natural indian viagra Search our medical news database advanced search register login hot topics breast cancer aging neuroscience dentistry kidneys more home newsletter for purchase medical topics products about us contact verticalnews congenital myasthenic syndromes new findings from max-planck-institute for medical research in the area of congenital myasthenic syndromes published published in genomics and genetics weekly , march 16th, 2012 2012 mar 16 -- a new study, "a new mouse model for the slow-channel congenital myasthenic syndrome induced by the achr el221f mutation," is now available. "we have generated a new mouse model for congenital myasthenic syndromes by inserting the missense mutation l221f into the e subunit of the acetylcholine receptor by homologous recombination. This mutation has been identified in man to cause a mild form of slow-channel congenital myasthenic syndrome with variable penetrance," scientists writing in the journal neurobiology of disease report. much viagra 100mg viagra funziona yahoo cost of viagra effectiveness of viagra for daily use viagra side effects cough "in our mouse model we observe as in human patients prolonged endplate currents. The summation of endplate potentials may account for a depolarization block at increasing stimulus frequencies, moderate reduced muscle strength and tetanic fade. Calcium and intracellular vesicle accumulation as well as junctional fold loss and organelle degeneration underlying a typical endplate myopathy, were identified. Moreover, a remodeling of neuromuscular junctions occurs in a muscle-dependent pattern expressing variable phenotypic effects," wrote f. Chevessier and colleagues, max-planck-institute for medical research. The researchers concluded: "altogether, this mouse model provides new insight into the pathophysiology of congenital myasthenia and serves as a new tool for deciphering signaling pathways induced by excitotoxicity at peripheral synapses. " chevessier and colleagues published their study in neurobiology of disease (a new mouse model for the slow-channel congenital myasthenic syndrome induced by the achr el221f mutation. Neurobiology of disease, 2012;45(3):851-61). Additional information can be obtained by contacting f. Chevessier, dept. Of molecular neurobiology, max planck institute for medical research, jahnstrasse 29, 69120 heidelberg, germany. Keywords: city:heidelberg, country:germany, region:europe, genetics. This article was prepared by genomics & genetics weekly editors from staff and other reports. Copyright 2012, genomics & genetics weekly via newsrx. Com. Welcome to newsrx! Learn more about a six-week, no-risk free trial of genomics and genetics.