Previous studies have demonstrated that muscarinic, and nicotinic receptors increase free Ca2+ levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca2+ overl...Previous studies have demonstrated that muscarinic, and nicotinic receptors increase free Ca2+ levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca2+ overload can trigger either necrotic or apoptotic cell death. Gamma-aminobutyric acid (GABA), an important inhibitory neurotransmitter in the central nervous system, exists in the facial nerve nucleus. It is assumed that GABA negatively regulates free Ca2+ levels in the facial nerve nucleus. The present study investigated GABA type A (GABAA) receptor expression in the facial nerve nucleus in a rat model of facial nerve injury using immunohistochemistry and laser confocal microscopy, as well as the regulatory effects of GABAA receptor on nicotinic receptor response following facial nerve injury. Subunits α1, α3, α5, β1, β2, δ, and γ3 of GABAA receptors were expressed in the facial nerve nucleus following facial nerve injury. In addition, GABAA receptor expression significantly inhibited the increase in nicotinic receptor-mediated free Ca2+ levels in the facial nerve nucleus following facial nerve injury in a concentration-dependent fashion. These results suggest that GABAA receptors exhibit negative effects on nicotinic receptor responses following facial nerve injury.展开更多
The muscarinic receptor modulates intracellular free calcium ion levels in the facial nerve nucleus via different channels. In the present study, muscarinic receptor-mediated free calcium ions levels were detected by ...The muscarinic receptor modulates intracellular free calcium ion levels in the facial nerve nucleus via different channels. In the present study, muscarinic receptor-mediated free calcium ions levels were detected by confocal laser microscopy in the facial nerve nucleus following facial nerve injury in rats. There was no significant difference in muscarinic receptor expression at the affected facial nerve nucleus compared with expression prior to injury, but muscarinic receptor-mediated free calcium ion levels increased in the affected side following facial nerve injury (P 〈 0.01). At day 30 after facial nerve injury, 50 pmol/L muscarinic-mediated free calcium ion levels were significantly inhibited at the affected facial nerve nucleus in calcium-free artificial cerebrospinal fluid, and the change range was 82% of artificial cerebrospinal fluid (P 〈 0.05). These results suggest that increased free calcium ion concentrations are achieved by intracellular calcium ion release, and that the transmembrane flow of calcium ions is also involved in this process.展开更多
Previous studies have demonstrated that the cholinergic system, via nicotinic receptors, regulates intracellular free calcium levels in the facial nucleus under normal physiological conditions. However, the regulation...Previous studies have demonstrated that the cholinergic system, via nicotinic receptors, regulates intracellular free calcium levels in the facial nucleus under normal physiological conditions. However, the regulation of nicotinic receptors on free calcium levels following facial nerve injury remains unclear. In the present study, an animal model of facial nerve injury was established, and changes in nicotinic receptor expression following facial nerve injury in rats were detected using reverse transcription polymerase chain reaction. Nicotinic receptor-mediated changes of free calcium levels following facial nucleus injury were determined by laser confocal microscopy. Results showed no significant difference in nicotinic receptor expression between the normal group and the affected facial nerve nucleus. The nicotinic receptor a4132 subtype increased free calcium levels following facial nerve injury by promoting calcium transmembrane influx, and L-type voltage-gated calcium channel-mediated influx of calcium ions played an important role in promoting calcium transmembrane influx. The nicotinic receptor-mediated increase of free calcium levels following facial nerve injury provides an important mechanism for the repair of facial nerve injury.展开更多
Muscarinic receptors and nicotine receptors can increase free calcium ion levels in the facial nucleus via different channels following facial nerve injury. In addition, γ-aminobutyric acid A (GABAA) receptors have...Muscarinic receptors and nicotine receptors can increase free calcium ion levels in the facial nucleus via different channels following facial nerve injury. In addition, γ-aminobutyric acid A (GABAA) receptors have been shown to negatively regulate free calcium ion levels in the facial nucleus by inhibiting nicotine receptors. The present study investigated the influence of GABAA, γ-aminobutyric acid B (GABAB) and C (GABAc) receptors on muscarinic receptors in rats with facial nerve injury by confocal laser microscopy. GABAA and GABAB receptors exhibited significant dose-dependent inhibitory effects on increased muscarinic receptor-mediated free calcium ion levels following facial nerve injury. Results showed that GABAA and GABAB receptors negatively regulate muscarinic receptor effects and interplay with cholinergic receptors to regulate free calcium ion levels for facial neural regeneration.展开更多
Objective: To report an unusual case of pyriform sinus-pleural-mediastinal fistula secondary to internal penetrating trauma by a toothbrush, with emphasis on management options. Case report: A 26-year-old woman swallo...Objective: To report an unusual case of pyriform sinus-pleural-mediastinal fistula secondary to internal penetrating trauma by a toothbrush, with emphasis on management options. Case report: A 26-year-old woman swallowed a toothbrush in a violent manner 8 months ago in an attempt of self-mutilation. She immediately complained of neck pain and dysphagia. She was diagnosed with pyriform sinus-pleural-mediastinal fistula. The fistula was repaired. Primary closure was performed and covered with the sternocleidomastoid muscle flap, and reinforced with thyroid tissue and surrounding tissues. The patient did not present any complications or recurrence, and she gained weight after the operation. Conclusion: Early recognition of hypopharyngeal perforation is important, and in selected cases, immediate repair of the perforation can lead to a good prognosis.展开更多
基金a Grant from the Youth Research Foundation of Qingdao University,No.2007
文摘Previous studies have demonstrated that muscarinic, and nicotinic receptors increase free Ca2+ levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca2+ overload can trigger either necrotic or apoptotic cell death. Gamma-aminobutyric acid (GABA), an important inhibitory neurotransmitter in the central nervous system, exists in the facial nerve nucleus. It is assumed that GABA negatively regulates free Ca2+ levels in the facial nerve nucleus. The present study investigated GABA type A (GABAA) receptor expression in the facial nerve nucleus in a rat model of facial nerve injury using immunohistochemistry and laser confocal microscopy, as well as the regulatory effects of GABAA receptor on nicotinic receptor response following facial nerve injury. Subunits α1, α3, α5, β1, β2, δ, and γ3 of GABAA receptors were expressed in the facial nerve nucleus following facial nerve injury. In addition, GABAA receptor expression significantly inhibited the increase in nicotinic receptor-mediated free Ca2+ levels in the facial nerve nucleus following facial nerve injury in a concentration-dependent fashion. These results suggest that GABAA receptors exhibit negative effects on nicotinic receptor responses following facial nerve injury.
基金Youth Scientific Research Foundation of Qingdao University (2007)
文摘The muscarinic receptor modulates intracellular free calcium ion levels in the facial nerve nucleus via different channels. In the present study, muscarinic receptor-mediated free calcium ions levels were detected by confocal laser microscopy in the facial nerve nucleus following facial nerve injury in rats. There was no significant difference in muscarinic receptor expression at the affected facial nerve nucleus compared with expression prior to injury, but muscarinic receptor-mediated free calcium ion levels increased in the affected side following facial nerve injury (P 〈 0.01). At day 30 after facial nerve injury, 50 pmol/L muscarinic-mediated free calcium ion levels were significantly inhibited at the affected facial nerve nucleus in calcium-free artificial cerebrospinal fluid, and the change range was 82% of artificial cerebrospinal fluid (P 〈 0.05). These results suggest that increased free calcium ion concentrations are achieved by intracellular calcium ion release, and that the transmembrane flow of calcium ions is also involved in this process.
基金Youth Research Fund of Qingdao University (2007)
文摘Previous studies have demonstrated that the cholinergic system, via nicotinic receptors, regulates intracellular free calcium levels in the facial nucleus under normal physiological conditions. However, the regulation of nicotinic receptors on free calcium levels following facial nerve injury remains unclear. In the present study, an animal model of facial nerve injury was established, and changes in nicotinic receptor expression following facial nerve injury in rats were detected using reverse transcription polymerase chain reaction. Nicotinic receptor-mediated changes of free calcium levels following facial nucleus injury were determined by laser confocal microscopy. Results showed no significant difference in nicotinic receptor expression between the normal group and the affected facial nerve nucleus. The nicotinic receptor a4132 subtype increased free calcium levels following facial nerve injury by promoting calcium transmembrane influx, and L-type voltage-gated calcium channel-mediated influx of calcium ions played an important role in promoting calcium transmembrane influx. The nicotinic receptor-mediated increase of free calcium levels following facial nerve injury provides an important mechanism for the repair of facial nerve injury.
基金the Youth Research Foundation of Qingdao University, No. 2007
文摘Muscarinic receptors and nicotine receptors can increase free calcium ion levels in the facial nucleus via different channels following facial nerve injury. In addition, γ-aminobutyric acid A (GABAA) receptors have been shown to negatively regulate free calcium ion levels in the facial nucleus by inhibiting nicotine receptors. The present study investigated the influence of GABAA, γ-aminobutyric acid B (GABAB) and C (GABAc) receptors on muscarinic receptors in rats with facial nerve injury by confocal laser microscopy. GABAA and GABAB receptors exhibited significant dose-dependent inhibitory effects on increased muscarinic receptor-mediated free calcium ion levels following facial nerve injury. Results showed that GABAA and GABAB receptors negatively regulate muscarinic receptor effects and interplay with cholinergic receptors to regulate free calcium ion levels for facial neural regeneration.
文摘Objective: To report an unusual case of pyriform sinus-pleural-mediastinal fistula secondary to internal penetrating trauma by a toothbrush, with emphasis on management options. Case report: A 26-year-old woman swallowed a toothbrush in a violent manner 8 months ago in an attempt of self-mutilation. She immediately complained of neck pain and dysphagia. She was diagnosed with pyriform sinus-pleural-mediastinal fistula. The fistula was repaired. Primary closure was performed and covered with the sternocleidomastoid muscle flap, and reinforced with thyroid tissue and surrounding tissues. The patient did not present any complications or recurrence, and she gained weight after the operation. Conclusion: Early recognition of hypopharyngeal perforation is important, and in selected cases, immediate repair of the perforation can lead to a good prognosis.