Fast cortical oscillation after thalamic degeneration: Pivotal role of NMDA receptor
| Autor: | Hisae Gemba, Shin-ichi Kyuhou |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
Purkinje cell Biophysics Gene Expression Auditory cortex Receptors N-Methyl-D-Aspartate Biochemistry Thalamic Diseases Synapse Mice Purkinje Cells Thalamus medicine Animals RNA Messenger Molecular Biology Visual Cortex Auditory Cortex Medial geniculate nucleus Fourier Analysis Chemistry Neurodegeneration Cell Biology Anatomy medicine.disease Mice Inbred C57BL Electrophysiology Visual cortex medicine.anatomical_structure Evoked Potentials Auditory NMDA receptor Female Dizocilpine Maleate Excitatory Amino Acid Antagonists Neuroscience |
| Zdroj: | Biochemical and Biophysical Research Communications. 356:187-192 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2007.02.116 |
| Popis: | We examined electrophysiological and molecular changes of the thalamocortical system after thalamic degeneration in Purkinje cell degeneration (pcd) mice. In pcd mice, neurons in specific thalamic nuclei including the ventral medial geniculate nucleus began to degenerate around postnatal day 50, whereas the visual thalamic nucleus and nonspecific thalamic nuclei remained almost intact. In association with the morphological changes, auditory evoked potentials in the primary auditory cortex (AC) began to decrease gradually. Fast Fourier transform analysis of spontaneous cortical field potentials revealed that fast oscillation (FO) around 25 Hz occurred in the AC but not in the visual cortex. Quantitative mRNA analysis demonstrated that expression of the N-methyl-D-aspartate (NMDA) receptor was up-regulated in the AC but not in the visual cortex. Systemic administration of an NMDA antagonist abolished the FO in the AC. These results indicate that increased NMDA activity may cause the FO in the AC of pcd mice. |
| Databáze: | OpenAIRE |
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