Penetration of an α-motor neuron is a good example of a technique used to study postsynaptic electrical activity. It is achieved by advancing a microelectrode through the ventral portion of the spinal cord. Puncture of a cell membrane is signaled by the appearance of a steady 70 mV potential difference between the microelectrode and an electrode outside the cell. The cell can be identified as a spinal motor neuron by stimulating the appropriate ventral root and observing the electrical activity of the cell. Such stimulation initiates an antidromic impulse that is conducted to the soma and stops at that point. Therefore, the presence of an action potential in the cell after antidromic stimulation indicates that the cell that has been penetrated is an α-motor neuron. Stimulation of a dorsal root afferent (sensory neuron) can be used to study both excitatory and inhibitory events in α-motor neurons (Figure 1).
Fig1. Excitatory and inhibitory synaptic connections mediating the stretch reflex provide an example of typical circuits within the CNS. A) The stretch receptor sensory neuron of the quadriceps muscle makes an excitatory connection with the extensor motor neuron of the same muscle and an inhibitory interneuron projecting to flexor motor neurons supplying the antagonistic hamstring muscle. B) Experimental setup to study excitation and inhibition of the extensor motor neuron. Top panel shows two approaches to elicit an excitatory (depolarizing) postsynaptic potential or EPSP in the extensor motor neuron–electrical stimulation of the whole Ia afferent nerve using extracellular electrodes and intracellular current passing through an electrode inserted into the cell body of a sensory neuron. Bottom panel shows that current passing through an inhibitory interneuron elicits an inhibitory (hyperpolarizing) postsynaptic potential or IPSP in the flexor motor neuron. (Reproduced with permission from Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. New York, NY: McGraw-Hill; 2000.)
Once an impulse reaches the presynaptic terminals, a response can be obtained in the postsynaptic neuron after a synaptic delay. The delay is due to the time it takes for the synaptic mediator to be released and to act on the receptors on the membrane of the postsynaptic cell. Because of it, conduction along a chain of neurons is slower if there are many syn apses compared to if there are only a few synapses. Because the minimum time for transmission across one synapse is 0.5 ms, it is also possible to determine whether a given reflex pathway is monosynaptic or polysynaptic (contains more than one synapse) by measuring the synaptic delay.
A single stimulus applied to the sensory nerves characteristically does not lead to the formation of a propagated action potential in the postsynaptic neuron. Instead, the stimulation produces either a transient partial depolarization or a transient hyperpolarization. The initial depolarizing response produced by a single stimulus to the proper input begins about 0.5 ms after the afferent impulse enters the spinal cord. It reaches its peak 11.5 ms later and then declines exponentially. During this potential, the excitability of the neuron to other stimuli is increased, and consequently the potential is called an excitatory postsynaptic potential (EPSP) (Figure 1).
The EPSP is produced by depolarization of the postsynaptic cell membrane immediately under the presynaptic ending. The excitatory transmitter opens Na+ or Ca2+ channels in the postsynaptic membrane, producing an inward current. The area of current flow thus created is so small that it does not drain off enough positive charge to depolarize the whole mem brane. Instead, an EPSP is inscribed. The EPSP due to activity in one synaptic knob is small, but the depolarizations produced by each of the active knobs summate.
EPSPs are produced by stimulation of some inputs, but stimulation of other inputs produces hyperpolarizing responses. Like the EPSPs, they peak 11.5 ms after the stimulus and decrease exponentially. During this potential, the excitability of the neuron to other stimuli is decreased; consequently, it is called an inhibitory postsynaptic potential (IPSP) (Figure 1).
An IPSP can be produced by a localized increase in Cl– transport. When an inhibitory synaptic knob becomes active, the released transmitter triggers the opening of Cl– channels in the area of the postsynaptic cell membrane under the knob. Cl– moves down its concentration gradient. The net effect is the transfer of negative charge into the cell, so that the mem brane potential increases.
The decreased excitability of the nerve cell during the IPSP is due to movement of the membrane potential away from the firing level. Consequently, more excitatory (depolarizing) activity is necessary to reach the firing level. The fact that an IPSP is mediated by Cl– can be demonstrated by repeating the stimulus while varying the resting membrane potential of the postsynaptic cell. When the membrane potential is at the equilibrium potential for chloride (ECl ), the postsynaptic potential disappears (Figure 2), and at more negative membrane potentials, it becomes positive (reversal potential).
Fig2. IPSP is due to increased Cl– influx during stimulation. This can be demonstrated by repeating the stimulus while varying the resting membrane potential (RMP) of the postsynaptic cell. When the membrane potential is at ECl , the potential disappears, and at more negative membrane potentials (eg, EK and below), it becomes positive (reversal potential).
Because IPSPs are net hyperpolarizations, they can be produced by alterations in other ion channels in the neuron. For example, they can be produced by opening of K+ channels, with movement of K+ out of the postsynaptic cell, or by closure of Na+ or Ca2+ channels.
