Ch.9
What is the reversal potential for ACh at the neuromuscular junction?
Since nicotinic ACh channels at the neuromuscular junction are equally permeable to sodium and potassium, the reversal potential is equal to the sum of the equilibrium potential for sodium and the equilibrium potential for potassium divided by 2. It is about -17mV at the frog neuromuscular junction.
An animal is discovered that uses ACh as a transmitter at some synapses in its nervous system. The ACh receptors of that animal are ligand gated receptors. However, their ACh receptors differ from those in other vertebrates in that when they bind ACh, the channel allows HCO3- as well as Cl- (instead of Na+ and K+) to go through equally well (the channel is equally permeable to HCO3- and Cl). Assuming that EHCO3 = -90 mV, and ECl = +10 mV, and the resting potential is -20 mV. a) What is the reversal potential for ACh at these synapses?
The reversal potential is -90 + (+10) /2= -40 mV. Thus, when the channels open, they would drive the membrane potential to a value more NEGATIVE than the resting potential and would evoke an IPSP!
What is the definition of a reversal potential?
The reversal potential is the potential to which the membrane is driven due to the opening of a ligand gated channel. The value is midway between the equilibrium potentials of the ions to which the channel is permeable.
Ligand gated channels that evoke inhibition are permeable to Cl-. What is the reversal potential that results from the binding of an inhibitory neurotransmitter?
The reversal potential would be the chloride equilibrium potential, since the channel is permeable to only one ion, Cl-. You would have to know the concentrations of chloride inside and outside the cell to calculate Ek, and thus the reversal potential for that channel.
List two major differences between a voltage-gated ion channel and a ligand-gated ion channel.
voltage gated ion channels are opened by the charge on the inside of the neuron while ligand gated channels are opened by a chemical neurotransmitter. In addition, voltage gated channels, at least the type we have discussed in class so far, are located all along the axon or, in the case of voltage gated Ca++ channels at the axon terminal, while ligand gated channels are located in the dendrites and cell body, at the site of the synaptic connection with the presynaptic axon.
Explain how the voltage clamp was used to evaluate the reversal potential at the neuromuscular junction.
By voltage clamping the muscle fiber at various holding or clamped potentials, one can follow the current coming into or out of the cell. The point is that when one clamps the membrane potential at -75 mV, Ek, there is a large influx of positive current, all of which is carried by Na+. As the membrane potential is clamped at progressively less negative values, the influx of positive current becomes progressively smaller. The reason is that driving force on Na+ is decreasing, causing a progressively smaller influx of Na+, while the driving force on K+ is increasing, causing a progressively larger efflux of positive charge carried by K+. When the membrane is clamped or held at a certain potential, there is no influx of positive current because at that potential, the reversal potential, the influx of Na+ is equal to the efflux of K+. At even a slightly more positive membrane potential, the current reverses; that is, now the influx of Na+ is smaller than the efflux of K+ (more positive current leaves the cell carried by K+ than enters the cell carried by Na+.
A nerve cell has a resting potential of -70 mV and a threshold of -55 mV. The reversal potential for one synapse on this neuron is -60 mV. In which direction does positive current cross the membrane during the action of the transmitter? Is the synapse excitatory or inhibitory? Why? What if there is a second synapse on the same neuron that has a reversal potential of -30 mV. If the same conductance change occurs at each synapse, which synapse will produce the largest EPSP?
The first synapse would be depolarizing and would generate an EPSP. That is, it would allow for an influx of positive charge and drive the membrane potential to -60, which is more depolarized than the resting potential. Notice that the membrane would never reach threshold, -55 mV, because the reversal potential is -60, which is below threshold. So while the evoked response would be a depolarizing EPSP, that EPSP would actually be inhibitory because it would in effect clamp the membrane potential at the reversal potential of -60 mV and prevent the membrane potential from reaching threshold. The second synapse would also be depolarizing and would generate an EPSP. However, the membrane would never get to the reversal potential of -30 mV because the membrane would reach threshold, -55 mV, and evoke an action potential.
