Abstract：
The reticular thalamic nucleus (RTN) is a thin shell that covers the dorsal thalamus and controls the overall information flow from the thalamus to the cerebral cortex through GABAergic projections that contact thalamo-cortical neurons (TC). RTN neurons receive glutamatergic afferents fibers from neurons of the sixth layer of the cerebral cortex and from TC collaterals. The firing mode of RTN neurons facilitates the generation of sleep-wake cycles; a tonic mode or desynchronized mode occurs during wake and REM sleep and a burst-firing mode or synchronized mode is associated with deep sleep. Despite the presence of cannabinoid receptors CB1 (CB1Rs) and mRNA that encodes these receptors in RTN neurons, there are few works that have analyzed the participation of endocannabinoid-mediated transmission on the electrical activity of RTN. Here, we locally blocked or activated CB1Rs in ketamine anesthetized rats to analyze the spontaneous extracellular spiking activity of RTN neurons. Our results show the presence of a tonic endocannabinoid input, since local infusion of AM 251, an antagonist/inverse agonist, modifies RTN neurons electrical activity; furthermore, local activation of CB1Rs by anandamide or WIN 55212-2 produces heterogeneous effects in the basal spontaneous spiking activity, where the main effect is an increase in the spiking rate accompanied by a decrease in bursting activity in a dose-dependent manner; this effect is inhibited by AM 251. In addition, previous activation of GABA-A receptors suppresses the effects of CB1Rs on reticular neurons. Our results show that local activation of CB1Rs primarily diminishes the burst firing mode of RTn neurons.
摘要：
网状丘脑核（RTN）是覆盖背侧丘脑的薄壳，并通过与丘脑皮质神经元（TC）接触的GABA能投射来控制从丘脑到大脑皮层的整体信息流。RTN神经元接受来自大脑皮层第六层神经元和TC侧支的谷氨酸能传入纤维。RTN神经元的激发模式促进了睡眠-觉醒周期的生成;在觉醒和REM睡眠期间发生强直模式或去同步模式,并且突发激发模式或同步模式与深度睡眠相关联。尽管在RTN神经元中存在大麻素受体CB1（CB1R）和编码这些受体的mRNA，很少有文献分析内源性大麻素介导的传递对RTN电活动的参与。这里,我们在氯胺酮麻醉的大鼠中局部阻断或激活CB1Rs，以分析RTN神经元的自发细胞外尖峰活性。我们的结果表明存在补品内源性大麻素输入，由于局部输注了AM251，一种拮抗剂/反向激动剂，改变RTN神经元的电活动；此外，通过anandamide或WIN55212-2对CB1R的局部激活在基础自发加标活性中产生异质作用，其中主要作用是增加加标速率，并以剂量依赖性方式降低爆裂活性；AM251抑制了这种作用。此外,先前激活的GABA-A受体抑制CB1R对网状神经元的作用。我们的结果表明，CB1R的局部激活主要减少了RTn神经元的爆发放电模式。
