Which Of The Following Changes In The Post Synaptic Neuron Could Cause An Epsp?

Postsynaptic conductance changes and the potential changes that accompany them alter the probability that an action potential volition be produced in the postsynaptic cell. At the neuromuscular junction, synaptic action increases the probability that an action potential will occur in the postsynaptic muscle cell; indeed, the large amplitude of the EPP ensures that an activeness potential ever is triggered. At many other synapses, PSPs actually subtract the probability that the postsynaptic cell volition generate an activeness potential. PSPs are chosen excitatory (or EPSPs) if they increase the likelihood of a postsynaptic activeness potential occurring, and inhibitory (or IPSPs) if they decrease this likelihood. Given that near neurons receive inputs from both excitatory and inhibitory synapses, it is important to empathize more precisely the mechanisms that determine whether a particular synapse excites or inhibits its postsynaptic partner.

The principles of excitation just described for the neuromuscular junction are pertinent to all excitatory synapses. The principles of postsynaptic inhibition are much the same as for excitation, and are besides general. In both cases, neurotransmitters bounden to receptors open or close ion channels in the postsynaptic jail cell. Whether a postsynaptic response is an EPSP or an IPSP depends on the type of channel that is coupled to the receptor, and on the concentration of permeant ions inside and outside the cell. In fact, the simply factor that distinguishes postsynaptic excitation from inhibition is the reversal potential of the PSP in relation to the threshold voltage for generating activity potentials in the postsynaptic cell.

Consider, for instance, a neuronal synapse that uses glutamate as the transmitter. Many such synapses accept receptors that, similar the ACh receptors at neuromuscular synapses, open ion channels that are nonselectively permeable to cations. When these glutamate receptors are activated, both Na⁺ and Thou⁺ flow across the postsynaptic membrane. The reversal potential (East _rev) for the postsynaptic current is approximately 0 mV, whereas the resting potential of neurons is approximately -lx mV. The resulting EPSP will depolarize the postsynaptic membrane potential, bringing it toward 0 mV. For the particular neuron shown in Figure vii.6A, the action potential threshold voltage is -forty mV. Thus, the EPSP increases the probability that the postsynaptic neuron will produce an action potential, defining this synapse every bit excitatory.

Figure 7.6

Reversal potentials and threshold potentials determine postsynaptic excitation and inhibition. (A) If the reversal potential for a PSP (0 mV) is more positive than the action potential threshold (-40 mV), the effect of a transmitter is excitatory, and (more...)

As an example of inhibitory postsynaptic action, consider a neuronal synapse that uses GABA every bit its transmitter. At such synapses, the GABA receptors typically open channels that are selectively permeable to Cl^-. When these channels open, negatively charged chloride ions can flow across the membrane. Assume that the postsynaptic neuron has a resting potential of -60 mV and an action potential threshold of -40 mV, every bit in the previous example. If East _Cl is -70 mV, as is typical for many neurons, transmitter release at this synapse volition inhibit the postsynaptic jail cell (considering E _Cl is more than negative than the action potential threshold). In this example, the electrochemical driving forcefulness (V _thou - Due east _rev) causes Cl^- to flow into the prison cell, generating an outward PSC (because Cl^- is negatively charged) and consequently a hyperpolarizing IPSP (Effigy vii.6B). Because East _Cl is more negative than the action potential threshold, the conductance change arising from the binding of GABA keeps the postsynaptic membrane potential more negative than threshold, thereby reducing the probability that the postsynaptic cell will fire an action potential.

Withal, not all inhibitory synapses produce hyperpolarizing IPSPs. For instance, in the neuron just described, if East _Cl were -50 mV instead of -70 mV, then the synapse would nonetheless be inhibitory because the reversal potential of the IPSP remains more negative than the activeness potential threshold (-40 mV). Considering the electrochemical driving force at present causes Cl^- to flow out of the jail cell, however, the IPSP is really depolarizing (Effigy vii.6C). Still, this depolarizing IPSP inhibits the postsynaptic jail cell because the cell's membrane potential is kept more negative than the threshold potential for activeness potential initiation. Another way to recall about this peculiarity is that if some other depolarizing input were to bring the prison cell'southward resting potential to -41 mV, just below threshold for firing an action potential, the opening of these GABA-activated channels would effect in a hyperpolarizing current, bringing the membrane potential closer to -50 mV, the reversal potential for these channels. Thus, while EPSPs depolarize the postsynaptic cell, IPSPs can hyperpolarize or depolarize; indeed, an inhibitory conductance change may produce no potential alter at all and nevertheless exert an inhibitory result.

Although the particulars of postsynaptic activeness tin can be complex, a elementary rule distinguishes postsynaptic excitation from inhibition: An EPSP has a reversal potential more positive than the action potential threshold, whereas an IPSP has a reversal potential more negative than threshold (Figure 7.6D). Intuitively, this rule tin be understood past realizing that an EPSP volition tend to depolarize the membrane potential so that information technology exceeds threshold, whereas an IPSP will always act to go on the membrane potential more than negative than the threshold potential.

Source: https://www.ncbi.nlm.nih.gov/books/NBK11117/

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