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cerisecamel639Lv1

28 Sep 2019

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?

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Jean KeelingLv2

28 Sep 2019

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A well-studied autoimmune and neuromuscular disease affects the neuromuscular junction of afflicted individuals. It turns out that antibodies attack the ligand receptor found on the skeletal muscle cells and reduces the number of these receptors, leading to weakness in eye muscles, facial muscles and in severe cases affects respiratory muscles.

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Which of the following statements is TRUE regarding sea anemones?

	None of the answer options is correct.
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	Low levels of calcium would not have any effect on synaptic transmission.
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Cephalization is: the

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	development of a brain within the head of an animal.
	concentration of sensory organs within the head end of an animal.
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Which of the following are TRUE about the resting membrane potential? (Select all that apply.)

	It results from voltage-gated sodium channels remaining open for long periods of time.
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Afferent and efferent neurons differ in:

	their size.
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	interneuron.
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Which of the following is NOT the role of an interneuron?

	stimulating a muscle to contract
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B)because blood decreases in pressure as it travels throughcirculation

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C)Na+, Ca2+, and Cl- are all more concentrated in theEXTRACELLULAR fluid

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