Overview plays a significant role in transmitting signals at chemical synapses. Voltage-gated channels are located within the presynaptic terminal. When an action potential invades the presynaptic membrane, these channels open and enters. A higher concentration of enables synaptic vesicles to fuse to the presynaptic membrane and release their contents (neurotransmitters) into the synaptic cleft to ultimately contact receptors in the postsynaptic membrane. The amount of neurotransmitter released is correlated with the amount of influx. Therefore, short-term<unk>  (STF) results from a build up of within the presynaptic terminal when action potentials propagate close together in time.<unk>  of excitatory post-synaptic current (EPSC) can be quantified as a ratio of subsequent EPSC strengths. Each EPSC is triggered by pre-synaptic calcium concentrations and can be approximated by: EPSC = k(presynaptic)4 = k(rest + influx + residual)4 Where k is a constant.<unk>  = EPSC2 / EPSC1 = (1 + residual / influx)4 - 1 Experimental evidence Early experiments by Del Castillo & Katz in 1954 and Dudel & Kuffler in 1968 showed that<unk>  was possible at the neuromuscular junction even if transmitter release does not occur, indicating that<unk>  is an exclusively presynaptic phenomenon. Katz and Miledi proposed the residual hypothesis. They attributed the increase in neurotransmitter release to residual or accumulated ("active calcium") within the axon membrane that remains attached to the membrane's inner surface. Katz and Miledi manipulated the concentration within the presynaptic membrane to determine whether or not residual remaining within the terminal after the first impulse caused an increase in neurotransmitter release following the second stimulus. During the first nerve impulse, concentration was either significantly below or nearing that of the second impulse. When concentration was approaching that of the second impulse,<unk>  was increased. In this first experiment, stimuli were presented in intervals of 100 ms between the first and second stimuli. An absolute refractory period was reached when intervals were about 10 ms apart. To examine<unk>  during shorter intervals, Katz and Miledi directly applied brief depolarizing stimuli to nerve endings. When increasing the depolarizing stimulus from 1-2 ms, neurotransmitter release greatly increased due to accumulation of active . Therefore, the degree of<unk>  depends on the amount of active , which is determined by the reduction in conductance over time as well as the amount of removed from axon terminals after the first stimulus.<unk>  is greatest when the impulses are closest together because conductance would not return to baseline prior to the second stimulus. Therefore, both conductance and accumulated would be greater for the second impulse when presented shortly after the first. In the Calyx of Held synapse, short term<unk>  (STF) has been shown to result from the binding of residual to neuronal sensor 1 (NCS1). Conversely, STF has been shown to decrease when chelators are added to the synapse (causing chelation) which reduce residual . Therefore, "active " plays a significant role in<unk> . In the synapse between Purkinje cells, short-term<unk>  has been shown to be entirely mediated by the<unk>  of currents through the voltage-dependent calcium channels.
Neural facilitation
Neural adaptation
Paraspinal inhibition
Co-stimulation
Presynaptic inhibition
Counterstimulation
Neurostimulation
Somatosensory amplification