4^th International Conference on
Neurology and Health Care

Mihoko Tomida graduated from School of Dentistry at Asahi University and Gifu University Graduate School of Medicine, and acquired Ph.D. After having worked as an oral surgeon for four years, she became a teacher of physiology at Tokyo Womens Medical University. And she started to investigate the relationship between pain and emotion by using rat and human. She found that the pain was involved with nerve cells of an amygdala and the cingulate cortex from animal experiment. After three years, she moved to Matsumoto Dental University.Beta endorphine expression in the periaqueductal gray (PAG) increased by inflammation and dynorphin in the PAG increased by giving electric stimulation at amygdala. She is interested in the expression of opioids in the brain. Now, she looks into the relation between pain or stress and opioid. expression.

Introduction: It is reported that excessive sports increase β-endorphin in the serum, but there are few reports about the expression of the opioid in the brain. Therefore we investigate a change of β-endorphin secreted in the rat brain after exercise. Methods: With male Wistar rats, we investigated the expression of β-endorphin in the periaqueductal gray (DM:dorsomedial, DL:dorsolateral, L:lateral, VL:ventrolateral) immunohistologically. The conditions are control group (only in a rota-rod treadmill), High-speed exercise group (11m/min), low-speed exercise group (6.6m/min). They exercises twice a day 7 days for 30 minutes. After 7 days, the corticosterone density in the rat blood was measured. The brain tissue of 20μm was immunostained by the free-floating method using an antibody of β- endorphin. Immunostaind section were photographed by a digital camera and immnopositive amount in a square of 100 μm was determined by using software. Results: The median of corticosterone density was control group: 294ug/ml, high-speed group: 349ug/ml and low-speed group: 345ug/ml. The significant difference was recognized between control and both exercise group. The median of endorphin expression in the periaqueductal gray is 27.9μm2, 51.0μm2, 23.5μm2. The significant difference was recognized between high-speed group and low-speed group or control group. By the part distinction, the expression of β-endorphin in DM and DL increase in particular when rats ran in high-speed.

Methadone is widely used in preventation of opiate withdrawal and also treatment opiate addiction. In addition to its clinical uses some studies demonstrated that methadone is associated with some alterations in seizure susceptibility. In this study, we tried to clarify the modulatory effect of methadone in clonic seizure threshold (CST) induced by pentylenetetrazole (PTZ) in mice, and we also further determined the probability role of N-Methyl-D- Aspartate (NMDA) receptor or Nitric oxide (NO) signaling in tolerance, dependence and seizure threshold of methadone. Our data showed that methadone (0.1,0.3,1, and 3 mg/kg) in acute administration has pro convulsive effect whereas chronic injection ( 3mg/kg, 3times/day for 5 days) enhanced seizure threshold. The non-effective (i.e., did not significantly alter the PTZ-induced seizure threshold by itself) doses of NMDA receptor antagonists [Ketamine (0.5 mg/kg) and MK-801(0.05 mg/kg)] were able to inhibit the pro-convulsive effect of methadone, while the non-effective doses of a nonspecific NOS inhibitor [L-NAME (10 mg/kg)] and a specific nNOS inhibitor [7-NI(15mg/kg)] could reversed the anti-convulsive effect of methadone in chronic administration. Additionally, the withdrawal syndrome signs, precipitated by naloxone and also anti-nociception effects of methadone were reduced by administration of NMDA receptor antagonists and NOS inhibitors accompanying methadone. These results suggest the involvement of NMDA receptors in pro and NO pathway in anti-convulsive effects of acute and chronic administration of methadone respectively and also both of them in dependence and tolerance.

Background: Alzheimers disease is the leading cause of dementia worldwide, and its prevalence is constantly increasing. Several theories, most significantly the amyloid beta and tau protein hypotheses, offer credible mechanistic explanations for the pathology of Alzheimers disease, and evidence for an infectious cause of the disease has steadily accumulated over 30 years including most recently a correlation between fungal colonisation of the brain at autopsy and occurrence of AD. The aim of this study was to perform a systematic review of preclinical studies of infectionrelated AD to: a) seek robustly characterised causal associations between infection and AD and b) identify best practice in experimental analysis of this complex disease to further analyse fungal infection and AD. Methods: The PubMed and SCOPUS databases were searched for studies published since the year 2000 which report animal or in vitro models of infection-related AD. Results: Initial searches yielded a total of 1100 publications, which after further scrutiny, was reduced to a cohort of n=24 studies conforming to defined inclusion criteria. 24 papers were identified to be the most suitable for discussion in this review. Conclusion: The literature on fungal infections and AD is very limited (n=3) and study design is inferior to that applied to bacterial or viral infections. More preclinical studies need to be done on the topic, based on well-designed studies of other infections, to bridge the gap and provide a better understanding. A good experimental model would be to use repeated low-dose fungal infection in non-transgenic mice long-term, and to use immunohistochemistry to detect any AD changes.