J
John M. Bissonnette
Researcher at Oregon Health & Science University
Publications - 95
Citations - 2809
John M. Bissonnette is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Rett syndrome & MECP2. The author has an hindex of 27, co-authored 94 publications receiving 2615 citations. Previous affiliations of John M. Bissonnette include University of Portland & Max Planck Society.
Papers
More filters
Journal ArticleDOI
A role for glia in the progression of Rett's syndrome.
Daniel T. Lioy,Saurabh K. Garg,Saurabh K. Garg,Caitlin E. Monaghan,Caitlin E. Monaghan,Jacob Raber,Jacob Raber,Kevin D. Foust,Brian K. Kaspar,Petra G. Hirrlinger,Frank Kirchhoff,John M. Bissonnette,Nurit Ballas,Gail Mandel,Gail Mandel +14 more
TL;DR: It is shown that glia, like neurons, are integral components of the neuropathology of RTT, and supports the targeting of glia as a strategy for improving the associated symptoms.
Journal ArticleDOI
Systemic delivery of MeCP2 rescues behavioral and cellular deficits in female mouse models of Rett syndrome.
Saurabh K. Garg,Daniel T. Lioy,Daniel T. Lioy,Hélène Cheval,James C. McGann,James C. McGann,John M. Bissonnette,Matthew J. Murtha,Kevin D. Foust,Brian K. Kaspar,Adrian Bird,Gail Mandel,Gail Mandel +12 more
TL;DR: It is shown that self-complementary AAV9, bearing MeCP2 cDNA under control of a fragment of its own promoter (scAAV9/MeCP2), is capable of significantly stabilizing or reversing symptoms when administered systemically into female RTT mice, the first potential gene therapy for females afflicted with RTT.
Journal ArticleDOI
Respiration and parturition affected by conditional overexpression of the Ca2+-activated K+ channel subunit, SK3.
Chris T. Bond,Rolf Sprengel,John M. Bissonnette,Walter A. Kaufmann,David Pribnow,Torben R. Neelands,Thorsten Storck,Manfred Baetscher,Jasna Jerecic,James Maylie,Hans-Günther Knaus,Peter H. Seeburg,John P. Adelman +12 more
TL;DR: The results implicate SK3 channels as potential therapeutic targets for disorders such as sleep apnea or sudden infant death syndrome and for regulating uterine contractions during labor.
Journal ArticleDOI
Correction of respiratory disorders in a mouse model of Rett syndrome
TL;DR: It is shown that apnea in RTT mice is characterized by excessive excitatory activity in expiratory cranial and spinal nerves, and GABA and serotonin 1a receptor activity are candidates for treatment of the respiratory disorders in Rett syndrome.
Journal ArticleDOI
Mechanisms regulating hypoxic respiratory depression during fetal and postnatal life
TL;DR: Tonic activity in early expiratory (postinspiratory) neurons may contribute to hypoxia-induced apneic episodes in the fetus and newborn and desensitization of alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid receptors has been demonstrated in respiratory-related neurons both in vivo and in vitro.