Electromyography and Fos immunostaining study establish a possible functional link between trigeminal proprioception and the oculomotor system in rats

The objective of this study was to explore whether there was a functional link between trigeminal proprioception and the oculomotor system mediated through jaw muscle afferents.Electromyography（EMG） was undertaken of the levator palpebrae（LP） and superior rectus（SR）,and Fos expression was detected in the brainstem following consecutive down-stretching of the lower jaw at 2-4 Hz in rats.Retrograde tracing was undertaken of the interstitial nucleus of Cajal and Darkschewitsch nucleus（INC/DN） pre-oculomotor neurons.FMG-like responses were recorded from the LP/SR during down-stretching of the lower jaw at 2-4 Hz in 3 out of 11 rats.Fos expression was induced by consecutive down-stretching of the lower jaw at 2-4 Hz for 20-30 seconds.Interestingly,Fos expression was distributed mainly in the bilateral INC/DN area.We also examined Fos-like immunoreactivity in central mesencephalic and paramedian pontine reticular formation that harbors premotor neurons controlling horizontal eye movement,but no Fos-like staining was observed therein.By injection of retrograde tracers into the oculomotor nucleus combined with Fos immunostaining,double labeled pre-oculomotor neurons were visualized to distribute in the INC/DN.In conclusions,there may exist a trigeminal proprioceptive-oculomotor system neural circuit through jaw muscle afferents in rats.Judging from Fos distribution pattern,this pathway might be related to vertical and torsional eye movements.

Is Marcus Gunn jaw winking a primitive reflex？ Rat neuroanatomy

AIM： To investigate a possible trigeminal proprioceptive- oculomotor neural pathway and explore possible synaptic connections between neurons in this pathway. Attempt to bring a new insight to mechanism of Marcus Gunn syndrome （MGS）. METHODS： Anterograde and retrograde tract tracing was applied and combined with immunofluorescent stain in rats. After electrophysiological identifying mesencephalic trigeminal nucleus （Vine） neurons, intracellular injection of tracer was performed to trace axon trajectory. RESULTS： Following injections of anterograde tracers into the Vine, labeled terminals were observed ipsilateral in oculomotor and trochlear nuclei （Ill/IV）, as well as in their premotor neurons in interstitial nucleus of Cajal and Darkschewitsch nucleus （INC/DN）. Combining with choline acetyltransferase （CHAT） immunofluorescent stain, it showed that Vme projecting terminals contact upon ChAT positive Ill/IV motoneurons under confocal microscope. By retrograde labeling premotor neurons of the III, it showed that Vme neuronal terminals contact with retrogradely labeled pre-oculomotor neurons in the INCIDN. Axons of intraceiiularly labeled Vme neurons that respond to electric stimuli of the masseter nerve traveled into the ipsilateral III. CONCLUSION： There may exist a trigeminal propdoceptive- oculomotor system neural circuit in the rat, which is probably related to vertical-torsional eye movements. Possible association of this pathway with MGS etiology was discussed.

Microglia activation mediated by toll-like receptor-4 impairs brain white matter tracts in rats

Microglia activation and white matter injury coexist after repeated episodes of mild brain trauma and ischemic stroke. Axon degeneration and demyelination can activate microglia; however, it is unclear whether early microglia activation can impair the function of white matter tracts and lead to injury. Rat corpus callosum（CC） slices were treated with lipopolysaccharide（LPS） or LPS ＋ Rhodobacter sphaeroides（RS）-LPS that is a toll-like receptor 4（TLR-4） antagonist. Functional changes reflected by the change of axon compound action potentials（CAPs） and the accumulation of β-amyloid precursor protein（β-APP） in CC nerve fibers. Microglia activation was monitored by ionized calcium binding adaptor-1 immunofluorescent stain, based on well-established morphological criteria and paralleled proportional area measurement. Input-output（I/O） curves of CAPs in response to increased stimuli were significantly downshifted in a dose-dependent manner in LPS（0.2, 0.5 and 1.0μg/mL）-treated slices, implying that axons neurophysiological function was undermined. LPS caused significant β-APP accumulation in CC tissues,reflecting the deterioration of fast axon transport. LPS-induced I/O curve downshift and P-APP accumulation were significantly reversed by the pre-treatment or co-incubation with RS-LPS. RS-LPS alone did not change the I/O curve.The degree of malfunction was correlated with microglia activation, as was shown by the measurements of proportional areas. Function of CC nerve fibers was evidently impaired by microglia activation and reversed by a TLP-4 antagonist, suggesting that the TLP-4 pathway lead to microglia activation.