 IPSP 的振幅和频率，其时间进程与 A δ 纤维诱发的长 IPSP 的时间进程相似。谷氨酸诱导的膜超极化和长 IPSP 的幅度随着膜超极化而降低，并在 ‐70 +/- 6 mV 处反转极性。这些超极化反应被河豚毒素 (0.5 µM) 或荷包牡丹碱 (10 µM) 阻断。 5. 这些观察结果表明，初级传入 A δ 纤维主要通过非 NMDA 受体亚类激活甘氨酸能和/或 GABA 能中间神经元，并导致脊髓背角附近 SG 神经元的抑制。（摘要截断为 400 字）
1. The possible roles of glycine and gamma‐aminobutyric acid (GABA) as inhibitory transmitters in the spinal dorsal horn were studied by intracellular recordings from substantia gelatinosa (SG) neurones in transverse slices of the adult rat spinal cord which retained an attached dorsal root. 2. Stimulation of primary afferent A delta fibres evoked an initial excitatory postsynaptic potential (fast EPSP) followed by a short and/or long inhibitory postsynaptic potential (short and long IPSP). The short IPSP, observed in twenty‐nine SG neurones (37%) which received inhibitory inputs, had a mean latency of 3.6 ms and a half‐decay time of 11 ms, while the long IPSP had a mean latency of 3.7 ms and a half‐decay time of 42 ms and was observed in thirty‐seven SG neurones (47%). The remaining twelve neurones (16%) exhibited both short and long IPSPs. Both IPSPs reversed polarity at a membrane potential of ‐70 +/‐ 4 mV. The short IPSP was reversibly blocked by the glycine receptor antagonist strychnine (0.5‐2 microM), while the long IPSP was reversibly blocked by the GABAA receptor antagonist bicuculline (10‐20 microM). 3. In the majority of SG neurones, the short and long IPSPs appeared to be disynaptic and were blocked by the non‐N‐methyl‐D‐aspartic acid (non‐NMDA) receptor antagonist 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; 5‐10 microM). Both IPSPs were less sensitive (depressed by less than 30%) to the NMDA receptor antagonist DL‐2‐amino‐5‐phosphonovaleric acid (APV; 50‐100 microM). 4. In ten SG neurones (13%), bath‐applied glutamate (0.5‐2 mM) increased the amplitude and frequency of IPSPs, which had a similar time course to that of the short IPSP evoked by afferent A delta fibres. The glutamate‐induced short IPSPs were blocked by tetrodotoxin (0.5 microM) or strychnine (0.5‐1 microM). In twelve neurones (16%), glutamate hyperpolarized the membrane or increased the amplitude and frequency of IPSPs that had a similar time course to that of the A delta fibre‐evoked long IPSPs. The glutamate‐induced membrane hyperpolarization and long IPSPs decreased in amplitude with membrane hyperpolarization and reversed polarity at ‐70 +/‐ 6 mV. These hyperpolarizing responses were blocked by tetrodotoxin (0.5 microM) or bicuculline (10 microM). 5. These observations suggest that primary afferent A delta fibres activate glycinergic and/or GABAergic interneurones primarily through the non‐NMDA receptor subclass and result in inhibition of nearby SG neurones in the dorsal horn of the spinal cord.(ABSTRACT TRUNCATED AT 400 WORDS)