Asynchronous presynaptic glutamate release enhances neuronal excitability during the post-spike refractory period

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Post-spike afterhyperpolarizations (AHPs) functionally inhibit neuronal excitability for tens to hundreds of milliseconds following each action potential. This imposes a relative refractory period during which synaptic excitation is less effective at evoking spikes. Here we asked whether some synapses have mechanisms in place that allow them to overcome the AHP and drive spiking in target cells during this period of reduced excitability. We examined glutamate synapses onto oxytocin and vasopressin neurons in the paraventricular nucleus of the hypothalamus. These synapses can display pronounced asynchronous glutamate release following a single presynaptic spike, with the time course of release being similar to that of the post-spike AHP. To test whether asynchronous release is more effective at overcoming the relative refractory period, we evoked a single action potential with either a brief synchronous depolarization or an asynchronous potential and then assessed excitability at multiple time points following the spike. Neurons receiving asynchronous depolarizing synaptic inputs had a shorter relative refractory period than those receiving synchronous depolarizations. Our data demonstrate that synapses releasing glutamate in an asynchronous and delayed manner are ideally adapted to counter the AHP. By effectively overcoming the relative refractory period, the kinetics of excitatory synaptic input can play an important role in controlling post-spike excitability.

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