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PURPOSE: This paper describes a new surgical procedure with electrical stimulation of the facial nerve for unresolved Bell's palsy and compares the facial nerve recovery with another group who underwent traditional middle cranial fossa decompression. RECENT FINDINGS: All patients with total unilateral facial paralysis had surgery by the senior author 3 months from onset of Bell's Palsy. Surgical decompression was performed in 13 patients between 1992-2012 (Group 1). Surgical exposure with intraoperative electrical stimulation of the facial nerve in the peri-geniculate region was performed in 47 patients between 2012-2022 (Group 2). The facial recovery at 1 month and 3 month were significantly better in Group 2. The degree of synkinesis was significantly less in Group 2. The trans-mastoid electrical stimulation of the facial nerve is less invasive, requires no hospital stay, and less time off work compared to the middle cranial fossa approach. The earlier facial movement at one month results in less long-term unwanted faulty regeneration or synkinesis.

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BACKGROUND: Facial nerve hemangiomas (FNHs) are rare tumors that primarily occur near the geniculate ganglion in the temporal bone. Despite their rarity, they can cause significant facial nerve dysfunction. The optimal management approach for FNHs remains uncertain, with surgery being the mainstay but subject to debate regarding the extent of resection and preservation of the facial nerve. METHODS: Systematic review was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We queried the PubMed/Medline (accessed on 5 March 2024) electronic database using combinations of the following search terms and words text: "geniculate ganglion hemangioma", "ganglional hemangioma", "hemangioma of the facial nerve", "facial hemangioma", and "intratemporal hemangioma". RESULTS: We identified a total of 30 literatures (321 patients). The most common site involved for the facial nerve hemangioma was the geniculate ganglion area followed by internal auditory canal, tympanic segment, labyrinthine segment and mastoid involvement. All patients were treated with conservative management or surgery. We report a 48-year-old female patient with HB grade 2 facial palsy and hemifacial spasm underwent SRS using Cyberknife technology. The treatment targeted the FNH in the left internal acoustic canal near the geniculate ganglion. Six months post-treatment, clinical improvement was evident, and lesion control was confirmed in a follow-up brain MRI. CONCLUSION: The rarity of FNHs contributes to the lack of consensus on optimal management. This illustrative case demonstrates the feasibility of SRS as a standalone treatment for FNHs.

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BACKGROUND: The suprageniculate fossa (SGF) is located between the geniculate ganglion, the middle cranial fossa (MCF) and the anterior semicircular canal (ASCC). An endoscopic transcanal approach has been recently proposed to treat the different lesions in this area. The aim of the study is to describe the anatomical pathway of this approach by measuring the dimensions of its boundaries while checking their correlation with the pneumatization of the SGF area. METHODS: This is a retrospective anatomical analysis of Cone Beam CT scans of 80 patients, for a total of 160 temporal bones analyzed. Two checkpoints were measured for the SGF route, as an internal and an external window. These are triangles between the MCF dura, the geniculate ganglion and the ASCC on parasagittal and axial planes. The pneumatization of the SGF was also assessed, classified and correlated with the measured dimensions. RESULTS: The depth of the SGF was 7.5 ± 1.8 mm. The width of the external window was 7.5 ± 1.9, 5.6 ± 2.4 and 1.6 ± 1.6 mm for the posterior, middle and anterior points of measurement, respectively. The height of the internal window was 7.6 ± 1.2, 4.5 ± 1.5 and 1.7 ± 1.7 mm for the posterior, middle and anterior points of measurement, respectively. Type A pneumatization was found in 87 cases, type B in 34 and type C in 39. The degree of pneumatization directly correlated to the depth and height of the fossa. CONCLUSIONS: The suprageniculate approach route is defined by the internal and external windows which should be evaluated during a pre-surgery imaging assessment. The detailed anatomy of the approach and the novel classification of the pneumatization of the SGF are here described which may be useful to plan a safer procedure with minimal complications.

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PURPOSE: A variety of lesions could arise from the GG area, or extend into this region from adjacent sites. The management of perigeniculate lesions includes observation, surgery, and radiation, according to the nature, the size of the lesion, and the accompanying symptoms. Preliminary experiences on the exclusive transcanal endoscopic approach to the GG area have shown safety and feasibility avoiding of any postauricular incision, or brain manipulation. The experience from two referral centers on patients treated for a GG lesion with a totally endoscopic approach is herein reported. METHODS: Data about patients who underwent exclusive endoscopic approach to the GG area at the Otolaryngology Departments of the University Hospitals of Modena and Bologna between May 2017 and February 2022 were retrospectively collected. RESULTS: The total number of patients included in our study was 11. 10 patients (91%) had progressive unilateral facial paralysis and 1 patient (11%) presented with chronic otorrhea. The mean largest diameter of the treated lesions was of 8 mm. The resection was extended to the fundus of the IAC in 2 patients (expanded approach). The remaining 9 patients (82%) underwent partial ossicular replacement prosthesis (PORP). No major complications occurred. Facial nerve outcomes were good in all patients and the mean ABG worsened from 12 dB pre-operatively to 22 dB post-operatively. CONCLUSIONS: The exclusively endoscopic approach to GG lesions represents a viable alternative to traditional microscopic approaches and may be included in the armamentarium of ear surgeons.

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Schwannomas are rare nerve sheath tumors that can occur throughout the body, and are symptomatic based on location, size, and impingement on adjacent structures. These tumors are often benign lesions and occur sporadically or from genetic conditions such as neurofibromatosis. Schwannomas may arise from peripheral nerves, gastrointestinal nerves, spinal nerve roots and cranial nerves. Facial nerve schwannomas arise from cranial nerve VII, commonly involving the geniculate ganglion, labyrinthine segment, and internal auditory canal. While small lesions are asymptomatic, larger lesions can cause facial nerve paralysis, and facial spasms. Lesions in the internal auditory canal can cause hearing loss, tinnitus, vertigo, and otalgia. High-resolution CT imaging and MRI imaging are useful for distinguishing between other pathologies that arise from the same region. High-resolution CT scans can show bony degeneration of nearby structures such as the labyrinth or ossicles. MRI imaging shows hypo intensity on T1 imaging, and hyperintensity on T2 imaging. On T1 postcontrast, enhancement can be homogenous or heterogeneous with cystic degeneration if the lesion is large. Nodular enhancement is commonly seen on facial nerve schwannomas within the internal auditory canal. Vestibular schwannomas involving CN VIII are more common, and appear similar to facial nerve schwannomas, but can be distinguished apart due to growth in the geniculate ganglion and/or the labyrinthine segment. Management of asymptomatic or mild lesions is typically conservative with follow up imaging, and surgery for larger lesions. Here, we present a case of a facial nerve schwannoma in a 57-year-old woman.

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Facial nerve hemangiomas are a rare entity of skull base lesions that arise within the temporal bone and affect the seventh cranial nerve.1 They are vascular malformations arising from the vascular plexuses surrounding the nerve. Although slow growing and overall benign in nature, they can cause significant facial nerve dysfunction even at small sizes.2 Facial nerve hemangiomas can arise within different segments of the facial nerve within the temporal bone, but most commonly arise near the geniculate ganglion.3 We describe the case of a 34-year-old female who presented with progressive right facial palsy (House-Brackmann 4) and a calcified lesion arising from the petrous temporal bone. Resection of the lesion was performed with a posterior to anterior middle fossa approach, with identification of the greater superficial petrosal nerve and geniculate ganglion, sectioning of the middle meningeal artery, and identification of V2 and V3 segments of the trigeminal nerve (Video 1). The bony mass was peeled off the petrous temporal bone and the geniculate ganglion without sacrifice of the facial nerve. Postoperative imaging showed gross total resection, and the patient's facial palsy improved to House-Brackmann 1. A comprehensive literature review on surgical approaches and outcomes for the resection of hemangiomas involving the geniculate ganglion or the facial nerve is also provided.2,4-18 The case presentation, surgical anatomy, operative nuances with technical considerations, and postoperative course with imaging are reviewed. The patient and family provided informed consent for the procedure and publication of patient images.

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OBJECTIVE: To distinguish geniculate ganglion venous malformation (GGVM) from schwannoma (GGS) by using high-resolution CT (HRCT), routine MRI, and dynamic T1-weighted imaging (T1WI) characteristics. METHODS: Surgically confirmed GGVMs and GGSs between 2016 and 2021 were retrospectively included. Preoperative HRCT, routine MR, and dynamic T1WI were performed on all patients. Clinical data, imaging characteristics including lesion size, involvement of facial nerve (FN), signal intensity, enhancement pattern on dynamic T1WI, and bone destruction on HRCT were evaluated. Logistic regression model was developed to identify independent factors for GGVMs, and the diagnostic performance was accessed by receiving operative curve (ROC) analysis. Histological characteristics were explored for both GGVMs and GGSs. RESULTS: Twenty GGVMs and 23 GGSs with mean age of 31 were included. On dynamic T1WI, 18 GGVMs (18/20) showed "pattern A" enhancement (a progressive filling enhancement), while all 23 GGSs showed "pattern B" enhancement (a gradual whole-lesion enhancement) (p < 0.001). Thirteen GGVMs (13/20) showed the "honeycomb" sign whereas all GGS (23/23) showed extensive bone changes on HRCT (p < 0.001). Lesion size, involvement of FN segment, signal intensity on non-contrast T1WI and T2-weighted imaging (T2WI), and homogeneity on enhanced T1WI were obviously differed between two lesions (p < 0.001, p = 0.002, p < 0.001, p = 0.01, p = 0.02, respectively). Regression model showed the "honeycomb" sign and "pattern A" enhancement were independent risk factors. Histologically, GGVM was characterized by interwoven dilated and tortuous veins, while GGS was characterized by abundant spindle cells with dense arterioles or capillaries. CONCLUSIONS: The "honeycomb" sign on HRCT and "pattern A" enhancement on dynamic T1WI are the most promising imaging characteristics for differentiating GGVM from GGS. CLINICAL RELEVANCE STATEMENT: The characteristic sign and enhancement pattern on HRCT and dynamic T1-weighted imaging allow preoperative differentiation of geniculate ganglion venous malformation and schwannoma feasible, which will improve clinical management and benefit patient prognosis. KEY POINTS: • The "honeycomb" sign on HRCT is a reliable finding to differentiate GGVM from GGS. • GGVM typically shows "pattern A" enhancement (focal enhancement of the tumor on early dynamic T1WI, followed by progressive contrast filling of the tumor in the delayed phase), while "pattern B" enhancement (gradual heterogeneous or homogeneous enhancement of the whole lesion) is observed in GGS on dynamic T1WI.

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Geniculate ganglion hemangioma (GGH) is rarely presented in the neurosurgical literature. It extends extradurally on the middle fossa floor and displaces the intratemporal part of the facial nerve. Surgical treatment is advisable at early symptoms. Proposed techniques include fascicular-sparing resection or nerve interruption with grafting. No definitive conclusions exist about the superiority of a certain technique in preserving facial nerve integrity and function. Through the description of a surgically managed symptomatic GGH, we herein discuss literature data about the surgical results of fascicular-sparing resection versus grafting. A PRISMA-based literature search was performed on the PubMed database. Only articles in English and published since 1990 were selected and furtherly filtered based on the best relevance. Statistical comparisons were performed with ANOVA. One hundred sixteen GGHs were collected, 56 were treated by fascicular-sparing resection, and 60 were treated by grafting. The facial function was improved, or unchanged, in 53 patients of the fascicular-sparing group and 30 patients of the grafting one. Sixty-five patients achieved a good (House-Brackmann (HB) grade III) postoperative facial outcome, of which 47 and 18 belonged to the fascicular-sparing and grafting group, respectively. Greater efficacy of the fascicular-sparing technique in the achievement of a better facial outcome was found (p = 0.0014; p = 0.0022). A surgical resection at the earliest symptoms is critical to preserve the facial nerve function in GGHs. Fascicular-sparing resection should be pursued in symptomatic cases with residual facial function (I-III HB). Conversely, grafting has a rationale for higher HB grades (V-VI). Broader studies are required to confirm these findings and turn them into new therapeutic perspectives.

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The sense of taste starts with activation of receptor cells in taste buds by chemical stimuli which then communicate this signal via innervating oral sensory neurons to the CNS. The cell bodies of oral sensory neurons reside in the geniculate ganglion (GG) and nodose/petrosal/jugular ganglion. The geniculate ganglion contains two main neuronal populations: BRN3A+ somatosensory neurons that innervate the pinna and PHOX2B+ sensory neurons that innervate the oral cavity. While much is known about the different taste bud cell subtypes, considerably less is known about the molecular identities of PHOX2B+ sensory subpopulations. In the GG, as many as 12 different subpopulations have been predicted from electrophysiological studies, while transcriptional identities exist for only 3 to 6. Importantly, the cell fate pathways that diversify PHOX2B+ oral sensory neurons into these subpopulations are unknown. The transcription factor EGR4 was identified as being highly expressed in GG neurons. EGR4 deletion causes GG oral sensory neurons to lose their expression of PHOX2B and other oral sensory genes and up-regulate BRN3A. This is followed by a loss of chemosensory innervation of taste buds, a loss of type II taste cells responsive to bitter, sweet, and umami stimuli, and a concomitant increase in type I glial-like taste bud cells. These deficits culminate in a loss of nerve responses to sweet and umami taste qualities. Taken together, we identify a critical role of EGR4 in cell fate specification and maintenance of subpopulations of GG neurons, which in turn maintain the appropriate sweet and umami taste receptor cells.

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In order to master the surgical approaches to the middle cranial fossa, the surgeon needs to understand the relevant bony anatomy. However, she/he also needs to have a clear and sound understanding of the neural and vascular anatomy because, oftentimes, the osseous anatomy (except for the optic apparatus) should be removed to expose and protect the neurovascular anatomy. This is the second of a two-part article discussing the neurovascular anatomy of the middle cranial fossa. A brief discussion of the surgical approaches follows.

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Taste ganglion neurons are functionally and molecularly diverse, but until recently morphological diversity was completely unexplored. Specifically, taste arbors (the portion of the neuron within the taste bud) vary in structure, but the reason for this variability is unclear. Here, we analyzed structural variability in taste arbors to determine which factors determine their morphological diversity. To characterize arbor morphology and its relationship to taste bud cells capable of transducing taste stimuli (taste-transducing cell) number and type, we utilized sparse cell genetic labeling of taste ganglion neurons in combination with whole-mount immunohistochemistry. Reconstruction of 151 taste arbors revealed variation in arbor size, complexity, and symmetry. Overall, taste arbors exist on a continuum of complexity, cannot be categorized into discrete morphological groups, and do not have stereotyped endings. Arbor size/complexity was not related to the size of the taste bud in which it was located or the type of taste-transducing cell contacted (membranes within 180 nm). Instead, arbors could be broadly categorized into three groups: large asymmetrical arbors contacting many taste-transducing cells, small symmetrical arbors contacting one or two taste-transducing cells, and unbranched arbors. Neurons with multiple arbors had arbors in more than one of these categories, indicating that this variability is not an intrinsic feature of neuron type. Instead, we speculate that arbor structure is determined primarily by nerve fiber remodeling in response to cell turnover and that large asymmetrical arbors represent a particularly plastic state.

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Ramsay Hunt syndrome is the complication of the virus varicella-zoster and the infection caused by it, which shows apparent geniculate ganglion involvement. This article discusses the etiology, epidemiology, and pathology of Ramsay Hunt syndrome. Clinically it may be presented as a vesicular rash on the ear or even in the mouth, pain in the ear, and facial paralysis. Some other rare symptoms may also be present, which are also discussed in this article. Skin involvement is also seen in some cases as patterns due to anastomoses between cervical and cranial nerves. This article provides an overview of how the varicella-zoster virus causes facial paralysis and other neurological symptoms. Knowing about this condition and its clinical features is essential to make an early diagnosis and, thus, provide a good prognosis. A good prognosis is required to reduce the nerve damage, prevent further complications, and start an early therapy of acyclovir and corticosteroid. This review also presents a clinical picture of the disease and its complications. The incidence of Ramsay Hunt syndrome has gradually decreased over time because of the development of the varicella-zoster vaccine and better health facilities. The paper also talks about how the diagnosis of Ramsay Hunt syndrome is made and the various treatment options available. Facial paralysis in Ramsay Hunt syndrome presents differently than Bell's Palsy. If not treated for too long, it may cause permanent muscle weakness and may also cause a loss of hearing. It may be confused with simple herpes simplex virus outbreaks or contact dermatitis.

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Taste sensation is the process of converting chemical identities in food into a neural code of the brain. Taste information is initially formed in the taste buds on the tongue, travels through the afferent gustatory nerves to the sensory ganglion neurons, and finally reaches the multiple taste centers of the brain. In the taste field, optical tools to observe cellular-level functions play a pivotal role in understanding how taste information is processed along a pathway. In this review, we introduce recent advances in the optical tools used to study the taste transduction pathways.

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Oral sensory neurons of the geniculate ganglion (GG) innervate taste papillae and buds on the tongue and soft palate. Electrophysiological recordings of these neurons and fibers revealed complexity in the number of unique response profiles observed, suggesting there are several distinct neuronal subtypes. Molecular descriptions of these subpopulations are incomplete. We report here the identification of a subpopulation of GG oral sensory neurons in mice by expression of tyrosine hydroxylase (TH). TH-expressing geniculate neurons represent 10-20% of oral sensory neurons and these neurons innervate taste buds in fungiform and anterior foliate taste papillae on the surface of the tongue, as well as taste buds in the soft palate. While 35-50% of taste buds on the tongue are innervated by these TH+ neurons, 100% of soft palate taste buds are innervated. These neurons did not have extragemmal processes outside of taste buds and did not express the mechanosensory neuron-associated gene Ret, suggesting they are chemosensory and not somatosensory neurons. Within taste buds, TH-expressing fibers contacted both Type II and Type III cells, raising the possibility that they are responsive to more than one taste quality. During this analysis we also identified a rare TH+ taste receptor cell type that was found in only 12-25% of taste buds and co-expressed TRPM5, suggesting it was a Type II cell. Taken together, TH-expressing GG oral sensory neurons innervate taste buds preferentially in the soft palate and contact Type II and Type III taste bud receptor cells.

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OBJECTIVE: Facial nerve (FN) schwannomas are extremely rare. According to their origin and involved segment(s), they constitute distinct subtypes. Intact FN function presents a management challenge, particularly in the cerebellopontine angle cisternal subtype that masquerades as a vestibular schwannoma. Fascicular-sparing technique with subtotal resection can maintain a good FN function. This study focuses on management to maintain good FN function. METHODS: A retrospective analysis of a cohort of 13 patients harboring FN schwannoma. Patient demographics, clinical findings, imaging, surgical intervention, and outcomes were analyzed. RESULTS: Five women and 8 men, with an average age of 55.3 years (39-75 years), harbored 6 cisternal, 2 ganglion, and 5 combined tumors. Average tumor size was 28.3 mm (16-50 mm). Eleven patients underwent surgery. Seven patients had fascicle-sparing technique, 5 of whom maintained their preoperative FN function, whereas 2 patients with near-total removal had a deterioration in FN function. Two patients with preoperative complete facial paralysis had gross total removal with interposition nerve graft. CONCLUSIONS: FN schwannomas management is individualized according to the subtype and the FN function at presentation. When FN function is normal, observation can be applied for prolonged period of time. At the early sign of deterioration, sub- or near-total resection with fascicle sparing technique can be performed. The cisternal subtype masquerade as vestibular schwannoma and should be recognized at the initial exposure by the appearance of finely splayed nerve fascicles at the perimetry of the tumor which elicits a motor response at low threshold stimulation.

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PURPOSE: To describe the suprameatal-transzygomatic root endoscopic approach (STEA) to the geniculate ganglion (GG), the labyrinthine facial nerve (FN) and epitympanum. METHODS: The feasibility and limits of the STEA, maintaining the integrity of the ossicular chain, were analysed. Ten human cadaveric ears were dissected. Step-by-step description of the technique and relevant measurements were taken during the approach. The visualization and surgical working field on the anterior and posterior medial epitympanum, GG, greater superficial petrosal nerve, the labyrinthine FN and suprageniculate area were evaluated. The range of motion through the approach and the rate of the decompression of the GG and the labyrinthine portion of the FN were assessed as well. CT-scan measurements were compared with those obtained during the dissection. RESULTS: A complete exploration of the epitympanum was possible in every specimen. Decompression of the GG and first portion of the FN was achieved without any trauma to the ossicular chain in nine ears. The endoscope movements were mainly limited by the distance between bony buttress-short process of the incus-tegmen. The working space, during GG and labyrinthine FN decompression, was limited by the distance between malleus head-medial epitympanic wall and malleus head-GG. Radiologic measurements were consistent with those obtained during the dissections. CONCLUSION: The STEA is a promising minimally invasive approach for decompression of the GG and FN's labyrinthine portion. The applications of this corridor include the exploration and surgery of the medial epitympanum, preserving the ossicular chain.

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This review summarizes our understanding of ATP signaling in taste and describes new directions for research. ATP meets all requisite criteria to be considered a neurotransmitter: (1) presence in taste cells, as in all cells; (2) release upon appropriate taste stimulation; (3) binding to cognate purinergic receptors P2X2 and P2X3 on gustatory afferent neurons, and (4) after release, enzymatic degradation to adenosine and other nucleotides by the ectonucleotidase, NTPDase2, expressed on the Type I, glial-like cells in the taste bud. Importantly, double knockout of P2X2 and P2X3 or pharmacological inhibition of P2X3 abolishes transmission of all taste qualities. In Type II taste cells (those that respond to sweet, bitter, or umami stimuli), ATP is released non-vesicularly by a large conductance ion channel composed of CALHM1 and CALHM3, which form a so-called channel synapse at areas of contact with afferent taste nerve fibers. Although ATP release has been detected only from Type II cells, it is also required for the transmission of salty and sour stimuli, which are mediated primarily by the Type III taste cells. The source of the ATP required for Type III cell signaling to afferent fibers is still unclear and is a focus for future experiments. The ionotropic purinergic receptor, P2X3, is widely expressed on many sensory afferents and has been a therapeutic target for treating chronic cough and pain. However, its requirement for taste signaling has complicated efforts at treatment since patients given P2X3 antagonists report substantial disturbances of taste and become non-compliant.

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The fungiform papilla (FP) is a gustatory and somatosensory structure incorporating chorda tympani (CT) nerve fibers that innervate taste buds (TB) and also contain somatosensory endings for touch and temperature. Hedgehog (HH) pathway inhibition eliminates TB, but CT innervation remains in the FP. Importantly, after HH inhibition, CT neurophysiological responses to taste stimuli are eliminated, but tactile responses remain. To examine CT fibers that respond to tactile stimuli in the absence of TB, we used Phox2b-Cre; Rosa26LSL-TdTomato reporter mice to selectively label CT fibers with TdTomato. Normally CT fibers project in a compact bundle directly into TB, but after HH pathway inhibition, CT fibers reorganize and expand just under the FP epithelium where TB were. This widened expanse of CT fibers coexpresses Synapsin-1, ß-tubulin, S100, and neurofilaments. Further, GAP43 expression in these fibers suggests they are actively remodeling. Interestingly, CT fibers have complex terminals within the apical FP epithelium and in perigemmal locations in the FP apex. These extragemmal fibers remain after HH pathway inhibition. To identify tactile end organs in FP, we used a K20 antibody to label Merkel cells. In control mice, K20 was expressed in TB cells and at the base of epithelial ridges outside of FP. After HH pathway inhibition, K20 + cells remained in epithelial ridges but were eliminated in the apical FP without TB. These data suggest that the complex, extragemmal nerve endings within and disbursed under the apical FP are the mechanosensitive nerve endings of the CT that remain after HH pathway inhibition.

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Schwannomas are benign tumors arising from Schwann cells which are a protective casing of nerves, composing myelin sheath and can develop in any nerve where Schwann cells are present. Most common are vestibulocochlear nerve schwannomas. Facial nerve schwannomas (FNSs) are uncommon tumors involving seventh nerve of which geniculate ganglion involvement is most common. Clinical presentations and the imaging appearances of FNSs are influenced by the topographical anatomy of the facial nerve and vary according to the segments involved. We report a case of 73-year-old man presenting with right side facial weakness of lower motor neuron type involvement. Computed tomography and magnetic resonance imaging are clinching the diagnosis. An early diagnosis is important in containing the disease facilitating early surgical intervention.

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Taste buds consist of specialized epithelial cells which detect particular tastants and synapse onto the afferent taste nerve innervating the endorgan. The nature of the neurotransmitter released by taste cells onto the nerve fiber was enigmatic early in this century although neurotransmitters for other sensory receptor cell types, e.g. hair cells, photoreceptors, was known for at least a decade. A 1999 paper by Burnstock and co-workers (Bo et al., 1999) showing the presence of P2X receptors on the afferent nerves served as a springboard for research that ultimately led to the discovery of ATP as the crucial neurotransmitter in the taste system (Finger et al., 2005). Subsequent work showed that a subpopulation of taste cells utilize a unique release channel, CALHM1/3, to release ATP in a voltage-dependent manner. Despite these advances, several aspects of purinergic transmission in this system remain to be elucidated.

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