1. Why might a muscle cell fail to show any EPSPs?
2. What is the main factor that determines the time course of the falling phase of the EPSP?
3. What is the pathway and the mechanism by which a sensory stimulus can change the EPSP frequency in the muscle? What would be the effect of this change in frequency on muscle contraction? That is, how is it that EPSPs are summating, and in this muscle, what are the functional consequences of the summation?
4. Explain why a depolarization of the cell membrane potential might make the IPSPs clearer.
5. In the crayfish neuromuscular junction and in the vertebrate nervous system, both presynaptic inhibition and postsynaptic inhibition are common. Both provide inhibition, so why do both forms exist?
1. Muscle cell EPSP is shown in response to a single action potential in a somatic efferent neuron. However, in conditions like myasthenia gravis, the decrease in ACh release cause EPSPs to fall as muscle fibers in the motor unit fail to fire action potentials.
2. The main factor that determines the time course of the falling phase of the EPSP the rates of binding and unbinding of ACh the rates of binding and unbinding of ACh.
4. An excitatory postsynaptic potential takes place when the membrane is depolarized by the ion movement.
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