MODEL FOR MODE OF ACTION OF GABA ON PRIMARY AFFERENT TERMINALS - DEPOLARIZING EFFECTS OF GABA APPLIED IONTOPHORETICALLY TO NEURONS OF MAMMALIAN DORSAL ROOT GANGLIA
MODEL FOR MODE OF ACTION OF GABA ON PRIMARY AFFERENT TERMINALS - DEPOLARIZING EFFECTS OF GABA APPLIED IONTOPHORETICALLY TO NEURONS OF MAMMALIAN DORSAL ROOT GANGLIA
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DOI：
10.1016/0028-3908(74)90145-2
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发表时间：
1974-01-01
影响因子：
4.7
通讯作者：
RASMINSKY, M
中科院分区：
文献类型：
--
作者：
FELTZ, P;RASMINSKY, M
在戊巴比妥钠麻醉的大鼠上，测定了腰脊神经节感觉神经元对γ-氨基丁酸（GABA）的反应。细胞内的记录，从他们的逆向背根刺激的反应确定的细胞。γ-氨基丁酸施加到刺穿的神经元的细胞外位点，在那里记录2 - 10 mV的单位诱发场电位。GABA的共同作用是膜电位的可逆去极化转变，可以直接从直流膜电位记录或间接从交流膜电位记录中确定记录逆向尖峰的分量的幅度变化：即峰值和超极化后电位。对GABA的去极化反应经常促进重复放电，并且通常经历快速的“脱敏”。GABA引起的膜电位变化与膜电阻的一致性降低有关，这种降低可以通过直接测量输入电阻或间接测量峰电位幅度与膜极化之间的关系来确定，本文建议进一步研究GABA对脊神经节神经元的这种去极化作用，作为确定GABA去极化的离子依赖性的模型这些反应可能介导初级传入终末的突触前抑制。
In rats under pentobarbitone anaesthesia, γ-aminobutyric acid (GABA) was tested on sensory neurones of lumbar spinal ganglia. Intracellular recordings were made from cells identified by their response to antidromic dorsal root stimulation. γ-Aminobutyric acid was applied to the impaled neurones by microiontophoresis at extracellular sites where unitary evoked field potentials of 2 10 mV were recorded. The common effect of GABA was a reversible depolarizing shift of the membrane potential, ascertained either directly from d.c. membrane potential recordings or indirectly from a.c. recordings of changes in amplitude of the components of the antidromic spike: i.e. peak and hyperpolarizing after-potential. The depolarizing response to GABA often promoted repetitive firing and generally underwent rapid “desensitization”. The changes in membrane potential induced by GABA were associated with a consistent decrease in the membrane resistance ascertained either by direct measurements of the input resistance or indirect estimates from changes of the relationship between spike amplitude and membrane polarization.It is proposed to investigate further this depolarizing action of GABA on spinal ganglia neurones as a model for the determination of the ionic dependency of GABA depolarizing responses which are likely to mediate presynaptic inhibition on primary afferent terminals.