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首页> 外文期刊>Neurochemical Research >Norepinephrine Homogeneously Inhibits α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate- (AMPAR-) Mediated Currents in All Layers of the Temporal Cortex of the Rat
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Norepinephrine Homogeneously Inhibits α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate- (AMPAR-) Mediated Currents in All Layers of the Temporal Cortex of the Rat

机译:去甲肾上腺素均质抑制大鼠颞皮质各层中α-氨基-3-羟基-5-甲基-4-异恶唑丙酸酯-(AMPAR-)介导的电流

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摘要

The primary auditory cortex is subject to the modulation of numerous neurotransmitters including norepinephrine (NE), which has been shown to decrease cellular excitability by yet unclear mechanisms. We investigated the possibility that NE directly affects excitatory glutamatergic synapses. We found that bath applications of NE (20 μM) decreased glutamatergic excitatory post-synaptic currents (EPSCs) in all cortical layers. Changes in the kinetics of synaptic EPSCs, invariance of pair pulse ratio and of the coefficient-of-variation, together with the decrease of responses to pressure-application of AMPA (500 μM), indicated the postsynaptic nature of the adrenergic effect. Pharmacological experiments suggested that the NE-induced depression of EPSCs is caused by the activation of α1 adrenoceptors, PLC, and a Ca2+-independent PKC. We speculate that the decrease in temporal cortex excitability might promote a posterior-to-anterior shift in cortical activation together with a decrease in spontaneous background activity, resulting eventually in more effective sensory processing.
机译:初级听觉皮层受到包括去甲肾上腺素(NE)在内的多种神经递质的调节,这已经通过尚不清楚的机制降低了细胞的兴奋性。我们调查了NE直接影响兴奋性谷氨酸能突触的可能性。我们发现NE的沐浴液(20μM)可降低所有皮质层的谷氨酸能兴奋性突触后电流(EPSC)。突触EPSCs动力学的变化,脉冲对比率的不变性和变异系数,以及对AMPA(500μM)施加压力的响应减少,表明肾上腺素能效应的突触后性质。药理实验表明,NE诱导的EPSC抑制是由α1肾上腺素受体,PLC和Ca 2 + 非依赖性PKC的激活引起的。我们推测,颞皮质兴奋性的降低可能促进了皮层激活的从后向前移动以及自发背景活动的减少,最终导致了更有效的感觉处理。

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