Fenik Victor B
Department of Veterans Affairs Greater Los Angeles Healthcare System , Los Angeles, CA , USA ; Websciences International , Los Angeles, CA , USA.
Front Neurol. 2015 Dec 1;6:254. doi: 10.3389/fneur.2015.00254. eCollection 2015.
We reassessed and provided new insights into the findings that were obtained in our previous experiments that employed the injections of combined adrenergic, serotonergic, GABAergic, and glycinergic antagonists into the hypoglossal nucleus in order to pharmacologically abolish the depression of hypoglossal nerve activity that occurred during carbachol-induced rapid-eye-movement (REM) sleep-like state in anesthetized rats. We concluded that noradrenergic disfacilitation is the major mechanism that is responsible for approximately 90% of the depression of hypoglossal motoneurons, whereas the remaining 10% can be explained by serotonergic mechanisms that have net inhibitory effect on hypoglossal nerve activity during REM sleep-like state. We hypothesized that both noradrenergic and serotonergic state-dependent mechanisms indirectly control hypoglossal motoneuron excitability during REM sleep; their activities are integrated and mediated to hypoglossal motoneurons by reticular formation neurons. In addition, we proposed a brainstem neural circuit that can explain the new findings.
我们重新评估了先前实验中的发现，并提供了新的见解。在先前的实验中，我们向舌下神经核注射了肾上腺素能、血清素能、GABA能和甘氨酸能拮抗剂，以药理学方法消除在麻醉大鼠中卡巴胆碱诱导的快速眼动（REM）睡眠样状态期间发生的舌下神经活动抑制。我们得出结论，去甲肾上腺素能去易化是导致约90%舌下运动神经元抑制的主要机制，而其余10%可由血清素能机制解释，该机制在REM睡眠样状态期间对舌下神经活动具有净抑制作用。我们假设，去甲肾上腺素能和血清素能状态依赖性机制在REM睡眠期间间接控制舌下运动神经元的兴奋性；它们的活动由网状结构神经元整合并介导至舌下运动神经元。此外，我们提出了一个脑干神经回路来解释这些新发现。
