Orexinergic systems responsible for the mechanisms of involved in the initiation and selection of emotional motor behaviors.

穹隆周围外侧下丘脑的食欲素能神经元投射到中脑的结构，包括黑质和桥中被盖。这些区域包括中脑运动区(MLR)，以及在快速眼动(REM)睡眠中调节张力的桥脚核和背外侧被盖核(PPN/LDT)。食欲素能系统的缺陷导致发作性睡病，这表明这些投射与运动和肌肉张力之间的切换有关。本研究描述了这些食欲素能投射到中脑的作用。在去大脑的猫中，将食欲素-A(60μM至1.0 mm，0.20至0.25μ1)注入MLR可降低在跑步机上诱导运动所需的电刺激强度(4只猫)，甚至在没有电刺激的情况下引发运动运动。另一方面，当向PPN或黑质网状部(SNR)注射增食欲素时，PPN的刺激强度需要增加才能引起肌肉松弛。向PPN内注射GABA_A受体拮抗剂荷包牡丹碱(5 mM，0.2~0.25μL)，可逆转增食欲素对PPN和SNR的影响。这些结果表明，兴奋性食欲素能驱动可以通过增加MLR神经元的兴奋性来维持较高水平的运动活动，同时增强GABA能对可能是胆碱能的PPN神经元的影响，从而抑制肌肉松弛。我们得出结论，从下丘脑到中脑的食欲素能投射在调节运动行为、控制清醒和睡眠时的姿势肌张力和运动运动方面发挥着重要作用。此外，由于在没有食欲素的情况下兴奋性会减弱，当食欲素能系统功能正常时，向中脑发出的信号可能会诱导运动行为，但当食欲素能系统的功能受到干扰时，会引起紧张症或发作性睡病。

Orexinergic neurons in the perifornical lateral hypothalamus project to structures of the midbrain, including the substantia nigra and the mesopontine tegmentum. The areas contain the mesencephalic locomotor region (MLR), and the pedunculopontine and laterodorsal tegmental nuclei (PPN/LDT) which regulate atonia during rapid eye movement (REM) sleep. Deficiencies of the orexinergic system result in narcolepsy, suggesting that these projections are concerned with switching between locomotor movements and muscular atonia. The present study characterizes the role of these orexinergic projections to the midbrain. In decerebrate cats, injecting orexin-A (60μM to 1.0mM, 0.20 to 0.25μ1) into the MLR reduced the intensity of the electrical stimulation required to induce locomotion on a treadmill (4 cats) or even elicit locomotor movements without electrical stimulation. On the other hand, when orexin was injected into either the PPN or the substantia nigra pars reticulata (SNr), an increased stimulus intensity at the PPN was required to induce muscle atonia. The effects of orexin on the PPN and the SNr were reversed by subsequently injecting bicuculline (5mM, 0.20 to 0.25μl), a GABA_A receptor antagonist, into the PPN. These findings indicate that excitatory orexinergic drive could maintain a higher level of locomotor activity by increasing the excitability of neurons in the MLR, while enhancing GABAergic effects on presumably cholinergic PPN neurons, to suppress muscle atonia.We conclude that orexinergic projections from the hypothalamus to the midbrain play an important role in regulating motor behavior and controlling postural muscle tone and locomotor movements when awake and during sleep. Furthermore, as the excitability is attenuated in the absence of orexin, signals to the midbrain may induce locomotor behavior when the orexinergic system functions normally but elicit atonia or narcolepsy when the orexinergic function is disturbed.