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Conclusions. Data about the recovery course of facial function after intratemporal facial nerve reconstruction using interposition nerve graft would provide useful information for clinicians to understand the regenerative process of the facial nerve after this type of surgery. It would also enable them to obtain informed consent from the patients by preoperatively explaining the predicted outcome of the postoperative facial paralysis. Objective. The purpose of this study was to describe the recovery course of facial movement and electrophysiological findings after intratemporal facial nerve reconstruction using interposition graft. Patients and methods. Five patients who underwent reconstruction of the facial nerve using interposition nerve graft immediately after facial nerve excision during surgery for temporal bone lesions were included in this study. Each patient was evaluated for facial movement (Yanagihara score), blink reflex (BR), and electroneurography (ENoG) preoperatively and postoperatively. Results. Improvement in facial movement began 8-10 months postoperatively. The score then gradually increased, and reached a plateau level by 2 years following surgery. The final score in four of the five patients ranged from 20 to 24 points, while the facial score of one patient only reached 12 points even at 3 years after surgery. All patients demonstrated moderate to severe synkinesis. The reappearance of R1 in BR occurred 7-10 months postoperatively, almost simultaneously with the beginning of recovery of facial movement. The latency of R1 on the operated side became shortened with increasing postoperative time, although it remained considerably longer than that on the unoperated side, even after 2 postoperative years. The onset of recovery of ENoG value (10-12 months postoperatively) was always delayed compared with the actual facial movement recovery and never returned to the level in the unoperated side. [ABSTRACT FROM AUTHOR]

Conclusion. The present study demonstrated the age-related decrease in the axonal diameter of the olfactory nerve. This finding may represent the maturational change of the olfactory receptor neurons. Objectives. The aim of this study was to investigate age-related changes in the axonal diameter of the olfactory nerve in the lamina propria. Materials and methods. Female ICR mice, postnatal age 10 days, 3 months, 7 months, and 16 months, were studied. The electron micrographs of septal olfactory mucosa were used to measure the axonal diameters of olfactory nerves. Results. The distribution of the diameter shifted toward the thinner side between 10-day-old and 3-month-old mice. The axonal diameter showed significant decreases (p < 0.001) from the age of 10 days to that of 3 months. [ABSTRACT FROM AUTHOR]

Conclusion. This study suggested that nitric oxide (NO) takes part in the parasympathetic nerve control functions mainly through m3 receptors and subsequently through m1 receptors. Objectives. The regulation of glandular secretions and vasomotor tone in human nasal mucosa implicates muscarinic receptors. There are five recognized classes (m1-m5) of muscarinic receptor subtypes. NO is a free radical gas that has been found to be produced in neuronal cells by the action of enzyme neural nitric oxide synthase (nNOS). The aim of this study was to identify the colocalization of muscarinic receptor subtypes (m1-m5) and nNOS in the human inferior turbinate mucosa. Materials and methods. Human inferior turbinate mucosa was stained by using the antibody of muscarine receptor subtypes and nNOS in an immunohistochemical double-staining method. Results. The colocalization of m3 receptors and nNOS-immunoreactive nerve fibers was most extensively distributed on glands, vessels, and epithelium in all muscarinic receptor subtypes. These findings lead us to propose that NO also acts as a neurotransmitter in glands, vessels, and epithelium of the human nasal mucosa and can be assigned to parasympathetic nerve structures through m3 receptors mainly and m1 receptors subsequently. [ABSTRACT FROM AUTHOR]

In a previous study we showed that, in rat spiral ganglion neurons (SGNs), the adenosine 5'-triphosphate (ATP)-evoked currents were a combination of the activation of ionotropic receptors (the first fast current) and the activation of metabotropic receptors which secondarily opened non-selective cation channels. These two conductances imply the involvement of different receptor subtypes. In the present study, we tested three subtype-specific purinergic ligands: α,β-methylene ATP (α,β-meATP) for P2X receptors, uridine 5′-triphosphate (UTP) for P2Y receptors and 2′-3′-O-(4-benzoylbenzoyl) ATP (Bz-ATP) for P2Z (P2X 7 ) receptors. Application of 100 μM α,β-meATP did not trigger any significant change in membrane conductance, while the SGNs were responsive to ATP. Pressure application of UTP (100 μM, 1 s) evoked an inward current averaging 344±169 pA at a holding potential of -50 mV. The conductance developed after a latency averaging 1.5±0.6 s, took 4-6 s to peak and reversed slowly within 15-30 s. The current-voltage curve reversed near 0 mV, suggesting a non-selective cation conductance, like the second component of the ATP conductance. Bz-ATP evoked an inward current which developed without latency, was sustained during ligand application and was rapidly inactivated at the end of application: the same characteristics as the first component of the ATP-evoked current. The Bz-ATP conductance reversed around -10 mV, indicating also a non-selective cation conductance. These results suggest that, in SGNs, ATP acts via two different receptor subtypes, ionotropic P2Z receptors and metabotropic P2Y receptors, and that these two receptor subtypes can assume different physiological roles. [ABSTRACT FROM AUTHOR]