Synkinesis after severe facial nerve paralysis has been related to the processes of aberrant reinnervation and increased excitability of the facial nucleus. 
In order to help understanding the physiological role of neuronal OMgp, we examined the change of OMgp expression in the facial nucleus after the facial nerve transection. Real-time RT-PCR and Western blot analysis showed a down-regulation of OMgp expression in the facial nucleus 5-7 (mRNA) or 5-14 (protein) days after transection.
The corticobulbar tract fibers descend near the corticospinal tract, mostly to the upper medulla, where they decussate and ascend in the dorsolateral medulla to connect with the contralateral facial nucleus.
In the first dog, a lesion at the level of the medulla oblongata was thought to cause primary irritation of the facial nucleus, with consequently permanent contraction of the ipsilateral facial muscles.
However, quantitative estimation of large motor neuron populations in the facial nucleus revealed a significant deficit in motor cells (-16%) in Clu-/- compared with WT mice.
Moreover, fluorescent retrograde tracing analysis by application of Fluoro-Gold into the regenerated nerves demonstrated the presence of Fluoro-Gold-positive motor neurons in the facial nucleus of the rat brain.
Blink reflex studies were partly consistent with midpontine lesions in the vicinity of the facial nucleus ipsilateral to SPHC.
NPR-C immunoreactivity was detected in several regions, including the periaqueductal gray, oculomotor nucleus, red nucleus and trochlear nucleus of the midbrain; the pontine nucleus, dorsal tegmental nucleus, vestibular nucleus, locus coeruleus, trigeminal motor nucleus, nucleus of the trapezoid body, abducens nucleus and facial nucleus of the pons; and the dorsal motor nucleus of the vagus, hypoglossal nucleus, lateral reticular nucleus, nucleus ambiguus and inferior olivary nucleus of the medulla oblongata. Interestingly, NPR-C immunoreactivity was detected in the cholinergic neurons of the oculomotor nucleus, trochlear nucleus, dorsal tegmental nucleus, motor trigeminal nucleus, facial nucleus, dorsal motor nucleus of the vagus, nucleus ambiguus and hypoglossal nucleus.
Injections that included dental afferents also labeled the mesencephalic nucleus of V, whereas injections into the skin of the face labeled cell bodies in the facial nucleus, and in most cases the motor nucleus of 5.
We performed comparative Nissl, Klüver-Barrera and Golgi staining studies of the mammalian facial nucleus to classify the morphologically distinct subdivisions and the neuronal types in the rat, rabbit, ferret, Japanese monkey (Macaca fuscata), pig, horse, Risso's dolphin (Grampus griseus), and bottlenose dolphin (Tursiops truncatus).
The four groups were compared with double retrograde tracing of the facial nucleus, electrophysiological and histomorphometrical assessment of the reconstructed facial nerve. Retrograde tracing of facial nucleus revealed significantly higher number of double-labeled neurons in group I although the total number of labeled neurons was not different between the two groups.
Neurons with collateral axonal projections to NTS and Amb (14% and 10%, respectively) were observed predominantly within a region of RVMM that extended co-extensively with approximately the rostrocaudal extent of the facial nucleus.
A high density of calcitonin gene-related peptide-immunoreactive perikarya was found in the superior colliculus, the dorsal nucleus of the raphe, the trochlear nucleus, the lateral division of the marginal nucleus of the brachium conjunctivum, the motor trigeminal nucleus, the facial nucleus, the pons reticular formation, the retrofacial nucleus, the rostral hypoglossal nucleus, and in the motor dorsal nucleus of the vagus, whereas a high density of fibers containing calcitonin gene-related peptide was observed in the lateral division of the marginal nucleus of the brachium conjunctivum, the parvocellular division of the alaminar spinal trigeminal nucleus, the external cuneate nucleus, the nucleus of the solitary tract, the laminar spinal trigeminal nucleus, and in the area postrema.
As previously reported, activated microglia facilitate the expression of a glial cell-type glutamate transporter, glutamate transporter-1 (GLT-1; EAAT2), around injured motoneurons in axotomized rat facial nucleus.
Cleaved SNAP-25 also appeared in the facial nucleus after injection of the toxin into rat whisker muscles.
First, we quantified the extent of total synaptic input to motoneurons in the facial nucleus using synaptophysin immunocytochemistry following FFA with and without subsequent MS.
The lateral facial nucleus is the sole output structure whose neuronal activity leads to whisker movements. To understand how single facial nucleus neurons contribute to whisker movement we combined single-cell stimulation and high-precision whisker tracking. Our data suggest the following coding scheme for whisker movements in the facial nucleus. 2) The facial nucleus neurons are heterogeneous with respect to the movement properties they encode. 3) facial nucleus spikes are translated in a one-to-one manner into whisker movements..
In 700-microm-thick slices with unilaterally exposed preBötC, a kernel <100 microm thick, centered 0.5 mm caudal to the facial nucleus, is necessary for rhythm generation.
Our method allowed us to identify neurons of the facial nucleus and the supratrigeminal nucleus, as well as assessing cellular distribution within layers of the dorsal cochlear nucleus.
The regions of the red nucleus receiving basal gangliar input project to the contralateral facial nucleus and upper segments of the cervical spinal cord.
P2X7 hybridization signals were also observed in the motor neurons of the trigeminal motor nucleus, facial nucleus, hypoglossal nucleus, and the anterior horn of the spinal cord.
A novel region ventrolateral to the facial nucleus, the para-facial respiratory group (pFRG), was found and has been considered to also generate respiratory rhythm.
We also tested the impact of cd39-deletion in a model of ischemia, in an entorhinal cortex lesion and in the facial nucleus after facial nerve lesion.
In the present study, we have examined somatic motor neurons of the lumbar spinal cord, and branchiomotor neurons of the facial nucleus in bcl-2-null mice to determine the differential dependence among motor neuron populations with respect to Bcl-2-mediated survival.
We performed the subtracted library screening of the facial nucleus after the facial nerve axotomy.
The primate facial nucleus is a prominent brainstem structure that is composed of cell bodies giving rise to axons forming the facial nerve. These observations advance our understanding of the morphological organization of the primate facial nucleus and provide structural features for comparative studies, interpreting afferent influence on OO function and for designing studies pinpointing structural alterations in OO motor neurons that may accompany disorders affecting facial movement..
In the hindbrain, generation of the facial nucleus involves complex developmental processes that will lead to the formation of a structure composed of motor neurons, astrocytes and oligodendrocytes. To uncover the cellular mechanisms regulated by LIFR beta during facial nucleus development, we first analyzed its expression pattern in the hindbrain. We also show that LIFR beta is implicated in astrocyte and oligodendrocyte differentiation, specifically within the facial nucleus..
Within a recent study on the recovery of vibrissae motor performance after facial nerve repair in blind (strain SD/RCS) and sighted (strain SD) rats, we found that, despite persisting myotopic disorganization in the facial nucleus, the blind animals fully restored vibrissal whisking.
GAD67-ir cells were found at the ventrolateral pontomedullary border in areas adjacent to the A5 noradrenergic cell group and overlapping the facial nucleus lateral subnuclei and para-facial zones. The PV-ir cells of RVM and caudal pons were found medial to the facial nucleus and lateral to the pyramid in a column distinct from the GAD67-ir cells.
In addition, it was observed for the first time that ZnT3 mRNA was expressed in the facial nucleus. The function of ZnT3 in facial nucleus awaits further study..
Motoneuron number and expression of cytoplasmic RNA and ribosomal RNA (rRNA) gene transcription activity in the facial nucleus were examined quantitatively and chronologically for up to 4 weeks in rats after facial nerve axotomy and avulsion in order to elucidate interrelationships in axonal changes. The number of large motoneurons in the facial nucleus was reduced by 40% 2 weeks after avulsion and by 70% 4 weeks after avulsion but displayed a 19% loss even 4 weeks after axotomy. rRNA gene transcription activity in the large motoneurons of the facial nucleus decreased significantly beginning 30 min after both axotomy and avulsion, but the severity of the decrease was far more marked in the avulsion group, showing a 59% loss from the control value 4 weeks after avulsion.
We also confirmed that a large number of ChAT-positive motor neurons in the oculomotor nucleus, facial nucleus, hypoglossal nucleus, and spinal motor neurons contained FGF1.
A phenomenon-in which microglia are activated in axotomized rat facial nucleus suggests that a certain neuronal stimulus triggers the activation of microglia.
The transient expression of estrogen receptor alpha (ERalpha) in the facial nucleus of rats during development was already reported. Thus, it is possible that ERalpha expression in the facial nucleus during development plays important roles in the development of motoneurons and/or external pinna muscles..
OBJECTIVE: There are two hypotheses for the pathogenesis of hemifacial spasm (HFS): abnormal cross-transmission between the facial nerve fibers at a site of vascular compression, and hyperactivity of the facial nucleus. We applied chronic electrical stimulation (CES) to the facial nucleus in rats, and clarified functional and morphological changes in the nucleus. METHOD: Under anesthesia, a novel intracranial electrode was stereotactically implanted in the facial nucleus of six rats. CES of the facial nucleus via the implanted electrode was applied for 5 min daily for three weeks (CES animals). Facial electromyograms (EMGs) were recorded at rest and during electrical stimulation to study the excitability of the facial nucleus at 1, 2, and 4 weeks after initiating CES. CONCLUSIONS: CES of the facial nucleus can produce an abnormal EMG response very similar to the abnormal muscle response (AMR) characteristic of HFS patients. Kindling-like hyperactivity of the facial nucleus induced by CES is the cause of the AMR, suggesting a pathogenesis of HFS..
Recordings of Vi/Vc neurons identified by antidromic activation from stimulation of the facial nucleus and non-identified Vi/Vc neurons reveal two neuron types, phasic and tonic.
Consistent with single-unit recordings in more intact preparations, respiratory networks were distributed bimodally along the rostrocaudal axis, with respiratory neurons concentrated at the caudal pole of the facial nucleus, and 350 microns caudally, at the level of the pFRG and the preBötC, respectively.
A survey of the literature reveals that the only area meeting all these criteria is a region, reaching from the parvocellular pontine reticular formation just above the superior olive through the lateral reticular formation around the facial nucleus and nucleus ambiguus down to the caudalmost medulla, including the dorsal and ventral reticular nuclei and nucleus retroambiguus.
Glutamate stimulation of the dorsal facial area, an area located dorsal to the facial nucleus, increases common carotid arterial blood flow.
Here, we employed electrophysiology, quantitative PCR, and immunohistochemistry to investigate the subunit composition of NMDA receptors in postnatal motor neurons of the Wistar rat facial nucleus (FN).
We show that neurons located in SupV and the reticular formation dorsal to the facial nucleus most likely excite JCMNs.
Anterograde tracers placed directly into M3 and M4 revealed the amygdala connection to be reciprocal and documented corticofugal projections to the facial nucleus, surrounding pontine reticular formation, and spinal cord.
Within a recent study on the vibrissae motor performance after facial nerve repair in strains of blind (SD/RCS) and sighted (SD) rats we found that, despite persisting myotopic disorganization in the facial nucleus, the blind animals fully restored vibrissal whisking.
The objective of this study was to anatomically map the extent of axotomy-induced cell death and immune cell rescue in the facial nucleus to study the differential survival capabilities of each subpopulation. At 4 weeks post-axotomy, topographical mapping of axotomy-induced cell death throughout the rostro-caudal extent of the facial nucleus was accomplished in accordance with previously published maps of the subnuclear arrangement of the facial neurons. The results indicate that all 3 subpopulations of FMN can be found in each of the subnuclear groups throughout the entire rostro-caudal extent of the facial nucleus.
Light microscopic autoradiography failed to detect V1b binding sites in the facial nucleus.
In the presence of Ca(2+) (0.8 mM), lesioning experiments suggested a physiological difference in perifacial RTN/pFRG VMS between the lateral VMS (beneath the ventrolateral part of the facial nucleus) and the middle VMS (beneath the ventromedial part of the facial nucleus), at least in newborn rats.
The present study compares the neuronal activity of this area with that of three motoneuron pools involved in phonation, namely the trigeminal motor nucleus, facial nucleus, and nucleus ambiguous.
V (trigeminal nucleus), VII (facial nucleus), and XII (hypoglossal nucleus), and spinal cord compared to non-transgenic wild-type mice and transgenic mice over-expressing the non-mutated wild-type human SOD1 (tg-SOD1).
Whisker motor neurons are located in the lateral facial nucleus and their cellular properties might contribute to the rhythmicity of whisking. Numerous structures provide input to the lateral facial nucleus, the most mysterious and important one being the putative central pattern generator (CPG).
NPW-ir fibers were observed in several brain regions, including the lateral septum, bed nucleus of the stria terminalis, dorsomedial and posterior hypothalamus, central amygdaloid nucleus, CA1 field of hippocampus, interpeduncular nucleus, inferior colliculus, lateral parabrachial nucleus, facial nucleus, and hypoglossal nucleus.
Normally there was a considerable number of GFAP-positive cells in nonnucleus regions but few inside the facial nucleus region.
Transection of rat adult facial nerve leads to an increase in the number of activated microglia in the facial nucleus (FN), with a peak in proliferation 3 days after transection.
Furthermore, the distributions of vacuoles and LBHIs were examined in the pons including the facial nucleus, where pathological changes occur in ALS patients and G93A mice. In the facial nucleus of G1L mice, where the number of motor neurons was significantly reduced, only a few LBHIs were detected along with prominent vacuole formation. In contrast, significantly more LBHIs with little vacuole formation were evident around the facial nucleus in G1L mice.
At the end of the study, quantitative analysis of neurons in the facial nucleus was carried out, and axons were stereologically counted.
In addition, glial apoptosis was seen in the facial nucleus after both distal and proximal axotomy.
In each adult rat, the organisation of the facial nucleus and the cortical motor output corresponding to the normal side were compared with those corresponding to the reinnervated side.
Cell counts revealed a significant reduction in motor neuron number in the facial nucleus at 4 months after onset of expression of TrkB.T1, suggesting that a proportion of TrkB.T1-expressing motor neurons became undetectable as a result of severe atrophy or was lost because of cell death.
Previous publications have provided different descriptions of the topographical organization of the facial nucleus of the pig. Since swine is used in biomedical research due to its embryological, anatomical and physiological similarities to human, we have reinvestigated the anatomical organization of the facial nucleus with application of fluorescent retrograde tracer Fast Blue, antibody to choline acetyltransferase and acetylcholinesterase histochemistry.
While respiratory commands were monitored electrically from third to fifth cervical ventral roots, activity was measured optically over areas containing groups of respiratory neurones, or single neurones, along the medulla from the facial nucleus to the pre-Bötzinger complex.
By contrast, binding in the ipsilateral facial nucleus decreased, compared with the control side, by 7 days after the lesion and showed some recovery toward symmetry by 2 months after lesion, and there was no evidence for contralateral changes.
Moreover, completely transecting the brainstem at the caudal end of the facial nucleus abolished active expirations, while rhythmic inspirations continued. We hypothesize that inspiration and expiration are generated by coupled, anatomically separate rhythm generators, one generating active expiration located close to the facial nucleus in the region of the retrotrapezoid nucleus/parafacial respiratory group, the other generating inspiration located more caudally in the preBötzinger Complex..
Using microarray analysis we identified an increase in the expression of 60 genes (at a false discovery rate of 0.1, genes were significant P < 0.004) within the facial nucleus as a consequence of nerve injury.
Cervical dislocation showed the least VLM labelling, limited to a discrete area approximately 0.6-1.4 mm caudal to the facial nucleus.
Lectin histochemistry in the unoperated facial nucleus revealed aging-related morphological changes in resting microglia, including hypertrophy of the cytoplasm with dense perinuclear staining. We propose that aging-related changes in morphology in conjunction with a less regulated proliferative response in the aged facial nucleus may be a reflection of microglial senescence..
Four weeks after the injections, GFP and synaptophysin-GFP labeling of axons and putative presynaptic terminals was detected in the lateral portion of the facial nucleus (FN), in close proximity to motor neurons identified morphologically and by axonal back-labeling from the whisker follicles.
The highest density of immunoreactive fibers was found in the motor trigeminal nucleus, the laminar and alaminar spinal trigeminal nuclei, the facial nucleus, the marginal nucleus of the brachium conjunctivum, the locus coeruleus, the cuneiform nucleus, the dorsal motor nucleus of the vagus, the postpyramidal nucleus of the raphe, the lateral tegmental field, the Kölliker-Fuse nucleus, the inferior central nucleus, the periaqueductal gray, the nucleus of the solitary tract, and in the inferior vestibular nucleus.
Clinical as well as electrophysiological features plead for mechanisms of the disease in structural lesions at the neural fibers (putatively: focal demyelination at origin of ephapses) and functional changes in the nuclear cells (hyperactivity of the facial nucleus).Lateral Spread Responses (LSRs) elicited by stimulation of the facial nerve branches testify of these electrophysiological perturbations.
Single-pulse electrical stimulation of the supratrigeminal region (SupV) and the reticular formation dorsal to the facial nucleus (RdVII) elicited masseter EMG response at mean (+/-SD) latencies of 2.22 +/- 0.59 ms and 3.10 +/- 1.14 ms, respectively.
FOS positive neurons were induced by hypoxia and mainly existed in the nucleus of solitary tract, area postrema, hypoglossal nucleus, lateral reticular nucleus, inferior olivary nucleus, nucleus raphe pallidus, facial nucleus, trapezoid nucleus, but in the group of hypoxia plus TMP, the level of FOS immunoreactivity decreased remarkably, compared with the group of hypoxia (P<0.05).
Stimulation of the sphenopalatine ganglion (SPG), a parasympathetic ganglion of the facial nerve, or the dorsal facial area (DFA), an area in the lateral tegmental field just dorsal to the facial nucleus, induces an increase in blood flow of the common carotid artery (CCA). All HRP-labeled neurons were distributed in the reticular areas dorsal and lateral to the superior olivary nucleus and the facial nucleus, extending from the caudal half of the superior olivary nucleus to the rostral 3/4 of the facial nucleus on the HRP-injected side. They were grouped into five clusters, namely lateral circumference of the superior olivary nucleus, dorsal circumference of the superior olivary nucleus, lateral circumference of the facial nucleus, dorsal circumference of the facial nucleus, and the DFA.
In this study we investigated the effect of minocycline specifically on microglial mitotic activity and neuronal regeneration within the facial nucleus following a nerve crush injury. Proliferation was measured by labeling the dividing microglia with 3H-thymidine and quantifying labeled cells throughout the facial nucleus on days 2, 3 and 4 post-axotomy.
OBJECTIVE: To compare the electrophysiological excitability characteristics of the facial nucleus and related structures in hemifacial spasm (HFS), post-facial palsy synkinesis (PFPS) and facial myokymia (FM). CONCLUSIONS: PFPS and HFS cases had similar enhanced excitability patterns at the facial nucleus and related brain-stem structures, more marked on the symptomatic side and more obvious in the PFPS group.
RESULTS: After 1 d of survival times, many labeled cell bodies were found in 1-4 cervical spinal ganglia, anterior horn of 1-4 cervical spinal cord, ventromedial division of facial nucleus, accessory facial nucleus ipsilaterally. CONCLUSION: Fengch'ih may bring into full play its effect by correlation of posterior ear branch of facial nerve and anterior branch of 2-3 cervical nerve with 1-4 cervical the anterior horn of the spinal cord, ventromedial division of facial nucleus, accessory facial nucleus..
Normal facial nucleus (Mo7) had 20% large motoneurons in contrast with 10% in hypothyroid pups.
Both the CTbeta and PRV injections also resulted in labeling of neurons in all four vestibular nuclei, the prepositus hypoglossi, the reticular formation, the inferior olivary nucleus, the medullary raphe nuclei, the spinal and principal trigeminal nuclei, the facial nucleus, and the lateral reticular nucleus.
Second, solitarii-facial projections were analyzed following injections of anterograde and retrograde tracers into the NTS and the facial nucleus, respectively. NTS neurons, except those of the rostrolateral part, reached the dorsal aspect of the facial nucleus. Finally, simultaneous injections of anterograde tracer in the STC and retrograde tracer in the facial nucleus gave retrogradely labeled neurons in the NTS receiving contacts from anterogradely labeled trigeminal boutons.
Colchicine treatment and blockade of action potential by tetrodotoxin significantly decreased GABA(A)alpha1 immunoreactivity in the axotomized facial nucleus after 7 days.
We studied the effects of transplanting Schwann cells, mixed olfactory ensheathing cells, and S-type olfactory ensheathing cells on the histological and functional organization of the connections between the facial nucleus and distal muscles. The site of lesion and the somatotopic organization of the facial nucleus were assessed histologically, after application of different retrograde fluorescent tracers simultaneously to the buccal and temporal divisions of the facial nerve. RESULTS: The rate of recovery of eye closure was increased by the use of the cell transplants, but the disorganization of the facial nucleus and aberrant nerve branching were unchanged.
Also, MS-treated rats showed an enhanced accumulation of glycogen in neurons of the facial nucleus, the nucleus ambiguus, and the hypoglossal nucleus, structures that regulate respiratory activity and airway patency.
In the rats of hypoxia group, the level of nNOS immunoreactivity was enhanced remarkably in the lateral reticular nucleus, nucleus of trapezoid, hypoglossal nucleus and the facial nucleus compared with the control group (P<0.05).
Assuming the presence of intercellular interactions between injured motoneurons and microglia in the axotomized facial nucleus, we investigated the effects of neuronal conditioned medium (NCM) on the release of urokinase-type plasminogen activator (uPA) from microglia.
In contrast, in E17-E18 specimens, pre-inspiratory activity could not be detected in the rostral medulla at the level of the facial nucleus. Strong activity then developed in the facial nucleus and peaked in the post-inspiratory phase.
The rabbit has eight auricular muscles that are innervated by motoneurons originating from the facial nucleus located on the ventral side of the medulla oblongata. However, the distribution within the facial nucleus of the motoneurons that innervate each auricular muscle has not been defined clearly. Our results show that the medial subnucleus of the facial nucleus projects primarily to the auricular muscles, and that each auricular muscle is innervated by a specific group of motoneurons distributed in a particular region of the medial subnucleus.
Localization of the retrogradely labeled neurons within the ipsilateral facial nucleus was confirmed for all facial muscles examined. buccinator pars buccalis were distributed within the dorsal part of the intermediate subnucleus of the facial nucleus in the both species. levator labii superioris showed the difference in the distribution within the facial nucleus among the species. depressor anguli oris was innervated by the neurons distributed within the intermediate subnucleus of the facial nucleus in the rabbit.
The abundance of GlyR subunits and gephyrin fell sharply in the axotomized facial nucleus.
As has also been shown for Slack, Slick is expressed in the olfactory bulb, red nucleus, facial nucleus, pontine nucleus, oculomotor nucleus, substantia nigra, deep cerebellar nuclei, vestibular nucleus, and the thalamus.
We demonstrate, using in vitro and in vivo recordings, that the trigeminal loop consists of excitatory pathways from vibrissa sensory inputs to vibrissa motoneurons in the facial nucleus.
Injections of biotinylated dextran amine into the CPA resulted in numerous labeled fibers with varicosities in the ipsilateral subnucleus reticularis dorsalis, commissural subnucleus of the nucleus tractus solitarii, lateral medulla, medial facial nucleus, A5 area, lateral vestibular nucleus, and internal lateral subnucleus of the parabrachial complex. The projection to the facial nucleus arises from nearby reticular neurons, whereas projections to the vestibular nucleus arise from the lateral reticular nucleus.
In addition, strong hybridization signals were localized in various nuclei: main and accessory olfactory bulb, compact part of the substantia nigra, pontine gray matter, tegmental reticular nucleus, Edinger-Westphal nucleus, trigeminal motor nucleus, locus coeruleus, mesencephalic trigeminal nucleus, raphe nuclei, facial nucleus, ambiguus nucleus, dorsal motor vagal nucleus, and inferior olivary nucleus.
In bone marrow chimeras, ganciclovir blocked microglial activation in the facial nucleus upon axotomy and repressed the development of experimental autoimmune encephalomyelitis.
We show that the migration of motor neurons of the facial nucleus from rhombomere 4 to 6 is also affected in sdf1a morphants (embryos injected with morpholine-conjugated antisense oligonucleotides).
The phenomenon in which urokinase-type plasminogen activator (uPA) is induced in the axotomized facial nucleus suggests an interaction between injured motoneurons and microglia. Thus, uPA induction in the axotomized facial nucleus may be explained by a neuronal stimulus leading to uPA induction in microglia..
We investigated the discharge response of respiratory neurons (RNs) in the pre-Bözinger complex (PBC) to electrical stimulation of the facial nucleus in which the motor neurons were retrogradely degenerated and the antagonistic effects of microiontophoresis of CNQX, bicuculline (BIC), strychnine (Stry) and atropine on the discharge responses of the neurons. The response of pre-inspiratory (Pre-I) (24 / 26) and inspiratory (I) (30 / 35) neurons to the electrical stimulation of the facial nucleus was mainly excitatory, and the response of expiratory (E) (20 / 22) and inspiratory-expiratory phase-spanning (I-E) (28 / 33) neurons was mainly inhibitory. These results suggest that non-motoneurons in the facial nucleus may participate in the modulation of respiration by affecting the activities of RNs in the PBC and that Glu, GABA and Gly serve as neurotransmitters or modulators to regulate the activities of the RNs in the PBC and hence the rhythmic respiratory movement..
A tract tracing study was performed to examine the localization of the facial nucleus in the brain stem of the pond turtle, Pseudemys scripta elegans. The results showed that the facial nucleus has two subnuclei, a medial group and a lateral group. Double labeling studies showed that the medial cell group of the facial nucleus lies between the principal and accessory abducens nuclei in the pons, whereas the lateral group lies adjacent to the accessory abducens nucleus. The facial nucleus of pond turtles largely overlaps the rostrocaudal extent of the accessory abducens nucleus, but extends well beyond it into the medulla. These data elucidate the position and distribution of the facial nucleus in the brain stem of pond turtles and contribute to the body of comparative neuroanatomical literature on the distribution of the cranial nerve nuclei of reptiles..
However, with migration of cell groups such as the facial nucleus from the pons to the medulla during ontogeny, the boundaries of the adult pons are sometimes difficult to precisely define.
METHOD: facial nucleus injection and isotopic-label tracer with liquid scintillation counting techniques were used to investigate the changes of radioactivity after guinea pig facial nerve compressed.
Blink reflex findings were consistent with an injury in the pons, mainly in the vicinity of the left facial nucleus.
Hyperintensities, indicative of neuropathology, were observed in several areas including the nucleus ambiguus, facial nucleus, trigeminal motor nucleus, rostroventrolateral reticular nucleus, lateral paragigantocellular nucleus and the substantia nigra.
Projections of the interneurons of the facial nucleus to respiration-related areas in the brainstem of the rat were revealed by unilateral, iontophorectic injection of the anterograde neuronal tracer, Phaseolus vulgaris leucoagglutinin (PHA-L), into the facial nucleus after motor neurons degeneration had been induced by axotomy of the facial nerve. These results revealed that the interneurons in the facial nucleus have widespread projections to the respiratory groups in the brainstem, and suggest that the facial nucleus is involved not only in the control of muscles for facial expression but also in the regulation of functional respiratory activity..
The facial nucleus (FN) has been known as a motor nucleus to control the activity of the facial skeletal muscles by its efferent somatic motoneurons.
Both preferentially give rise to bilateral projections to parts of the facial nucleus that innervate the upper facial musculature as demonstrated in the monkey. The facial representation of M1, LPMCv, and M4 preferentially give rise to contralateral axonal projections ending in parts of the facial nucleus that innervate the lower facial musculature.
In the present study, GDNF expression in motoneurons of SOD1(G93A) transgenic mice was assessed by facial nucleus or intraspinal injection of lentiviral vectors (LV) encoding GDNF. In contrast, LV-GDNF induced a significant rescue of motoneurons in the facial nucleus and prevented motoneuron atrophy. The differential effect of GDNF on facial nucleus versus spinal motoneurons suggests different vulnerability of motoneurons in ALS..
Then, the labeled motoneurons into the facial nucleus could really be the expression of axonal projections from facial motoneurons to the hypoglossus nerve and facial muscles.
Although facial nucleus supersensitivity is more accepted as the main cause of hemifacial spasm.
RESULTS: In situ hybridization and immunohistochemistry demonstrated a strong up-regulation of SCD at mRNA and protein level in regenerating neurons of the rat facial nucleus whereas non-regenerating Clarke's and Red nucleus neurons did not show an induction of this gene.
Galectin-1 mRNA was predominantly observed in the cell bodies of neurons such as oculomotor nucleus (III), trochlear nucleus (IV), trigeminal motor nucleus (V), abducens nucleus (VI), facial nucleus (VII), hypoglossal nucleus (XII), red nucleus, and locus ceruleus.
Strong expression was also seen in several cranial motor nuclei, including the nucleus of ambiguus, hypoglossal nucleus, facial nucleus and dorsal vagus motor nucleus.
It was possible to localize the points at which regenerating fibres became aberrant in their course by studying the number of labelled motoneurons in the facial nucleus after application of the tracer to the temporal branch of the nerve: this was similar in the distal and proximal hemisection groups, suggesting that aberrant axonal development occurred throughout the length of the nerve.
However, activation of a discrete region of the MM at the level of the caudal pole of the facial nucleus (CP7) consistently caused a dramatic reduction in phrenic nerve amplitude and/or frequency and, in six rats, produced a prolonged apnea.
In response to facial nerve axotomy, we observed an increase in GABA(B) receptor expressing microglial cells in the facial nucleus.
Three months after FFA all retrogradely labeled motoneurons were scattered throughout the entire facial nucleus.
The respiratory rhythm is generated within the hindbrain reticular formation, rostrally in the vicinity of the facial nucleus and caudally within the vagal/glossopharyngeal domain.
Testosterone propionate (TP) administration coincident with facial nerve axotomy in the hamster attenuates glial fibrillary acidic protein (GFAP) expression in the facial nucleus that is normally increased following axotomy alone.
OBJECTIVE: To study the effects of constitutive nitric oxide synthase inhibitor L-nitroarginine on the recovery of traumatic facial paralysis in rats and the changes of the expression of cNOS and OX42 in the facial nucleus. and the changes of cNOS and OX42 positive neurons were studied in facial nucleus. The cNOS immunoactivity was obvious inhibited in facial nucleus, while the OX42 immunoactivity was obvious increased.
In contrast, beta1 gene expression in the axotomized facial nucleus decreased compared to controls as soon as day post-lesion 3..
Two of the groups then received either three or six sessions of tone-alone extinction training while the motor nuclei that mediate expression of the CR (facial nucleus and accessory abducens) were reversibly inactivated with microinjections of the GABA agonist muscimol.
The effects of neonatal food restriction upon the dendritic development of facial nucleus (FN) motor neurons of Wistar rats were analyzed.
An upregulation of Nrg-1 type-I mRNA, probably type- I-alpha, was observed in reactive astrocytes of the facial nucleus 1 d postaxotomy.
T-cells and in the microglial immunoreactivity for the alpha5beta1, alpha6beta1, and alphaMbeta2 integrins at day 4 in the facial nucleus and in the crushed facial motor nerve.
In the brainstem of symptomatic SOD1(G93A) transgenic mice, significantly increased immunoreactivity for MnSOD was observed in abducens nucleus, facial nucleus, dorsal motor nucleus of vagus, hypoglossal nucleus, medullary and pontine reticular formation, superior and inferior olivary nucleus, and cochlear nucleus.
To investigate the involvement of ciliary neurotropic factor (CNTF) in the postlesional response of motoneurons, we studied the activation of STAT3 signaling, the main signal transduction pathway of CNTF-like cytokines, in the facial nucleus of wildtype and CNTF-deficient mice following peripheral nerve transection. As shown by immunocytochemistry and immunoblot analysis, phosphorylation and nuclear translocation of STAT3 was maximally induced within 12 h postlesion in motoneurons of the ipsilateral facial nucleus of wildtype mice and is maintained for at least 3 days.
RESULTS: Under normal situation, the motoneurons contributing buccall and marginal mandibular branches were primarily distributed in the intermedial and lateral subnucleus in facial nucleus and almost completely overlapped.
After tracer injection into the superior rectus and medial rectus muscles, retrogradely labeled neurons were seen not only in the ipsilateral facial nucleus (16%) but also in the contralateral nucleus (8%).
RESULTS: The fluorescence labeled facial motoneurons were all in the lateral subnucleus of facial nucleus after BTX-A injection at rat whisker pad.
CONCLUSION: The vascular compression at the root of the facial nerve is a main cause of IHFS, and the abnormal function of the facial nucleus is also one of the causes.
Double-labeled neurons were consistently found in the nerve-crushed facial nucleus (3.2%), and their number increased in the nerve-transected facial nucleus (12.2%).
RESULTS: BDNF mRNA and its protein were observed in widespread areas of normal rat facial nucleus, and those increased 1 day after axotomy. FGF-2 mRNA and its protein were mainly localized in normal FMNs of ventral facial nucleus.
facial nucleus was treated with bcl-2 monoclonal antibody or bcl-2 DIG-labelling probe and studied with immunohistochemistry and in situ hybridization. After facial nerve transected, the reduction of bcl-2 expression was more significant when facial nerve transected close to facial nucleus than that far from facial nucleus (P < 0.05).
For this purpose, axotomy induced changes of regenerating facial nucleus neurons, and non-regenerating red nucleus and Clarke's nucleus neurons have been analyzed in an intra-animal side-to-side comparison.
In the lower brainstem, fibers terminated in the pontine and medullary reticular formation, locus coeruleus, nucleus subcoeruleus, medial parabrachial nucleus, nucleus of the spinal trigeminal tract, solitary tract nucleus and facial nucleus.
After transection and suture of the facial nerve trunk, the zygomatic ramus contained axons of 328 +/- 50 motoneurons dispersed throughout the whole facial nucleus.
The VRG organization was mapped systematically using injections of the excitatory amino acid DL-homocysteic acid (DLH; 5-20 mM, 2-6 nl) from single- or double-barrel pipettes at 100-200 microm intervals between the facial nucleus and the calamus scriptorius.
We also detected moderate to high levels of PR gene expression in several regions, such as the trapezoid nucleus, facial nucleus, periaqueductal gray regions, and rostral ventrolateral medulla.
Studies in anesthetized rats have implicated GABAA receptors in the region of the medullary raphe pallidus (RP) at the level of the facial nucleus in sympathetic nervous regulation of both heart rate and thermoregulatory mechanisms.
Quantitative analysis showed that age does not affect the glial response to axotomy in the lesioned facial nucleus; however, an aging-related contralateral effect with enhanced GFAP-labeling was observed.
This RVLM area was determined to be ventrolateral to the facial nucleus and close to the ventral surface.
By way of the representative application of the recommended investigation procedure to 100 microm serial sections through the patient's brain stem stained for lipofuscin pigment and Nissl material, we observed neuronal loss together with astrogliosis in nearly all of the ingestion-related lower brain stem nuclei (motor, principal and spinal trigeminal nuclei; facial nucleus; parvocellular reticular nucleus; ambiguous nucleus, motor nucleus of the dorsal glossopharyngeal and vagal area; gelatinous, medial, parvocellular and pigmented solitary nuclei; hypoglossal nucleus).
OBJECTIVE: To explore the discharge patterns of non-motoneurons in the facial nucleus of rats. METHODS: After retrograde degeneration of the facial motoneurons induced by section of the facial nerve, the discharge of non-motoneurons in the facial nucleus was extracellularly monitored, and their phase relations to the respiratory cycle were investigated. RESULTS: In 18 rats, totally 142 non-motoneurons with spontaneous discharge were recorded in the facial nucleus. CONCLUSION: There exist different kinds of nonmotoneurons in the facial nucleus. The results of this study suggest that the facial nucleus not only controls the movement of the facial skeletal muscles, but also participates in the regulation of other functions such as respiration..
OBJECTIVE: In order to study the changes of CGRP activity in facial nucleus of guinea pig after facial nerve injury. RESULT: It was showed the there were CGRP-immunoreactivity (IR) in normal facial nucleus and its' subnucleus. We noticed distinct bundle-shaped CGRP fibers elongated to the peripheral part from ventral facial nucleus in the period of 14 d-35 d.
Third, conspicuous projections from branches of these ascending collaterals to the area dorsolateral to the facial nucleus were found.
Immunofluorescence study revealed HSV-1 in the geniculate ganglion, the descending root, and the facial nucleus at this stage. In contrast, the facial nucleus neurons showed no remarkable degeneration, despite HSV-1 particles in their cytoplasm.
Retrograde labeling with fluorogold revealed 981 +/- 450 (n = 5) and 53 +/- 38 (n = 5) retrogradely labeled motoneurons in the facial nucleus in the presence of GDNF and NT-3, respectively.
In order to determine the possible involvement of androgens in regulation of pro UII mRNA expression, we have studied the co-localization of pro UII mRNA and AR immunoreactivity and the effect of castration and dihydrotestosterone (DHT) replacement therapy on pro UII mRNA in the rat facial nucleus and ventral horn of the spinal cord. By in situ hybridization, pro UII mRNA was only detected in motoneurons in both the facial nucleus and ventral horn of the spinal cord. Three weeks after castration, pro UII mRNA expression, as measured by semi-quantitative in situ hybridization, was increased by 17% and 58% in the ventral horn of the spinal cord and the facial nucleus, respectively.
Virus uptake involved exclusively orbicularis oculi motoneurons in the dorsolateral division of the facial nucleus.
The earliest time point at which WGA-HRP was detected in the axotomized facial nucleus occurred at 3 hpo.
Sympathetic axons sprouted into the axotomized facial nucleus of both NGF/p75(+/+) and NGF/p75(-/-) following injury, due to transgene expression of NGF in reactive astrocytes.
We previously reported that trigeminal rhythmic activities could be induced by some pharmacological applications in an isolated brainstem preparation with a rostral boundary at the border between the inferior and superior colliculus, and a caudal border at the level of the rostral facial nucleus.
Signals for VAMP2 and -3 mRNAs in the facial nucleus were increased from 3 to 28 days after axotomy. On the contrary, VAMP1 mRNA, which was abundantly expressed in the control facial nucleus, was transiently decreased from 3 to 21 days after axotomy.
A few labeled neurons were found in the inferior salivatory nucleus, the rostral division of the dorsal motor nucleus of the vagus (DMX), the accessory facial nucleus and the lateral column of lamina IX at the C2 and C3 levels. When CTb was injected into the sternomastoid muscle, many labeled neurons were found in the medullary reticular formation, the facial nucleus, the medial column at the C1-C3, C5 and C6 levels, and the lateral column at the C2, C3, C5 and C6 levels.
We compare the tracers Fast Blue (FB), Fluoro-ruby, Fluoro-emerald, Fluoro-Gold (FG), and DiI in the rat facial nucleus after application to the buccal division of the nerve. FB and FG resulted in strong retrograde labelling of the facial nucleus after only 2 days from injection.
Concomitantly, a significant increase in the number of c-fos expressing neurons was observed in the rostral ventrolateral medulla (+63%), in particular in its most anterior part (+78%), and in the medullary region surrounding the caudal part of the facial nucleus (+91%). In contrast, under the same alpha-chloralose/urethane anesthesia, systemic infusion of sodium nitroprusside appeared to produce a hypotension and a marked increase in the density of such double c-fos and tyrosine hydroxylase expressing cells in the rostral ventrolateral medulla and the caudal medullary region surrounding the caudal part of the facial nucleus.These data indicate that medullary catecholaminergic C1 and A1 neurons are not involved in the pressor effect elicited by 5-HT(3) receptor stimulation in the nucleus tractus solitarii.
In situ hybridization studies showed an increase in alpha-internexin mRNA expression in the facial nucleus at 7 and 14 d after injury. Retrograde transport of fluorogold from the whisker pads to the facial nucleus was seen only in motoneurons that lacked alpha-internexin immunoreactivity, supporting the idea that target reinnervation and inhibitory signals from the periphery regulate the expression of alpha-internexin.
Muscimol dialysis through probes that were placed along the ventral medullary surface from approximately 1 mm rostral to the facial nucleus to approximately 0.5 mm caudal to the facial nucleus augmented the respiratory inhibition associated with acute increases in blood pressure.
We aimed to study the natural course of HFS and especially, to examine the relationships with psychological status or physical activities, in order to assess the possible role of the facial nucleus in the pathogenesis. In conclusion, HFS is a movement disorder of the facial nerve which is highly influenced by emotional status to support an involvement of the facial nucleus in the pathogenesis.
The location of the facial nucleus and pathway of facial neurofibers in the pons were observed. RESULTS: The distances from the facial nucleus to the ventral surface of pons, the median line, and the ventroexterior surface were 12.0-12.5 mm, 6.0 mm, and 7.5-9.0 mm respectively. But in cases who do not have vascular compression at the REZ, there might be dysfunction of the facial nucleus.
The motoneurones controlling this behaviour are located in various nuclei in the pons (trigeminal motor nucleus), medulla (facial nucleus, nucl.
mOPA1 was expressed widely in the mouse brain, especially in neurons of olfactory bulb, cerebral cortex, piriform cortex, hypothalamus, hippocampus, red nucleus, cochlear nucleus, motor trigeminal nucleus, facial nucleus, cerebellar nucleus, and Purkinje cells.
We describe an animal model of facial nerve lesion, repair, and regeneration that demonstrates abnormal organization of the facial nucleus; this model may be used to study synkinesis. The distribution of the tracers in the facial nucleus was assessed in both the lesioned animals and in a nonlesioned group (n = 20). RESULTS: In the control animals, muscle groups were somatotopically represented in the facial nucleus. After lesioning, repair, and regeneration, the somatotopy of the facial nucleus was disrupted. Axons projected from the facial nucleus to incorrect peripheral muscle groups, and aberrant branches were observed to simultaneously innervate different subdivisions of the facial nerve.
No labeled motoneurons were found in the facial nucleus.
The facial nucleus, the prepositus hypoglossal nucleus, and the sympathetic ganglia also showed P2X(3) immunoreactivity, even though these are not sensory associated. P2X(3) immunoreactivity in the facial nucleus, spinal trigeminal tract, the mesencephalic trigeminal nucleus, and the vestibular nucleus were undetectable in postnatal day 16 rat brainstem.
Injections of the retrograde tracer cholera toxin subunit B into physiologically identified wFMNs in the lateral facial nucleus resulted in dense, bilateral labeling throughout the brainstem reticular formation and in the ambiguus nucleus as well as predominantly ipsilateral labeling in the paralemniscal, pedunculopontine tegmental, Kölliker-Fuse, and parabrachial nuclei.
AT(1a) mRNA expression is present from E19 onward in the median preoptic nucleus, the vascular organ of the lamina terminalis, the paraventricular nucleus, the periaqueductal gray, the nucleus raphe pallidus, the motor facial nucleus, and very weakly in the nucleus of the solitary tract and the ambiguous nucleus, and at E21 in the subfornical organ, the anterior olfactory nucleus and the piriform cortex.
Of the five mouse strains tested in the current study, four--Balb/C, FVB, C57Bl/6, and C3H/N--showed vigorous granulocyte influx (60-90 cells per 20-microm section in axotomized facial nucleus, 20-40 cells per section on the contralateral side).
This method revealed that the normal facial nucleus contained approximately 3200 motoneurons (n=12 rats).
Although previous studies indicated many points of similarity between this mutant rat and the reeler mouse, nonlaminated structures such as the facial nucleus have not been studied in this mutant rat. Nissl-stained sections through the brainstem showed that the cytoarchitecture of the facial, motor trigeminal, and ambiguus nuclei was abnormal in SRK, especially in the lateral cell group of the facial nucleus and the compact formation of the ambiguus nucleus.
Labeled preganglionic neurons were cholinergic and were located immediately dorsolateral to the rostral-most portion of the facial nucleus and caudal superior olive, where they intermingled with A5 noradrenergic cells.
The reflex arc probably descends more medially and ventrally on its course to the facial nucleus..
Cold-activated raphé-spinal neurons were found in the nuclei raphé magnus and pallidus, centred at the level of the caudal part of the facial nucleus.
Transgenic deletion of IL6 caused a massive decrease in the recruitment of CD3-positive T-lymphocytes and early microglial activation during the first 4 days after injury in the axotomized facial nucleus.
He had an isolated lesion of the right facial nucleus in the pontine tegmentum.
In the majority of patients the corticofacial fibres travel within the ventromedial base of the pons and cross the midline at the level of the facial nucleus. In other patients the corticofacial fibres loop down into the ventral part of the upper medulla, cross the midline and ascend in the dorsolateral medullary region ipsilaterally to the facial nucleus.
ICAM-1 immunoreactivity in the normal mouse facial nucleus was restricted to the vascular endothelium. Transection of the facial nerve led to a fast upregulation of ICAM-1 on activated microglia in the axotomized facial nucleus and the infiltration of ICAM-1-positive lymphocytes.
A nerve tracer was injected into the mimic muscles innervated by the nerve to label the surviving motor neurons within the facial nucleus. After the regenerative period, a mean loss of 15% of the total cell number was observed within the facial nucleus compared with the opposite side.
The calcium flow inhibitor, nimodipine, has been shown to promote motor neuron survival in the facial nucleus after intracranial facial nerve transection.
In addition, a high level of NB-2 expression was observed in the accessory olfactory bulb, thalamic nuclei, facial nucleus, and inferior olive.
Early recruitment of CD3(+) T-lymphocytes to the facial nucleus 24 hours after injury was reduced by 60%.
The facial nucleus (FN) of the rat is composed of multipolar neurons generated between gestational days G12 and G15.
Nitric oxide synthase, revealed by NADPH-diaphorase histochemistry, OX-42-immunoreactive microglia, and expression of the cell death repressor gene bcl-2, investigated with nonradioactive in situ hybridization and immunohistochemistry, were evaluated in the facial nucleus.
Injections of retrograde tracers into the facial nucleus consistently labeled neurons in the hypoglossal nucleus. Reverse experiments - injections of anterograde tracers into the hypoglossal nucleus - labeled fine varicose nerve fiber terminals in the facial nucleus. These fiber terminals were concentrated in the intermediate subdivision of the facial nucleus, with a strong ipsilateral prevalence. Hypoglossal internuclear interneurons projecting to the facial nucleus, as well as those neurons of the parvocellular reticular formation that project to both facial and hypoglossal nuclei, could be involved in oro-facial coordination..
orbicularis oculi for the spontaneous blinks is reduced in patients with Parkinson's disease, because the motoneurones of the facial nucleus innervating the m.
These were the olfactory tubercle, nucleus accumbens, ventral mesencephalon, periventricular gray from the hypothalamus to the pons, facial nucleus, subdivisions of the inferior olive, and the intermediolateral nucleus in the spinal cord.
Areas expressing a high level of AT2 receptors follow: inferior colicullus (IC), dorso tegmental nucleus, central (DTgC), subcoeruleus, alpha, sensory root of the trigeminal nerve, principal sensory root trigeminal nucleus (Pr5, Pr5VL) supragenual nucleus, genu facial nerve, facial nucleus, cerebellar peduncles, vestibular and lateral nuclei.
RESULTS: Retrograde tracer injections into the facial nucleus consistently labeled small neurons in the hypoglossal nucleus. In reverse experiments the injection of anterograde tracers into the hypoglossal nucleus labeled fine caliber varicose nerve fibers, but no somata in the facial nucleus. CONCLUSIONS: Both, hypoglossal interneurons projecting to the facial nucleus and neurons of the parvocellular reticular formation double-projecting to the facial and hypoglossal nucleus might play an important role in coordinated orofacial movements.
Some of the ascending axons could be traced as far as the level of the facial nucleus and some of the descending axons beyond the spinomedullary junction.
The corticobulbar projection to musculotopically defined subsectors of the facial nucleus was studied from the face representation of the primary (M1), supplementary (M2), rostral cingulate (M3), caudal cingulate (M4) and ventral lateral pre- (LPMCv) motor cortices in the rhesus monkey. In the same animals, the musculotopic organization of the facial nucleus was defined by injecting fluorescent retrograde tracers into individual muscles of the upper and lower face. The facial nucleus received input from all face representations.
The distribution of fibers included additionally the substantia nigra, all the trigeminal nerve nuclei, the facial nucleus and a restricted portion of the inferior olive.
These findings suggest that an aberrant supranuclear pathway, looping around the nucleus ambiguus to the facial nucleus exists in our patient..
CONCLUSION: Developmental abnormalities of the facial nucleus itself constitute an important, and previously ignored, cause of monosymptomatic unilateral CFP..
CO(2)-responsive rostral and caudal units projected to either the thalamic posterior nucleus/zona incerta region (PO/ZI) or the superior salivatory/facial nucleus region (SSN/VII).
Here we show that, following facial nerve axotomy under conditions allowing (nerve anastomosis) or not subsequent regeneration (nerve resection), galectin-3 is not expressed by microglia in the corresponding facial nucleus 1-112 days after lesion.
In the present report, long-term protection of these neurons was evaluated by continuously expressing the neurotrophic factor glial cell line-derived neurotrophic factor (GDNF) within the facial nucleus using a lentiviral vector system. The viral vector was injected unilaterally into the facial nucleus of 4-month-old Balb/C mice. This is the first evidence that viral-mediated delivery of GDNF close to the motoneuron cell bodies of the facial nucleus of adult mice can lead to complete and long-term protection against lesion-induced cell death..
It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus..
In the present study, we have developed a procedure to study the membrane properties of identified, in situ microglia in acutely isolated brain slices from rat cortex, striatum and facial nucleus. To study the consequences of microglial activation on the membrane channel pattern, we compared cells in the normal facial nucleus and at defined times after facial nerve axotomy. Seven days after the lesion, at a time of major regenerative processes in the facial nucleus, the physiological properties of microglial cells had reverted to those present prior to the pathological event.
At E16.5, it was expressed in the premamillary hypothalamic nucleus, superficial gray matter of the superior colliculus, external germinal and Purkinje cell layers of the cerebellum, and facial nucleus.
In the axotomized facial nucleus of transgenic mice at the same time point, microglia activation was enhanced and exhibited phagocytic features. The findings show that in the facial nucleus microglial cells react to motoneuron disease caused by the SOD1 mutation and to axotomy-induced damage of facial motoneurons..
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