Synaptic potentials, according to our definition, are actually graded potentials. On the presynaptic cell this is caused by an influx of calcium, while in the postsynaptic cell the potential may be caused by one or a few different ions flowing across the membrane. In the presynaptic cell the action potential propagates along the axon until it reaches the very ends of the telodendria. Here many of the vgsc?s are replaced by voltage gated calcium channels. These channels are stimulated in much the same way as the vgsc?s. As calcium floods into the cell, it stimulates the release of neurotransmitter via exocytosis. The mechanism behind this integral action is currently the focus of more than one study. As such, it will not be dealt with in this section.

Synaptic potentials in the post synaptic membrane may be classified as either EPSP (excitatory post synaptic potential), or IPSP (inhibitory post synaptic potential). The determining factor in this classification scheme is the ion that the postsynaptic membrane becomes more permeable to. If the neurotransmitter binds to a receptor that lets in an ion that causes a depolarization (i.e. sodium) then that event is labeled as an EPSP, as it pushes the neuron toward threshold. On the other hand if the ion that experiences an increase in conductance is one that causes a hyperpolarization of the membrane (i.e. chlorine) then it is considered an IPSP. This is because it makes it harder for the neuron to achieve threshold, it has an inhibitory effect. These polarization events occur at sites on the neuron that contain the appropriate neurotransmitter receptor, either on the cell body or the dendritic membrane. Individually EPSPs and IPSPs are small and alone have no noticeable effect on membrane potential. However when the individual postsynaptic potentials are summated (added together) there is a marked effect on the membrane potential. Either an action potential has been stimulated or the cell was hyperpolarized making an action potential that much harder to generate. The summation point, is the axon hillock, also known as the integration center of the neuron. It is here that the results of all the IPSP and EPSP potentials are added together to determine if an action potential is generated (whether or not the total postsynaptic potential was a depolarization of threshold strength). It is thought that the axon hillock may have the lowest value for threshold potential in the neuron. This is because there are a large number of voltage gated sodium and potassium channels concentrated in this area.

During both EPSPs and IPSPs membrane resistance and conductance changes. Generally there is a conduction increase and associated resistance decrease, caused by the opening of ion channels due to stimulation by the neurotransmitter. Sometimes in IPSPs resistance actually increases, making it harder for the membrane to polarize. The fact that membrane resistance changes however can be experimentally verified. The experiment is a simple one based on the fact that neurons follow ohms law. Ohms law states that voltage is equal to the resistance times the current. V=I(R). In the experiment two micropippettes are inserted into the postsynaptic membrane during an EPSP. One is used to measure voltage, while the other periodically sends out pulses of electrical current. During the EPSP current is pulsed into the membrane and the resulting voltage is recorded. Before the EPSP similar voltage tests were run to show that the voltage remained constant. During the EPSP, the resulting voltage is shown to have decreased. Since the current was unaltered, a reduced voltage could mean only one thing, a reduction in membrane resistance.

The next question one should be asking, is which ions exactly are experiencing this increase in conductance. One way of testing this is to alter the membrane potential to the reversal potential. At the reversal potential there is no net current flow across the membrane upon stimulation. Consequently there is no change in the potential either. If the postsynaptic potential is caused by just one ion, the reversal potential will be that ions equilibrium potential. If more than one ion is let into the cell upon stimulation the reversal potential will be an intermediate of the equilibrium potentials for the ions in question. For most EPSPs the reversal potential is approximately -10mV. Since that is not the equilibrium potential for any one ion, the data suggest that more than one ion is responsible for this reversal potential. In fact -10 mV is about midway between the equilibrium potentials for sodium and potassium (potassium has an equilibrium potential around -90 mV and sodium?s is around +50mV). Thus during an EPSP sodium and potassium conductance increases, causing sodium to flow in and potassium out of the cell, eliciting a depolarization event. One should understand that ion channels are more permeable to some ions than to others. Theoretically this means that the reversal potential could be anywhere from -70mV to +50mV for an EPSP. Most EPSPs have a reversal potential between 0 and -20 mV. This shows that the ion channels are about equally permeable to both ions and gives a good explanation for the potential difference in various EPSPs of neurons.

IPSPs are known to hyperpolarize the neuronal membrane. Thus the neuron will experience an efflux of positive charge (K⁺) and/or an influx of negative charge(Cl^-). This theory is readily acceptable since both ions will flow the appropriate directions along their concentration gradient. IPSPs that have a reversal potential near -70mV are known to be dependent only on chlorine conductance increase. Those with more negative reversal potentials allow both chlorine and potassium to experience an increase in conductance.