![]() ![]() This effect displayed the same pharmacological profile as the electrically induced LTD recently published ( 4) and independently confirmed ( 7), suggesting that the conformational changes measured in the NMDARcd are associated with LTD induction. In the accompanying study ( 16), Förster resonance energy transfer (FRET)-fluorescence lifetime imaging microscopy (FLIM) imaging was used to show that agonist binding to the NMDAR produces conformational movement of the NMDARcd. Results Transient NMDAR Agonist Binding Without Ion Flux Depresses Spontaneous Excitatory Postsynaptic Currents. ![]() An important test of an ion-flow-independent model would be to measure directly signaling actions by NMDARs in the absence of ion flow. Studies supporting an ion-flow-independent role for NMDARs in LTD ( 4– 7) and other processes ( 7– 13) stand in contrast to studies proposing that flow of Ca 2+ through NMDAR is required for LTD ( 14) (see ref. However, this model is not consistent with recent studies suggesting that no change in i is required for LTD, and instead invokes metabotropic signaling by the NMDAR ( 4). #Ucsd cplot series#A model was developed ( 2, 3) to explain how activation of NMDAR could produce these opposing phenomena: strong stimuli during LTP induction drive a large flux of Ca 2+ through NMDARs, leading to a large increase in intracellular calcium ion concentration ( i) that activates one series of biochemical steps leading to synaptic potentiation a weaker stimulus during LTD induction drives a more reduced flux of Ca 2+ through NMDARs, producing a modest increase in i that activates a different series of biochemical steps, leading to synaptic depression. Surprisingly, activation of NMDARs can produce plasticity in opposite directions, with LTP enhancing transmission and LTD reducing transmission. Agonist binding to the NMDAR is required for two major forms of synaptic plasticity: long-term potentiation (LTP) and long-term depression (LTD) ( 1). ![]()
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