When the neuron is at rest, there is a baseline level of ion flow through leak channels. However, the ability of neurons to function properly and communicate with other neurons and cells relies on ion flow through channels other than the non-gated leak channels. We will cover how these channels open in a later lesson.
This chapter will examine ion flow through these channels after a stimulus and how the membrane potential changes in response. Postsynaptic potentials are changes in membrane potential that move the cell away from its resting state. For our purposes, postsynaptic potentials are measured in the dendrites and cell bodies. Ion channels that are opened by a stimulus allow brief ion flow across the membrane. A stimulus can range from neurotransmitters released by a presynaptic neuron, to changes in the extracellular environment, like exposure to...
to heat or cold, interactions with sensory stimuli like light or odors, or other chemical or mechanical events. The changes in membrane potential in response to the stimulus will depend on which ion channels are opened by the stimulus. An excitatory postsynaptic potential, or EPSP, occurs when sodium channels open in response to a stimulus. The electrochemical gradient drives sodium to rush into the cell. When sodium brings its positive charge into the cell, the cell's membrane potential becomes more positive, or depolarizes.
This change is called a depolarization because the cell's membrane potential is moving toward 0 millivolts. and the membrane is becoming less polarized. At 0 millivolts there is no potential or polarization across the membrane, so moving toward zero would be a decrease in potential.
This depolarization increases the likelihood a neuron will be able to fire an action potential, which makes this ion flow excitatory. Therefore, an EPSP is an excitatory change in the membrane potential of a postsynaptic neuron. A postsynaptic potential is typically brief, with ion channels closing quickly after the stimulus occurs. If there is not another stimulus, the cell will return to the resting membrane potential. An inhibitory postsynaptic potential, or IPSP on the other hand, is caused by the opening of chloride channels.
The equilibrium potential of chloride is negative 65 millivolts. So if the neuron is at rest, and negative 60 millivolts, when the chloride channels open, the electrochemical gradients drive chloride to flow into the cell. Chloride brings its negative charge into the cell, causing the cell's membrane to be damaged. membrane potential to become more negative, or hyperpolarize.
This change is called a hyperpolarization because the cell's membrane potential is moving away from 0 mV, and the membrane is becoming more polarized. An IPSP decreases the likelihood a neuron will be able to fire an action potential, which makes this flow inhibitory. Therefore, an IPSP is an inhibitory change in the membrane potential.
of a postsynaptic neuron. Like an EPSP, an IPSP is also typically brief and the membrane potential will return to rest if no additional stimulation occurs. In the previous example, the resting membrane potential of that cell was negative 60 millivolts, so chloride moved into the cell.
If the resting membrane potential was instead equal to chloride's equilibrium potential, of negative 65 millivolts, then chloride would be at equilibrium and move into and out of the cell, but there would be no net movement of the ion. Even though this would lead to no change in membrane potential, the opening of chloride channels continues to be inhibitory. Increased chloride conductance would make it more difficult for the cell to depolarize and to fire an action potential. If the resting membrane potential of the cell was more negative than chloride's equilibrium potential, for example at 70 millivolts, then chloride would leave the cell in order to move the membrane potential toward negative 65 millivolts. This would result in a depolarization of the membrane potential.
However, the overall effect is still inhibitory because once the cell reaches negative 65 millivolts, the driving forces acting on chloride would try to keep the cell at that membrane potential. making it more difficult for the cell to depolarize further and fire an action potential. A good rule of thumb is to remember that opening sodium channels is excitatory, whereas opening chloride channels is inhibitory.
If an excitatory stimulus is followed by additional excitatory stimuli, the sodium channels will either remain open or additional sodium channels will open. The increased sodium conductance will cause the EPSPs to summate, depolarizing the cell further than one EPSP alone. Each neuron has a threshold membrane potential, at which the cell will fire an action potential. The summation of EPSPs causes the neuron to reach that threshold.
EPSPs can summate via temporal or spatial summation. Temporal summation occurs when a presynaptic neuron, which is input 1 in the animation, stimulates the postsynaptic neuron multiple times in a row. Spatial summation occurs when more than one presynaptic neuron will be inputs 1 through 4 in the animation each stimulate the postsynaptic neuron at the same time. In both cases, the EPSPs of each stimulation will add together to cause a stronger depolarization of the membrane potential of the postsynaptic neuron than one excitatory stimulus alone.
In addition to the summation of excitatory inputs, EPSPs can also summate with inhibitory inputs. If an inhibitory input stimulates the postsynaptic neuron at the same time as an excitatory input, the result is a decrease in the amount of depolarization or the complete prevention of depolarization depending on the strength of the inhibitory input. In the case of combined inhibitory and excitatory stimuli, both chloride and sodium channels will open.
As sodium enters the cell trying to move the membrane potential to positive 60 millivolts, the equilibrium potential of sodium, chloride will also enter, trying to keep the cell near negative 65 millivolts, the equilibrium potential of chloride.