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首页> 外文期刊>The European Journal of Neuroscience >Chronic stress attenuates GABAergic inhibition and alters gene expression of parvocellular neurons in rat hypothalamus.
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Chronic stress attenuates GABAergic inhibition and alters gene expression of parvocellular neurons in rat hypothalamus.

机译：慢性应激会减弱大鼠下丘脑中GABA能的抑制作用并改变小细胞神经元的基因表达。

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Abstract Chronic stress causes disinhibition of the hypothalamus-pituitary-adrenal axis. Consequently, the brain is overexposed to glucocorticoids which in humans may precipitate stress-related disorders, e.g. depression. The hypothalamus-pituitary-adrenal activity is strongly regulated by GABAergic input to parvocellular neurons in the hypothalamic paraventricular nucleus. We here report a reduced frequency of miniature inhibitory postsynaptic currents (mIPSCs) in parvocellular neurons of rats exposed to 3 weeks of unpredictable stress. The mIPSC amplitude and kinetic properties were unchanged, pointing to a presynaptic change caused by chronic stress. Because paired-pulse inhibition was unaffected by chronic stress, the number of functional GABAergic synaptic contacts rather than the release probability seems to be reduced after chronic stress. Linearly amplified RNA from postsynaptic cells was hybridized with multiple cDNA clones of interest, including most GABA(A) receptor subunits. In agreement with the electrophysiological observations, relative expression of the prevalent GABA(A)alpha1, alpha3, gamma1 and gamma2 receptor subunits, which largely contribute to the recorded responses, was not altered after chronic stress. However, expression of the extra-synaptic GABA(A)alpha5 subunit, earlier linked to depression in humans, and of the delta receptor subunit were found to be significantly changed. In conclusion, chronic stress leads to presynaptic functional alterations in GABAergic input to the paraventricular nucleus which could contribute to the observed disinhibition of the hypothalamus-pituitary-adrenal axis; additionally other aspects of GABAergic transmission may also be changed due to transcriptional regulation of specific receptor subunits in the parvocellular neurons.
机译：摘要慢性应激引起下丘脑-垂体-肾上腺轴的抑制。因此，大脑过度暴露于糖皮质激素，而糖皮质激素可能在人体内引起与压力有关的疾病，例如精神分裂症。萧条。下丘脑-垂体-肾上腺的活动受到下丘脑室旁核小细胞神经元的GABA能量输入的强烈调节。我们在这里报告暴露于不可预测的压力3周的大鼠小细胞神经元中的微型抑制突触后电流（mIPSCs）的频率降低。 mIPSC振幅和动力学特性未改变，表明慢性应激引起的突触前变化。由于成对脉冲抑制不受慢性应激的影响，慢性应激后功能性GABA能突触接触的数量而非释放几率似乎降低了。将来自突触后细胞的线性扩增RNA与多个目标cDNA克隆（包括大多数GABA（A）受体亚基）杂交。与电生理学观察结果一致，慢性应激后，未改变的主要是GABA（A）alpha1，alpha3，γ1和gamma2受体亚基的相对表达，这在很大程度上有助于记录的反应。但是，发现与人的抑郁症早期相关的突触外GABA（A）alpha5亚基的表达和δ受体亚基的表达发生了显着变化。总之，慢性应激导致GABA能输入到脑室旁核的突触前功能改变，这可能有助于观察到的下丘脑-垂体-肾上腺轴的抑制作用。另外，由于细小细胞神经元中特定受体亚基的转录调控，GABA能传递的其他方面也可能改变。

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