The probability of a cell firing an action potential can be affected by the activation of an inhibitory synapse. In some cases, the synapse may not cause any change in potential if the membrane potential equals the Nernst potential for Cl- or K+. However, it may still result in a small depolarization. The reversal potential for the IPSP remains negative with respect to the threshold for eliciting a response, regardless of these outcomes. The strength of a synapse and the size of the postsynaptic potential (PSP) it generates can be influenced by various factors such as the size and number of synaptic contacts between cells, activity level, past history, and the probability of vesicle fusion. The strength of excitatory synapses is often measured by the safety factor, which is the ratio of EPSP amplitude to the amplitude needed to reach the threshold for triggering an action potential. Most synapses have low safety factors (<1), requiring multiple active synapses to sum their EPSPs and trigger an action potential in the postsynaptic neuron. This summation process is essential for synaptic integration. However, there are synapses with high safety factors (>1), such as those found at the neuromuscular junction. The neuromuscular junction has a high safety factor because each muscle cell is contacted by only one motor neuron, and when that motor neuron is firing, it signals the decision to contract the muscle. Certain diseases of the neuromuscular junction can reduce the size of end plate potentials (EPPs) to a point where the safety factor falls below 1, leading to weakness as the EPPs fail to trigger action potentials in the muscle fibers. The location of a synapse also plays a role in its overall effect. Action potentials are typically generated at the initial segment of a cell due to the high density of voltage-gated Na+ channels and the lower threshold for spike initiation. Therefore, the summed amplitudes of synaptic potentials at the initial segment are critical in determining whether a spike occurs. EPSPs generated by synapses close to the initial segment, such as those on the soma or proximal dendrites, produce a greater depolarization at the initial segment compared to EPSPs generated by synapses on distal dendrites.
However, in some cells, activation of an inhibitory affect the probability of the cell firing an action potential: synapse may produce no change in potential (if the mem-EPSPs increase the probability, whereas IPSPs decrease the brane potential equals the Nernst potential for Cl− or K+) or probability. may actually result in a small depolarization. Nevertheless, Safety factor. Synapses between cells vary in strength and in both these cases, the reversal potential for the IPSP thus in the size of the PSP generated in the postsynaptic cell. is still negative with regard to the threshold for eliciting Many factors determine synaptic strength, including the size and number of synaptic contacts between two cells, its activity level and past history, and the probability of vesicle fusion for the synapse. For excitatory synapses, the strength of the synapse may be quantified by what is known as its safety factor (the ratio of EPSP amplitude to the amplitude needed to reach the threshold to trigger an action potential). Most synapses have low safety factors (<1), and thus it takes the summed EPSPs of multiple active synapses to trigger an action potential in the postsynaptic neuron. This summation process is at the core of synaptic integration, which is taken up in the next section. Synapses with high (>1) safety factors exist, however, and the neuromuscular junction is one prominent example. When a motor neuron action potential triggers release of neurotransmitter at the neuromuscular junction, an end plate potential (EPP; the equivalent of an EPSP in a neuron) is generated in the muscle fiber. The EPP is so large that under normal circumstances it depolarizes the sarcolemma well above the action potential threshold and thus always triggers a spike, leading to contraction of the muscle cell. A high safety factor makes sense for the neuromuscular junction because each muscle cell is contacted by only a single motor neuron, and if that motor neuron is firing, the nervous system has basically made the decision to contract that muscle. In certain diseases of the neuromuscular junction, such as myasthenia gravis and Lambert-Eaton syndrome, the EPPs are reduced such that the safety factor can fall below 1, and thus the EPPs sometimes fail to trigger action potentials in the muscle fibers, leading to weakness.
The overall effect of a particular synapse is dependent on its location. To understand this concept fully, we must first recall that action potentials are typically generated at the initial segment of the cell because it has the highest density of voltage-gated Na+ channels and therefore the lowest threshold for initiation of a spike. Thus, it is the summed amplitudes of the synaptic potentials at this point, the initial segment, that is critical for the decision to spike. EPSPs generated by synapses close to the initial segment (i.e., synapses onto the soma or proximal dendrites) will result in a larger depolarization at the initial segment than will EPSPs generated by synapses on distal dendrites (
Fig.