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Release of dopamine and serotonin from Limax ganglia in vitro
Institution:1. Northwestern University, Feinberg School of Medicine, Chicago, IL, USA;2. Parkinson''s Disease and Movement Disorders Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA;3. HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain;4. Facultad HM de Ciencias de la Salud de la Universidad Camilo José Cela, Madrid, Spain;5. Instituto de Investigación Sanitaria HM Hospitales, Madrid, Spain;6. Aligning Science Across Parkinson’s (ASAP) Collaborative Research Network, Chevy Chase, MD 20815, USA;7. Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, Madrid, Spain;1. Banner Sun Health Research Institute, Sun City, AZ, USA;2. Department of Neurology, Mayo Clinic College of Medicine, Mayo Clinic Arizona, Scottsdale, AZ, USA;3. Department of Neurology, Barrow Neurological Institute, Phoenix, AZ, USA;4. Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ, USA;5. Brigham and Women''s Hospital and Harvard Medical School, Boston, MA, USA
Abstract:1. We wish to establish the kinetics of serotonin and dopamine release from Limax cerebral and buccal ganglia and find selective treatments to modify their release kinetics.2. The release of dopamine and serotonin from isolated ganglia was stimulated by high potassium exposure with and without prior treatment of ganglia with 6-hydroxydopamine (6-OHDA).3. Single ganglia release significant quantities of monoamines during a single 5 min high K+ exposure. Multiple high K+ exposures deplete a readily releasable transmitter store with little effect on storage pools.4. 6-OHDA exposure depletes readily releasable DA with little effect on total ganglion DA content or on serotonin.5. Feeding motor program responsiveness is suppressed reversibly by whole ganglion high K+ treatment.
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