An activity-dependent retrograde signal induces the expression of the high-affinity choline transporter in cholinergic neurons.

摘要: A well-accepted view of developing circuits is that synapses must be active to mature and persist, whereas inactive remain immature are eventually eliminated. We question this long-standing by investigating nonfunctional cholinergic nicotinic in the superior cervical ganglia (SCG) mice with a disruption alpha3 receptor (nAChR) subunit gene, gene essential for fast synaptic transmission sympathetic ganglia. Using imaging electrophysiology, we show persist at least 2-3 months without postsynaptic activity; however, presynaptic terminals lack high-affinity choline transporters (CHTs), as result, they quickly depleted transmitter. Moreover, demonstrate rescue experiments CHT induced signals downstream activity, converting capable sustaining transmitter release response high-frequency or continuous firing. Importantly, neurons continually maintain terminals.