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首页> 外文期刊>The European Journal of Neuroscience >Motor activity is modulated via different neuronal circuits in rats with chronic liver failure than in normal rats.
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Motor activity is modulated via different neuronal circuits in rats with chronic liver failure than in normal rats.

机译：与正常大鼠相比，慢性肝功能衰竭大鼠通过不同的神经元回路调节运动活动。

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The mechanisms by which liver failure alters motor function remain unclear. It has been suggested that liver disease alters the neuronal circuit between basal ganglia and cortex that modulates motor function. Activation of group I metabotropic glutamate receptors in the nucleus accumbens (NAcc) by injecting (S)-3,5-dihydroxyphenylglycine (DHPG) activates this circuit and induces locomotion We analysed by in vivo brain microdialysis the function of the circuits that modulate motor function in rats with liver failure due to portacaval shunt (PCS). We inserted cannulae in the NAcc and microdialysis probes in the NAcc, ventral pallidum (VP), substantia nigra pars reticulata (SNr), medio-dorsal thalamus (MDT), ventro-medial thalamus (VMT) or prefrontal cortex (PFCx). We injected DHPG in the NAcc and analysed extracellular neurotransmitters concentration in these areas. The results indicate that in control rats DHPG induces locomotion by activating the 'normal' neuronal circuit: NAcc --> VP --> MDT --> PFCx.In PCS rats this circuit is not activated. In PCS rats, DHPG injection activates an 'alternative' circuit: NAcc --> SNr --> VMT --> PFCx. This circuit is not activated in control rats. DHPG injection increases dopamine in the NAcc of control but not of PCS rats, and glutamate in PCS but not in control rats. DHPG-induced increase in dopamine would activate the 'normal' neuronal circuit, while an increase in glutamate would activate the 'alternative' circuit. The identification of the mechanisms responsible for altered motor function and coordination in liver disease would allow designing treatments to improve motor function in patients with hepatic encephalopathy.
机译：肝衰竭改变运动功能的机制仍不清楚。已经提出，肝脏疾病会改变基底神经节和皮质之间的神经元回路，从而调节运动功能。通过注射（S）-3,5-二羟基苯基甘氨酸（DHPG）激活伏伏核（NAcc）中的I组代谢型谷氨酸受体，可激活该电路并诱导运动。我们通过体内脑微透析分析了调节运动功能的电路的功能。在因门腔分流（PCS）而导致肝衰竭的大鼠中。我们在NAcc中插入了套管，并在NAcc，腹侧苍白球（VP），黑质黑质（SNr），中背丘脑（MDT），腹内侧丘脑（VMT）或前额叶皮层（PFCx）中插入了微透析探针。我们将DHPG注射到NAcc中，并分析了这些区域的细胞外神经递质浓度。结果表明，在对照大鼠中DHPG通过激活``正常''神经元回路来诱导运动：NAcc-> VP-> MDT-> PFCx。在PCS大鼠中，该回路未激活。在PCS大鼠中，DHPG注射会激活“替代”回路：NAcc-> SNr-> VMT-> PFCx。在对照大鼠中未激活该电路。 DHPG注射可增加对照组（而非PCS大鼠）的NAcc中的多巴胺，并增加PCS（而非对照大鼠）的谷氨酸盐。 DHPG诱导的多巴胺增加会激活“正常”神经元回路，而谷氨酸的增加会激活“替代”回路。鉴定引起肝病中运动功能和协调功能改变的机制，可以设计治疗方法，以改善肝性脑病患者的运动功能。

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