The mechanisms underlying neural facilitation are exclusively pre-synaptic; broadly speaking, PPF arises due to increased presynaptic Ca2+ concentration leading to a greater release of neurotransmitter-containing synaptic vesicles.
[1] Neural facilitation may be involved in several neuronal tasks, including simple learning, information processing,[2] and sound-source localization.
Therefore, short-term facilitation (STF) results from a build up of Ca2+ within the presynaptic terminal when action potentials propagate close together in time.
[7] Katz and Miledi manipulated the Ca2+ concentration within the presynaptic membrane to determine whether or not residual Ca2+ remaining within the terminal after the first impulse caused an increase in neurotransmitter release following the second stimulus.
To examine facilitation during shorter intervals, Katz and Miledi directly applied brief depolarizing stimuli to nerve endings.
Facilitation is greatest when the impulses are closest together because Ca2+ conductance would not return to baseline prior to the second stimulus.
In the Calyx of Held synapse, short term facilitation (STF) has been shown to result from the binding of residual Ca2+ to neuronal Ca2+ sensor 1 (NCS1).
[4] The type of synaptic enhancement seen in a given cell is also related to variant dynamics of Ca2+ removal, which is in turn dependent upon the type of stimuli; a single action potential leads to facilitation, while a short tetanus generally causes augmentation and a longer tetanus leads to potentiation.
STD occurs due to a decrease in the readily releasable pool of vesicles (RRP) as a result of frequent stimulation.
Likewise, synapses with high initial release probabilities serve as low-pass filters, responding to lower-frequency signals.
Synapses with an intermediate probability of release act as band-pass filters that selectively respond to a specific range of frequencies.