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Noradrenaline-stimulated inositol phospholipid breakdown in rat dorsal lateral geniculate nucleus neurones
Authors:John A. Kemp  C. Peter Downes  
Affiliation:1. Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, 00290, Finland;2. Molecular and Integrative Bioscience Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, 00790, Finland;3. Institute of Biotechnology, HiLIFE, University of Helsinki, Helsinki, 00790, Finland;4. Department of Neurosciences, Experimental Neurology and Leuven Brain Institute, KU Leuven – University of Leuven, 3000, Leuven, Belgium;5. VIB Center for Brain & Disease Research, Laboratory of Neurobiology, 3000, Leuven, Belgium;6. KU Leuven, Laboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine & Leuven Kanker Instituut, Leuven, 3000, Belgium;7. Clinical Neurosciences, Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, 00290, Finland;1. Department of Biomedical Sciences, University of Padova, Italy;2. Neuroscience Institute, National Research Council of Italy (CNR), Italy;3. Fondazione Istituto di Ricerca Pediatrica Città della Speranza (IRP), Italy;1. Department of Biochemistry and Molecular Biology, Structural Biology Imaging Center, McGovern Medical School at The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX 77030, USA;2. Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
Abstract:Noradrenaline-stimulated inositol phospholipid breakdown in matched vibratome sections through the rat dorsal lateral geniculate nucleus (dLGN). The response was measured as a large accumulation of [3H]inositol labelled inositol monophosphate and was mediated via activation of alpha 1-adrenergic receptors. Accumulation of [3H]inositol phosphates was reduced in kainic acid-lesioned animals, indicating that this response occurred within dLGN neurones and not afferent terminals. The results implicate inositol phospholipid breakdown as part of the mechanism of noradrenergic neurotransmission within the dLGN.
Keywords:noradrenaline   α  1-receptor   inositol phosphate   lateral geniculate nucleus
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