[Involvement of dopamine in amplification of cortical signals activating NMDA-receptors in the striatum (hypothetic mechanism)].
Possible mechanisms of amplification/attenuation of cortical signals opening or not opening NMDA-channels in striatal spine cells while passing through basal ganglio-thalamocortical network and relegated to either "strong" or "weak" signals, are considered. In absence of dopamine, a relative increase in intensity of the "strong" or "weak" cortical signals should result in the LTP/LTD on both striatonigral and striatopallidal cells, the thalamic cells being affected in the opposite way. Activation of the dopamine receptors on the striatonigral (striatopallidal) cells prompts the LTP/LTD expression. Thereof, the "strong" cortical signals are synergistically amplified whereas the "weak" signals are synergistically attenuated at the thalamic output.
Sil'kis
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IG
Institute of Higher Nervous Activity and Neurophysiology, Russian Acad Sci., Russia, 117485, Moscow, Butlerov St., 5a.
D003342:Corpus Striatum / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists*; D015398:Signal Transduction / Q000502:physiology*; D013788:Thalamus / Q000502:physiology
D016194:Receptors, N-Methyl-D-Aspartate; D004298:Dopamine