暂无摘要。

The neuroanatomical circuitry of jaw muscles has been mostly explored in non-human animals. A recent rodent study revealed a novel circuit from the central amygdala (CeA) to the trigeminal motor nucleus (5M), which controls biting attacks. This circuit has yet to be delineated in humans. Ultra-high diffusion-weighted imaging data from the Human Connectome Project (HCP) allow in vivo delineation of circuits identified in other species-for example, the CeA-5M pathway-in humans. We hypothesized that the CeA-5M circuit could be resolved in humans at both 7 and 3 T. We performed probabilistic tractography between the CeA and 5M in 30 healthy young adults from the HCP database. As a negative control, we performed tractography between the basolateral amygdala (BLAT) and 5M, as CeA is the only amygdalar nucleus with extensive projections to the brainstem. Connectivity strength was operationalized as the number of streamlines between each region of interest. Connectivity strength between CeA-5M and BLAT-5M within each hemisphere was compared, and CeA-5M circuit had significantly stronger connectivity than the BLAT-5M circuit, bilaterally at both 7 T (all p < .001) and 3 T (all p < .001). This study is the first to delineate the CeA-5M circuit in humans.

Psychological stress is commonly accepted to be closely associated with masticatory muscle disorder, which is the main symptom of temporomandibular disorder (TMD). Previous studies have confirmed that exposure to stress may cause masticatory muscle hyperactivity. However, the central mechanism underlying this process remains unclear. The mesencephalic trigeminal nucleus (Vme), which resides in the brainstem, is the primary afferent center for masticatory proprioception and plays a key role in oral-motor movements by projecting to the trigeminal motor nucleus (Vmo). Therefore, the present study was designed to examine the role of Vme neurons in masseter overactivity induced by chronic stress. We found that subjecting mice to restraint stress (6 h/day) for 14 days caused significant anxiety-like behavior, obvious masseter overactivity, and markedly enhanced electrophysiological excitability of Vme neurons. By using anterograde tract tracing combined with immunofluorescence staining methods, we observed vesicular glutamate transporter 1 (VGLUT1)-positive glutamatergic projections from the Vme to the Vmo. Moreover, chronic restraint stress (CRS) elevated the expression of VGLUT1 and choline acetyltransferase (ChAT) in Vmo. Furthermore, administration of VGLUT1-targeted short hairpin RNA (shRNA) into the bilateral Vme significantly suppressed the enhanced overexcitability of Vme neurons, downregulated the overexpression of VGLUT1 and ChAT in the Vmo, and attenuated the elevated overactivity of the masseter caused by CRS. Taken together, we showed that CRS can excite neurons in the Vme, enhancing glutamatergic excitatory projections from the Vme to the Vmo and resulting in masseter muscle overactivity. These findings provide us with a novel central mechanism underlying the correlation between psychological factors and TMD.

Proprioception from masticatory apparatus and periodontal ligaments comes through the trigeminal mesencephalic nucleus (Vmes). We evaluated the effects of tooth loss on neurodegeneration of the Vmes and trigeminal motor nucleus (Vmo). Bilateral maxillary molars of 2-month-old C57BL/6J mice were extracted under anesthesia. Neural projections of the Vmes to the periodontium were confirmed by injecting Fluoro-Gold (FG) retrogradely into the extraction sockets, and for the anterograde labeling adeno-associated virus encoding green fluorescent protein (AAV-GFP) was applied. For immunohistochemistry, Piezo2, ATF3, Caspase 3, ChAT and TDP-43 antibodies were used. At 1 month after tooth extraction, the number of Piezo2-immunoreactive (IR) Vmes neurons were decreased significantly. ATF3-IR neurons were detected on day 5 after tooth extraction. Dead cleaved caspase-3-IR neurons were found among Vmes neurons on days 7 and 12. In the Vmo, neuronal cytoplasmic inclusions (NCIs) formation type of TDP-43 increased at 1 and 2 months after extraction. These indicate the existence of neural projections from the Vmes to the periodontium in mice and that tooth loss induces the death of Vmes neurons followed by TDP-43 pathology in the Vmo. Therefore, tooth loss induces Vmes neuronal cell death, causing Vmo neurodegeneration and presumably affecting masticatory function.

Alzheimer\'s disease (AD) shows various symptoms that reflect cognitive impairment and loss of neural circuit integrity. Sensory dysfunctions such as olfactory and ocular pathology are also observed and used as indicators for early detection of AD. Although mastication is suggested to correlate with AD progression, changes in the masticatory system have yet to be established in transgenic animal models of AD. In the present study, we have assessed pathologic hallmarks of AD with the masticatory behavior of 5XFAD mice. We found that masticatory efficiency and maximum biting force were decreased in 5XFAD mice, with no significant change in general motor function. Immunohistochemical analysis revealed significant accumulation of Aβ (amyloid β), increased microglia number, and cell death in Vmo (trigeminal motor nucleus) as compared with other cranial motor nuclei that innervate the orofacial region. Masseter muscle weight and muscle fiber size were also decreased in 5XFAD mice. Taken together, our results demonstrate that Aβ accumulation in Vmo contributes to masticatory dysfunction in 5XFAD mice, suggesting a close association between masticatory dysfunction and dementia.

In the present report, we discussed the case of a 57-year-old man with unilateral masticatory muscle weakness, nystagmus, skew deviation and facial hypesthesia due to pontine tegmental infarction. Trigeminal motor neuropathy attributed to brain infarction is very rare. Brain magnetic resonance imaging revealed a small dot-like infarction lesion in the pontine tegmentum. Masticatory muscle weakness was confirmed by an electrophysiological study performed on the day after admission in which there was an incomplete interference pattern without spontaneous denervation activity, suggesting that the patient\'s masseter muscle weakness was caused by an infarction of the trigeminal motor nucleus proper or trigeminal motor nerve fascicles rather than Wallerian degeneration of the trigeminal nerve or the progression of masseter muscle degeneration.

暂无摘要。

Objective: To determine the opening and closing action of the external muscle, the projection pathway of the axon terminal of trigeminal motor nucleus (Vmo) neuron to the lateral pterygoid muscle was revealed. Methods: In this study, 10 SD rats of 8 weeks old were included. The left lateral pterygoid muscle of SD rats was surgically exposed, and the wound was closed after intramuscular injection of hydroxystilbamidine/fluorogold (FG) 3-5 μl. Seven days after the operation, the experimental animals were perfused, samples collected and sectioned for immunofluorescence staining. After FG injection into the lateral pterygoid muscle, the FG reversed in the Vmo neurons. Results: In the Vmo neurons on the FG injection side (left side), a large number of FG reversed neurons were found in the corpus luteum and dendrites. These neurons were not only distributed in the dorsolateral part of the trigeminal motor nucleus that innervated the closed muscle, but also in the ventral medial portion of the trigeminal nucleus of the open muscle. Conclusions: The neuronal conduction pathway between the Vmo and the lateral pterygoid muscle innervates the lateral pterygoid muscle. The neurons are distributed both in the dorsolateral and in the nucleus of the ventral ventricle. It is concluded that the lateral pterygoid muscle involve in the jaw closing and opening movement.
目的： 通过对SD大鼠三叉神经运动核（trigeminal motor nucleus，Vmo）-翼外肌神经元投射通路的定性研究分析，揭示Vmo神经元轴突终末向翼外肌的投射通路，以确定翼外肌的开闭口作用。 方法： 纳入8周龄SD大鼠10只，手术暴露SD大鼠左侧翼外肌，肌内注射荧光金3~5 μl后，关闭并缝合伤口。术后7 d，实验动物灌注、取材、切片后免疫荧光染色，荧光显微镜下观察荧光金注入翼外肌后，在三叉神经运动核内荧光金的逆行标记情况。 结果： 在荧光金注射侧的Vmo神经元内可见大量的荧光金逆标神经元的胞体和树突，这些神经元不仅分布于支配闭口肌的三叉神经运动核的背外侧部，也分布于支配开口肌的三叉神经运动核的腹内侧部。 结论： Vmo与翼外肌之间的神经元传导通路支配翼外肌，神经元既分布在背外侧部也分布在腹内侧部的核团内，推断翼外肌既在开口运动中发挥作用，又在闭口运动中发挥作用。.

Current scientific literature provides evidence that trigeminal sensorimotor activity associated with chewing may affect arousal, attention, and cognitive performance. These effects may be due to widespread connections of the trigeminal system to the ascending reticular activating system (ARAS), to which noradrenergic neurons of the locus coeruleus (LC) belongs. LC neurons contain projections to the whole brain, and it is known that their discharge co-varies with pupil size. LC activation is necessary for eliciting task-related mydriasis. If chewing effects on cognitive performance are mediated by the LC, it is reasonable to expect that changes in cognitive performance are correlated to changes in task-related mydriasis. Two novel protocols are presented here to verify this hypothesis and document that chewing effects are not attributable to aspecific motor activation. In both protocols, performance and pupil size changes observed during specific tasks are recorded before, soon after, and half an hour following a 2 min period of either: a) no activity, b) rhythmic, bilateral handgrip, c) bilateral chewing of soft pellet, and d) bilateral chewing of hard pellet. The first protocol measures level of performance in spotting target numbers displayed within numeric matrices. Since pupil size recordings are recorded by an appropriate pupillometer that impedes vision to ensure constant illumination levels, task-related mydriasis is evaluated during a haptic task. Results from this protocol reveal that 1) chewing-induced changes in performance and task-related mydriasis are correlated and 2) neither performance nor mydriasis are enhanced by handgrip. In the second protocol, use of a wearable pupillometer allows measurement of pupil size changes and performance during the same task, thus allowing even stronger evidence to be obtained regarding LC involvement in the trigeminal effects on cognitive activity. Both protocols have been run in the historical office of Prof. Giuseppe Moruzzi, the discoverer of ARAS, at the University of Pisa.

Functional imaging of the brainstem may open new avenues for clinical diagnostics. However, for reliable assessments of brainstem activation, further efforts improving signal quality are needed. Six healthy subjects performed four repeated functional magnetic resonance imaging (fMRI) sessions on different days with jaw clenching as a motor task to elicit activation in the trigeminal motor nucleus. Functional images were acquired with a 7 T MR scanner using an optimized multiband EPI sequence. Activation measures in the trigeminal nucleus and a control region were assessed using different physiological noise correction methods (aCompCor and RETROICOR-based approaches with variable numbers of regressors) combined with cerebrospinal fluid or brainstem masking. Receiver-operating characteristic analyses accounting for sensitivity and specificity, activation overlap analyses to estimate the reproducibility between sessions, and intraclass correlation analyses (ICC) for testing reliability between subjects and sessions were used to systematically compare the physiological noise correction approaches. Masking the brainstem led to increased activation in the target ROI and resulted in higher values for the area under the curve (AUC) as a combined measure for sensitivity and specificity. With the highest values for AUC, activation overlap, and ICC, the most favorable physiological noise correction method was to control for the cerebrospinal fluid time series (aCompCor with one regressor). Brainstem motor nuclei activation can be reliably identified using high-field fMRI with optimized acquisition and processing strategies-even on single-subject level. Applying specific physiological noise correction methods improves reproducibility and reliability of brainstem activation encouraging future clinical applications.