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Schizophrenia, Hypocretin (Orexin), and the Thalamocortical Activating System

机译:精神分裂症,促肾上腺皮质激素(Orexin)和丘脑皮质激活系统

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摘要

Diminished connectivity between midline-intralaminar thalamic nuclei and prefrontal cortex has been suggested to contribute to cognitive deficits that are detectable even in early stages of schizophrenia. The midline-intralaminar relay cells comprise the final link in the ascending arousal pathway and are selectively excited by the wake-promoting peptides hypocretin 1 and 2 (orexin A and B). This excitation occurs both at the level of the relay cell bodies and their axon terminals within prefrontal cortex. In rat brain slices, the release of glutamate from midline-intralaminar thalamocortical terminals induces excitatory postsynaptic currents (EPSCs) in layer V pyramidal cells in prefrontal cortex. When hypocretin is infused into medial prefrontal cortex of behaving animals, it improves performance in a complex cognitive task requiring divided attention. Chronic restraint stress causes atrophy of the apical dendritic arbors in layer V prefrontal pyramidal cells and leads to a reduction in hypocretin-induced EPSCs, indicating impairment in excitatory thalamocortical transmission. Thus, taken together with evidence for an underlying loss of excitatory thalamocortical connectivity in schizophrenia, stress in this illness could further exacerbate a breakdown in cortical processing of incoming information from the ascending arousal system.
机译:已提出中线-腹腔丘脑核与前额叶皮层之间的连通性降低会导致认知缺陷,甚至在精神分裂症的早期也可以检测到。中线-肠内中继细胞构成了上升的唤醒途径中的最后一个环节,并被促唤醒肽的hypocretin 1和2(orexin A和B)选择性地激发。这种激发同时发生在前额叶皮层的中继细胞体及其轴突末端的水平上。在大鼠脑切片中,谷氨酸从中线-腹腔内丘脑皮层末端释放,在额叶前皮质的V层锥体细胞中引起兴奋性突触后突触电流(EPSC)。当将降钙素注入行为动物的内侧前额叶皮层中时,它可以改善需要分立注意的复杂认知任务中的表现。慢性束缚应激会导致V层前额叶锥体细胞的顶端树突状树突萎缩,并导致降钙素诱导的EPSC减少,表明兴奋性丘脑皮质传递受到损害。因此,与精神分裂症中兴奋性丘脑皮质连通性基本丧失的证据一起,这种疾病中的压力可能会进一步加剧来自上升觉醒系统的传入信息的皮质处理能力的恶化。

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