Introduction: The thyroid hormones have profound effects on the development of neuromuscular system. These hormones exert their influence on both muscle fibers and related motoneurons during development. The masseter is one of the most important muscles for mastication in mammals. We attempted to evaluate the effect of thyroid hormone deficiency on the morphological characteristics of masseteric motoneurons in the period of alteration from sucking to biting and chewing in the rat. Materials and Methods: To induce hypothyroidism, timed pregnant dams received 50 ppm antithyroid drug propylthiouracil (PTU) in their drinking water and PTU was administered to the pups during suckling period. Horseradish peroxidase (HRP) was injected into the masseter (0.5-5 mlit, 40%) of normal and prenatal hypothyroid pups on postnatal days of 1, 7, 15, and 23 (n=24). After 24-48 hours, the 50 mm thick brainstem sections containing trigeminal motor nucleus were processed for TMB histochemical procedure and morphological characteristics of HRP labeled motoneurons and their HRP labeling intensity was evaluated. Student's t-test and two-way analysis of variance (ANOVA) were used for statistical analysis. Results: No significant morphological differences were observed at the end of first week of life. On day 15, hypothyroid labeled masseteric motoneurons consisted of 70% small and 30% medium neurons versus 40% and 60% in normal pups respectively (p<0.05). At the time of weaning, the number of large motoneurons dropped to 30% of normal value (p<0.001) with few, short, and disoriented dendrites. Conclusion: The alteration in particular patterns of masseteric motoneuron morphology and a severe delay in size transition could affect the development and plasticity of oral motor behavior under congenital hypothyroidism.

Permanent facial paralysis is a catastrophic event for involved patients. In long lasting paralysis with severe facial muscles atrophy, masseter muscle transfer is a very good choice. But its greatest problem is postoperative elongation of flap and gradual diminishing of early results and loss of symmetry.This article advocate a new modification for resolving this problem with concomitant elevation of mandibular periosteum with masseter muscle, as a unit for lip and midface elevation.

Introduction: Recently the neuroprotective role of uric acid (UA), as a natural biochemical substance, in neurodegenerative diseases has been proposed. Due to the critical role of apoptosis in many diseases of the nervous system, the present study was designed to investigate the anti-apoptotic effect of UA on motor neurons of the ventral spinal horn in neonate rats.Materials and Methods: Two-day-old rat neonates (n=10) were subdivided into experimental and control groups. In both groups, right sciatic nerve was transected. Experimental neonates were immediately treated with 10mg/kg UA intraperitoneally, while the control’s wound was closed without treatment. Five days after axotomy, transverse sections of spinal cord at L5 level were prepared for morphometric cell count and TUNNEL assay.Results: The motor neuron loss in axotomized side compared to intact side was 30.48%, which illustrates the effectiveness of axotomy in inducing motoneuron cell death. The TUNNEL assay confirmed the apoptotic characteristics of cell death. Comparing the mean motoneurons loss in the axotomized side of the control and UA-treated neonates, revealed a significant difference between the two groups (p<0.05). Also in both control and experimental groups, the difference between the apoptotic Index of the axotomized and intact sides was statistically significant (p<0.05).Conclusion: Neuroprotective effect of UA is possibly through inhibiting the apoptotic cell death, which occurred with the axotomized motoneurons in ventral spinal horn.

Background and Objective: Because of the critical role of cell death in the pathology of neurodegenerative diseases, its prevention is regarded as one of the most salient ends in neuroprotective strategies. Concerning the bulk of reports about the putative neuroprotective effects of erythropoietin (Epo), in the present study following axotomy, the effects of different doses of Epo on spinal moto neurons in neonates was investigated.Materials and Methods: Following transection of the right sciatic nerve of 20 two-day-old neonate rats and induction of apoptotic cell death in related moto neurons, the animals were subdivided into three experimental and one control groups. The experimental groups received different doses of 2500, 5000, 10000U/kg recombinant human Erythropoietin (rhEpo), and the control group was treated with equal volume of normal saline, intraperitoneally for 5 successive days. 24 hours following the last injection, histologic sections from the neonate spinal cords were prepared for counting of spinal moto neurons. In all samples, the intact side was regarded as the internal control.Results: The difference between moto neuron means of intact and axotomy sides was significant in all groups, which advocates the efficacy of axotomy in cell death induction. Comparison of axotomized side of different groups indicated significant differences between both 5000 and 10000U/kg groups with control, and also between 10000 and 2500 groups, but no significant differences could be seen between other groups. Thus, 5000U/kg of rhEpo can be considered as the neuroprotective dose which can prevent cell death of axotomized moto neurons.Conclusion: rhEpo has dose-dependent neuroprotective effects on axotomized spinal moto neurons.

Objective(s): Resveratrol has been recognized as a potential therapeutic drug in spinal cord injury (SCI). Sirtuin 1 (SIRT1) is vital in the regulation of apoptosis and cell stress response. In this research, our purpose was to explore the mechanisms of resveratrol on neuroprotection and to explore the role of SIRT1. Materials and Methods: We used lipopolysaccharide (LPS) in the VSC4. 1 spinal cord neuron cell line to mimic the micro-environment of the injured spinal cord. The apoptosis of VSC4. 1 motoneurons was assessed by TUNEL staining, Western blot, and RT-PCR. Immunofluorescence staining was used to observe the expression site of SIRT1, LC3-B, and Beclin-1, and their protein levels were measured by Western blot and RT-PCR. Results: Our results showed that resveratrol inhibits LPS-induced apoptosis in VSC4. 1 motoneurons. Levels of LC3-B, beclin-1, and SIRT1 indicated a significant increase after resveratrol treatment. But, if autophagy was inhibited, apoptosis in VSC4. 1 motoneurons significantly increased. When the cells were treated with EX527, a SIRT1 inhibitor, the protein contents of LC3-B and Beclin-1 were suppressed. Conclusion: Resveratrol inhibits apoptosis through promoting autophagy in VSC4. 1 motoneurons. SIRT1 was involved in autophagy activated by resveratrol in VSC4. 1 motoneurons.