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首页> 外文期刊>Journal of Neurophysiology >EPSP amplitude modulation at the rat Ia-alpha motoneuron synapse: effects of GABAB receptor agonists and antagonists.
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EPSP amplitude modulation at the rat Ia-alpha motoneuron synapse: effects of GABAB receptor agonists and antagonists.

机译：大鼠Ia-α运动神经元突触处的EPSP调幅：GABAB受体激动剂和拮抗剂的作用。

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The object of this study was to examine the relationship between excitatory postsynaptic potential (EPSP) amplitude, posttetanic potentiation, and EPSP amplitude modulation at synapses made by group Ia afferents on motoneurons in the rat. These relationships were evaluated in cells in untreated rats and in cells in rats treated with the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen and antagonist CGP-35348, which were used to manipulate Ca2+ entry into presynaptic terminals and consequently probability of transmitter release from them. There was no evidence for postsynaptic action of these drugs from measurement of their effects on motoneuron properties. During high-frequency stimulation (32 shock bursts at 167 Hz), EPSP amplitude either decreased (negative modulation) or increased (positive modulation) in response to successive stimuli at different connections. In untreated rats this frequency-dependent amplitude modulation behavior was inversely but weakly correlated with EPSP amplitude measured at low frequency. Intravenous (iv) administration of the GABAB agonist, baclofen, produced a marked and progressive decrease in EPSP amplitude measured at low frequency coincident with a change in frequency-dependent EPSP amplitude modulation toward more positive values (synaptic facilitation). In contrast, an increase in EPSP amplitude occurred after iv administration of the GABAB antagonist CGP-35348 that was accompanied by a negative shift in EPSP amplitude modulation during high-frequency stimulation. The negative shift in EPSP amplitude modulation (synaptic depression) after CGP-35348 application was much smaller than the positive shift induced by baclofen when normalized to the change in EPSP amplitude. Posttetanic potentiation decreased after baclofen but did not increase after CGP-35348. The relationship between modulation and EPSP amplitude was much steeper after GABAB receptor manipulation in either direction than that observed in the population of motoneurons in untreated preparations. This suggests that in the rat differences in probability of release play at most a small role in determining EPSP amplitude across the motoneuron pool.
机译：这项研究的目的是要检查兴奋性突触后电位（EPSP）振幅，破伤风后电位和在运动神经元的Ia组传入突触产生的突触之间EPSP振幅调制之间的关系。在未治疗的大鼠的细胞中以及在用γ-氨基丁酸-B（GABAB）受体激动剂巴氯芬和拮抗剂CGP-35348治疗的大鼠中的细胞中评估了这些关系，这些细胞被用来操纵Ca2 +进入突触前末端并因此控制递质的发生。从他们那里释放。通过测量它们对运动神经元特性的影响，没有证据表明这些药物具有突触后作用。在高频刺激期间（在167 Hz处有32个电击脉冲），EPSP振幅响应于不同连接处的连续刺激而减小（负调制）或增大（正调制）。在未经治疗的大鼠中，这种依赖于频率的幅度调制行为与低频测量的EPSP幅度成反比，但与之弱相关。静脉内（iv）施用GABAB激动剂巴氯芬导致低频下测得的EPSP振幅显着且逐渐下降，这与频率依赖性EPSP振幅调制向更正值的变化（突触促进）相吻合。相反，静脉内施用GABAB拮抗剂CGP-35348后，EPSP振幅增加，这伴随着高频刺激过程中EPSP振幅调制的负向移动。当将CGP-35348标准化为EPSP振幅变化后，施加CGP-35348后EPSP振幅调制的负位移（突触抑制）远小于巴氯芬引起的正位移。巴氯芬后强直性增强作用减弱，而CGP-35348后不增强。与未处理制剂中的运动神经元群体中观察到的相比，在任一方向上操纵GABA B受体后，调制度与EPSP振幅之间的关系要陡得多。这表明在大鼠中，释放概率的差异最多在确定整个运动神经元池中EPSP振幅中起很小的作用。

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