Trigeminal input exerts acute and chronic effects on the brain, modulating cognitive functions. Here, new data from humans and animals suggest that these effects are caused by trigeminal influences on the Locus Coeruleus (LC). In humans subjects clenching with masseter asymmetric activity, occlusal correction improved cognition, alongside with reductions in pupil size and anisocoria, proxies of LC activity and asymmetry, respectively. Notably, reductions in pupil size at rest on the hypertonic side predicted cognitive improvements. In adult rats, a distal unilateral section of the trigeminal mandibular branch reduced, on the contralateral side, the expression of c-Fos (brainstem) and BDNF (brainstem, hippocampus, frontal cortex). This counterintuitive finding can be explained by the following model: teeth contact perception loss on the lesioned side results in an increased occlusal effort, which enhances afferent inputs from muscle spindles and posterior periodontal receptors, spared by the distal lesion. Such effort leads to a reduced engagement of the intact side, with a corresponding reduction in the afferent inputs to the LC and in c-Fos and BDNF gene expression. In conclusion, acute effects of malocclusion on performance seem mediated by the LC, which could also contribute to the chronic trophic dysfunction induced by loss of trigeminal input.

三叉神经输入对大脑产生急性和慢性影响，调节认知功能。来自人类和动物的新数据表明，这些影响是由三叉神经对蓝斑 (LC) 的影响引起的。在咬肌不对称活动咬紧的人类受试者中，咬合矫正改善了认知能力，同时瞳孔大小和瞳孔不等小（分别代表 LC 活动和不对称性）减小。值得注意的是，高渗侧静息时瞳孔尺寸的减小预示着认知能力的改善。在成年大鼠中，三叉神经下颌支的远端单侧部分在对侧的 c-Fos（脑干）和 BDNF（脑干、海马、额叶皮层）的表达减少。这一违反直觉的发现可以通过以下模型来解释：病变侧的牙齿接触知觉丧失导致咬合力增加，从而增强了来自肌梭和后牙周受体的传入输入，而远端病变则不受此影响。这种努力导致完整侧的参与减少，相应地减少了 LC 的传入输入以及 c-Fos 和 BDNF 基因表达。总之，咬合不正对表现的急性影响似乎是由 LC 介导的，这也可能导致三叉神经输入损失引起的慢性营养功能障碍。