Long-Term Modification at Inhibitory Synapses in Developing Visual Cortex
Involvement of bidirectional modification at excitatory synapses in experience-dependent cortical maturation has been supported by various experimental data in visual cortex. Experiments using slice preparations demonstrated that cortical inhibitory synapses also undergo long-term potentiation (LTP) and depression (LTD) during the critical period. High-frequency stimulation (HFS) of excitatory and inhibitory inputs to pyramidal neurons induces LTD at inhibitory synapses when it elicits depolarizing responses large enough to activate NMDA receptors. HFS induces inhibitory LTP instead when it fails to activate NMDA receptors. Thus, the direction of modification is determined by postsynaptic NMDA receptors. LTD induction requires Ca2+ entry via NMDA receptors, whereas LTP induction requires IP3 receptor-mediated Ca2+ release, presumably triggered by GABAB receptor activation in the absence of substantial NMDA receptor activation. Intracellular Ca2+ release likely initiates BDNF release from the postsynaptic cell and activates TrkB receptors on inhibitory terminals, presumably leading to presynaptic enhancement of synaptic transmission. LTP maintenance requires presynaptic, but not postsynaptic, firing and associated Ca2+ entry at some intervals. This bidirectional modification at inhibitory synapses may contribute to the refinement and maintenance of visual responsiveness, and regulation of the critical period in visual cortex.
KeywordsDepression Tyrosine Heparin Serotonin Assure
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