Summation, which includes both spatial summation and temporal summation, is the process that determines whether or not an action potential will be generated by the combined effects of excitatory and inhibitory signals, both from multiple simultaneous inputs (spatial summation), and from repeated inputs (temporal summation). Depending on the sum total of many individual inputs, summation may or may not reach the threshold voltage to trigger an action potential. Neurotransmitters released from the terminals of a presynaptic neuron fall under one of two categories, depending on the ion channels gated or modulated by the neurotransmitter receptor. Excitatory neurotransmitters produce depolarization of the postsynaptic cell, whereas the hyperpolarization produced by an inhibitory neurotransmitter will mitigate the effects of an excitatory neurotransmitter. This depolarization is called an EPSP, or an excitatory postsynaptic potential, and the hyperpolarization is called an IPSP, or an inhibitory postsynaptic potential. Older models of neurons treated them mostly as simple integrators that just add up signals without much going on. Dendrites change that picture a lot. Modern studies point out they are not passive at all. They act like active parts that handle computations on their own. It seems like through voltage-gated channels, they manage this nonlinear summation. That allows for some local processing right there in the dendrites. Signals do not even make it to the axon hillock until after that step. The idea is dendrites do real work before everything else kicks in. Traditional views missed how dynamic that is. The only influences that neurons can have on one another are excitation, inhibition, and—through modulatory transmitters—biasing one another's excitability. From such a small set of basic interactions, a chain of neurons can produce only a limited response. A pathway can be facilitated by excitatory input; removal of such input constitutes disfacillitation. A pathway may also be inhibited; removal of inhibitory input constitutes disinhibition, which, if other sources of excitation are present in the inhibitory input, can augment excitation.
History The nervous system first began to be encompassed within the scope of general physiological studies in the late 1800s, when Charles Sherrington began to test neurons' electrical properties. His main contributions to neurophysiology involved the study of the knee-jerk reflex and the inferences he made between the two reciprocal forces of excitation and inhibition. He postulated that the site where this modulatory response occurs is the intercellular space of a unidirectional pathway of neural circuits. He first introduced the possible role of evolution and neural inhibition with his suggestion that "higher centers of the brain inhibit the excitatory functions of the lower centers". Much of today's knowledge of chemical synaptic transmission was gleaned from experiments analyzing the effects of acetylcholine release at neuromuscular junctions, also called end plates. The pioneers in this area included Bernard Katz and Alan Hodgkin, who used the squid giant axon as an experimental model for the study of the nervous system. The relatively large size of the neurons allowed the use of finely-tipped electrodes to monitor the electrophysiological changes that fluctuate across the membrane. In 1941 Katz's implementation of microelectrodes in the gastrocnemius sciatic nerve of frogs' legs illuminated the field. It soon became generalized that the end-plate potential (EPP) alone is what triggers the muscle action potential, which is manifested through contractions of the frog legs. One of Katz's seminal findings, in studies carried out with Paul Fatt in 1951, was that spontaneous changes in the potential of muscle-cell membrane occur even without the stimulation of the presynaptic motor neuron. These spikes in potential are similar to action potentials except that they are much smaller, typically less than 1 mV; they were thus called miniature end plate potentials (MEPPs). In 1954, the introduction of the first electron microscopic images of postsynaptic terminals revealed that these MEPPs were created by synaptic vesicles carrying neurotransmitters. The sporadic nature of the release of quantal amounts of neurotransmitter led to the "vesicle hypothesis" of Katz and del Castillo, which attributes quantization of transmitter release to its association with synaptic vesicles. This also indicated to Katz that action potential generation can be triggered by the summation of these individual units, each equivalent to an MEPP.
Types
At any given moment, a neuron may receive postsynaptic potentials from thousands of other neurons. Whether threshold is reached, and an action potential generated, depends upon the spatial (i.e. from multiple neurons) and temporal (from a single neuron) summation of all inputs at that moment. It is traditionally thought that the closer a synapse is to the neuron's cell body, the greater its influence on the final summation. This is because postsynaptic potentials travel through dendrites which contain a low concentration of voltage-gated ion channels. Therefore, the postsynaptic potential attenuates by the time it reaches the neuron cell body. The neuron cell body acts as a computer by integrating (adding or summing up) the incoming potentials. The net potential is then transmitted to the axon hillock, where the action potential is initiated. Another factor that should be considered is the summation of excitatory and inhibitory synaptic inputs. The spatial summation of an inhibitory input will nullify an excitatory input. This widely observed effect is called inhibitory 'shunting' of EPSPs.
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