Induction of NMDA and GABAA receptor-mediated Ca2+ oscillations with KCC2 mRNA downregulation in injured facial motoneurons.
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To clarify the changes that occur in gamma-aminobutyric acid type A (GABA(A)) receptor-mediated effects and contribute to alterations in the network activities after neuronal injury, we studied intracellular Ca(2+) concentration ([Ca(2+)](i)) dynamics in a rat facial-nerve-transection model. In facial motoneurons, an elevation of the resting [Ca(2+)](i), GABA-mediated [Ca(2+)](i) transients, enhancement of the glutamate-evoked [Ca(2+)](i) increases, and spontaneous [Ca(2+)](i) oscillations were induced by axotomy. All these axotomy-induced modifications were abolished by the GABA(A)-receptor antagonist bicuculline and N-methyl-d-aspartate (NMDA)-receptor antagonist d(-)-2-amino-5-phosphonopentanoic acid. A downregulation of K(+)-Cl(-) cotransporter (KCC2) mRNA, an increase in intracellular Cl(-) concentration ([Cl(-)](i)), and transformation of GABAergic hyperpolarization to depolarization were also induced by axotomy. We suggest that in axotomized neurons KCC2 downregulation impairs Cl(-) homeostasis and makes GABA act depolarizing, resulting in endogenous GABA inducing [Ca(2+)](i) oscillations via facilitation of NMDA-receptor activation. Such GABA(A)-receptor-mediated [Ca(2+)](i) oscillations may play a role in neural survival and regeneration. (+info)
Identification of regeneration-associated genes after central and peripheral nerve injury in the adult rat.
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BACKGROUND: It is well known that neurons of the peripheral nervous system have the capacity to regenerate a severed axon leading to functional recovery, whereas neurons of the central nervous system do not regenerate successfully after injury. The underlying molecular programs initiated by axotomized peripheral and central nervous system neurons are not yet fully understood. RESULTS: To gain insight into the molecular mechanisms underlying the process of regeneration in the nervous system, differential display polymerase chain reaction has been used to identify differentially expressed genes following axotomy of peripheral and central nerve fibers. 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. One hundred and thirty five gene fragments have been isolated, of which 69 correspond to known genes encoding for a number of different functional classes of proteins such as transcription factors, signaling molecules, homeobox-genes, receptors and proteins involved in metabolism. Sixty gene fragments correspond to genomic mouse sequences without known function. In situ-hybridization has been used to confirm differential expression and to analyze the cellular localization of these gene fragments. Twenty one genes (approximately 15%) have been demonstrated to be differentially expressed. CONCLUSIONS: The detailed analysis of differentially expressed genes in different lesion paradigms provides new insights into the molecular mechanisms underlying the process of regeneration and may lead to the identification of genes which play key roles in functional repair of central nervous tissues. (+info)
Earring lesions of the parotid tail.
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BACKGROUND AND PURPOSE: Masses in the parotid tail can be a source of consternation to radiologists and clinicians; inaccurate localization may lead to significant iatrogenic complication. We sought to review the pertinent anatomic localizing features of the parotid tail, relevant facial nerve anatomy, and sources of clinical and radiologic confusion. To conclude, we review imaging features that are helpful in generating a diagnosis in this location. METHODS: We retrospectively reviewed the imaging and clinical features of 111 parotid tail masses in 103 patients (56 male, 45 female, two of unknown sex; age range, 5 months-81 years). The following imaging findings were noted: size, enhancement, multiplicity of lesions, attenuation on CT scans, signal intensity on MR images, and appearance of the surrounding parotid gland. Diagnosis was confirmed by either surgical resection or biopsy findings or by specific clinical data or characteristic imaging findings. RESULTS: Seventeen types of parotid tail masses were identified. Benign lesions were: pleomorphic adenoma (n = 15), Warthin tumor (n = 14), infectious process (n = 13), venous malformation (n = 9), and Sjogren disease (n = 9), lymphatic malformations (n = 7), lipoma (n = 6), HIV lymphoepithelial lesion (n = 4), first brachial cleft cyst (n = 3), oncocytoma (n = 2), sarcoid (n = 1), and lymph node (n = 1). Malignant lesions were: Non-Hodgkin lymphoma (n = 14), metastatic disease (n = 7), mucoepidermoid carcinoma (n = 4), acinic cell carcinoma (n = 1), and undifferentiated carcinoma (n = 1). Eight patients had two diagnoses. CONCLUSION: Understanding normal parotid tail anatomy is important to radiologists, because accurate localization has implications for appropriate management of masses in this location, potentially reducing the occurrence of marginal mandibular nerve injury. (+info)
Surgical intervention in traumatic facial nerve paralysis.
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A four years review from June 1998 to June 2002 of traumatic facial nerve paralysis from temporal bone fractures that required surgical intervention is presented. The aim of this clinical presentation was to determine the current pattern of cases with traumatic facial paralysis which required surgical intervention at our center. There were six cases, of which four (66%) were longitudinal fractures, one each (17%) had transverse fracture and fracture over the lateral wall of mastoid. Hearing loss (83%) was the commonest associated clinical symptom. All cases underwent decompression via the transmastoid surgical approach. Intraoperative findings revealed oedema of facial nerve involving vertical segment and horizontal segment in three cases each respectively. Two cases had concomitant bony impingement. The facial nerve functions in four cases (66%) and one case recovered to House Brackmann grade 2 and 4, 12 months and 3 months respectively postsurgery. The case with transverse fracture remained as House Brackmann grade 5 after two years. (+info)
Regulation of stearoyl-CoA desaturase-1 after central and peripheral nerve lesions.
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BACKGROUND: Interruption of mature axons activates a cascade of events in neuronal cell bodies which leads to various outcomes from functional regeneration in the PNS to the failure of any significant regeneration in the CNS. One factor which seems to play an important role in the molecular programs after axotomy is the stearoyl Coenzyme A-desaturase-1 (SCD-1). This enzyme is needed for the conversion of stearate into oleate. Beside its role in membrane synthesis, oleate could act as a neurotrophic factor, involved in signal transduction pathways via activation of protein kinases C. 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. CONCLUSION: This differential expression points to a functionally significant role for the SCD-1 in the process of regeneration. (+info)
Turning on the machine: genetic control of axon regeneration by c-Jun.
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Upregulation of the transcription factor c-Jun has been correlated with axon regeneration after injury in multiple types of neurons. In this issue of Neuron, Raivich et al. use a nervous system-specific mutant to provide genetic evidence that c-Jun is necessary for efficient axon regeneration. (+info)
The AP-1 transcription factor c-Jun is required for efficient axonal regeneration.
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Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is highly expressed in response to neuronal trauma. Here we have investigated the role of c-jun during axonal regeneration using mice lacking c-jun in the central nervous system. After transection of the facial nerve, the absence of c-Jun caused severe defects in several aspects of the axonal response, including perineuronal sprouting, lymphocyte recruitment, and microglial activation. c-Jun-deficient motorneurons were atrophic, resistant to axotomy-induced cell death, and showed reduced target muscle reinnervation. Expression of CD44, galanin, and alpha7beta1 integrin, molecules known to be involved in regeneration, was greatly impaired, suggesting a mechanism for c-Jun-mediated axonal growth. Taken together, our results identify c-Jun as an important regulator of axonal regeneration in the injured central nervous system. (+info)
Incidence of cranial nerve injuries after carotid eversion endarterectomy with a transverse skin incision under regional anaesthesia.
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OBJECTIVES: The objective of this prospective study was to evaluate the incidence and distribution of cranial nerve injuries after carotid eversion endarterectomy (EEA) performed under regional anaesthesia using a transverse skin incision. PATIENTS AND METHODS: The study included 165 patients and 180 carotid arteries. All patients had a standard pre-operative assessment performed by a neurologist and ENT specialist. All carotid endarterectomies were performed by the eversion technique under regional anaesthesia. RESULTS: Ten cranial nerve injuries were observed. Seven patients had injuries of the marginal mandibular branch of the facial nerve, two patients had lesions of the hypoglossal nerve, and one patient had an injury of the recurrent laryngeal nerve. Eleven patients developed hoarseness without cranial nerve injury. Injuries of the marginal mandibular branch recovered after 3-8 months (mean 5.2 months). Both hypoglossal nerve injuries recovered after 4 months. The patient with the recurrent laryngeal palsy had no improvement after 19 months. Patients with hoarseness secondary to laryngeal haematoma recovered within 1 month. CONCLUSION: The incidence of cranial nerves injury after carotid EEA under regional anaesthesia is comparable to that reported for conventional carotid surgery. Postoperative hoarseness is most frequently due to laryngeal haematoma. (+info)