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首页> 外文期刊>Journal of Neurophysiology >Interactions between GABA and glycine at inhibitory amino acid receptors on rat olfactory bulb neurons.
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Interactions between GABA and glycine at inhibitory amino acid receptors on rat olfactory bulb neurons.

机译:GABA和甘氨酸在大鼠嗅球神经元的抑制性氨基酸受体上的相互作用。

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Whole cell voltage-clamp electrophysiology was used to examine interactions between GABA and glycine at inhibitory amino acid receptors on rat olfactory bulb neurons in primary culture. Membrane currents evoked by GABA and glycine were selectively inhibited by low concentrations of bicuculline and strychnine, respectively, suggesting that they activate pharmacologically distinct receptors. However, GABA- and glycine-mediated currents showed cross-inhibition when the two amino acids were applied sequentially. Application of one amino acid inhibited the response to immediate subsequent application of the other. In the majority of neurons, GABA inhibited subsequent glycine-evoked currents and glycine inhibited subsequent GABA-evoked currents. In a small proportion of neurons, however, GABA inhibited glycine-evoked currents but glycine had little effect on GABA-evoked currents. The reverse was true in other neurons, suggesting that alterations in chloride gradients alone did not account for the cross-inhibition. Furthermore, no cross-inhibition was observed between GABA- and glycine-evoked currents in some neurons. The amplitude of the current evoked by the coapplication of saturating concentrations of GABA and glycine in these neurons was nearly the sum of the currents evoked by GABA and glycine alone. In contrast, the currents were not additive in neurons demonstrating cross-inhibition. These results suggest that olfactory bulb neurons heterogeneously express a population of inhibitory amino acid receptors that can bind either GABA or glycine. Interactions between GABA and glycine at inhibitory amino acid receptors may provide a mechanism to modulate inhibitory synaptic transmission.
机译:全细胞电压钳电生理用于检查原代培养中大鼠嗅球神经元的抑制性氨基酸受体上的GABA与甘氨酸之间的相互作用。 GABA和甘氨酸引起的膜电流分别被低浓度的小分子和士的宁选择性抑制,表明它们激活了药理学上不同的受体。但是,当依次施加两个氨基酸时,GABA和甘氨酸介导的电流显示出交叉抑制作用。一种氨基酸的应用抑制了对另一种氨基酸的立即后续应用的响应。在大多数神经元中,GABA抑制随后的甘氨酸诱发电流,而甘氨酸抑制随后的GABA诱发电流。然而,在小部分神经元中,GABA抑制了甘氨酸诱发的电流,但是甘氨酸对GABA诱发的电流影响很小。相反,在其他神经元中也是如此,这表明仅氯化物梯度的改变不能解释交叉抑制作用。此外,在某些神经元中,在GABA和甘氨酸诱发的电流之间未观察到交叉抑制。在这些神经元中共同施加饱和浓度的GABA和甘氨酸引起的电流幅度几乎等于GABA和甘氨酸单独引起的电流之和。相反,电流在证明交叉抑制的神经元中不加和。这些结果表明,嗅球神经元异质表达可结合GABA或甘氨酸的抑制性氨基酸受体。 GABA和甘氨酸在抑制性氨基酸受体之间的相互作用可能提供调节抑制性突触传递的机制。

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