Accumulation of K+ in the synaptic cleft modulates activity by influencing both vestibular hair cell and calyx afferent in the turtle

摘要: Key points In the synaptic cleft between type I hair cells and calyceal afferents, K+ ions accumulate as a function of activity, dynamically altering driving force permeation through ion channels facing cleft. High-fidelity transmission is possible due to large conductances that minimize cell afferent time constants in presence significant membrane capacitance. Elevated potassium maintains near potential where transduction currents are sufficient depolarize them voltages necessary for calcium influx vesicle fusion. Elevated depolarizes postsynaptic by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, contributes depolarizing potentials single EPSP (quantum) can generate an action potential. With increased stimulation, depolarization increases frequency quanta released, elevates [K+]cleft at which smaller EPSPs would be trigger APs. Abstract Fast neurotransmitters act conjunction with slower modulatory effectors restricted spaces found giant synapses such endings auditory vestibular systems. Here, we used dual patch-clamp recordings from turtle their neurons show accumulating modulated extended range information transfer. High-fidelity was minimized capacitance. Increased concentration maintained promoted fusion. The elevated also depolarized neuron channels. This enabled reliably evoked AMPA-dependent EPSPs. Depolarization could elevate cleft, other enveloped same neuritic process increasing fidelity neurotransmission those well. Collectively, these data demonstrate neuronal activity gives rise accumulation, suggest on HCN modulate neurotransmission, preserving high-speed shifting resting both presynaptic cells.