首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Stress-induced, glucocorticoid-dependent strengthening of glutamatergic synaptic transmission in midbrain dopamine neurons.
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Stress-induced, glucocorticoid-dependent strengthening of glutamatergic synaptic transmission in midbrain dopamine neurons.

机译:应激诱导的中脑多巴胺神经元中谷氨酸能突触传递的糖皮质激素依赖性增强。

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摘要

Stress facilitates development of addictive behaviors in part by stress-induced increase in the strength of glutamatergic synapses at dopamine (DA) neurons within the ventral tegmental area (VTA). Here, we further demonstrate that this stress-induced synaptic adaptation is glucocorticoid-dependent and is progressively developed. Activation of glucocorticoid receptors (GRs) either by in vivo injection of dexamethasone (Dex) or incubation of the VTA slice with Dex potentiate the synaptic strength of glutamatergic synapses at VTA DA neurons, whereas preventing the activation of GRs by Ru486 abolishes this effect. These results suggest that the VTA GRs play a critical role in stress-induced cellular adaptations.
机译:应激促进上瘾行为的发展,部分原因是应激引起的腹侧被盖区(VTA)内多巴胺(DA)神经元的谷氨酸能突触强度增加。在这里,我们进一步证明这种应激诱导的突触适应是糖皮质激素依赖性的,并且是逐步发展的。通过体内注射地塞米松(Dex)或将VTA切片与Dex一起孵育来激活糖皮质激素受体(GRs),可以增强VTA DA神经元的谷氨酸能突触的突触强度,而通过Ru486阻止GRs的激活可以消除这种作用。这些结果表明,VTA GRs在应激诱导的细胞适应中起关键作用。

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