Heurotransmitters and their respective receptors influence the propagation of action potentials. Why does ACh release at skeletal muscles cause excitation and muscle contractions whereas ACh release at the heart causes inhibition and a slowing down of the heart rate and force of heart contractions? O the ACh released at skeletal muscles and the heart are not similar skeletal muscles have more ACh receptors the properties of the ACh receptors are different a and b

The sympathetic postganglionic neurons release only norepinephrine while the adrenal medulla secretes mainly epinephrine (80%) and a small amount of norepinephrine (20%). The sympathetic postganglionic neurons do not secrete epinephrine because; Group of answer choices a. Epinephrine is not as widely used in the nervous system as norepinephrine b. Phenylethanolamine-N-methyltransferase (PNMT) which converts norepinephrine to epinephrine is present in the adrenal medulla, but not in sympathetic postganglionic adrenergic neurons c. Acetylcholine which stimulates the secretion of epinephrine does not act on postganglionic neurons d. Dopamine beta hydroxylase in hyperactive in the adrenal medulla

threshold resting membrane potential decrease calcium channels increase action potentials The autonomic nervous system influences the heart rate. A sympathetic signal (norepinephrine) results in opening. This accelerates the process of reaching thereby resulting in a in time between successive action potentials. A parasympathetic signal (acetylcholine) results in the dropping to -70mV. This results in an in time for cells to reach threshold, thereby increasing the time between successive

neurotransmitters 1 In what way may drugs be used to affect neurotransmitters? Select an answer and submit. For keyboard navigation, use the up/down arrow keys to select an answer. A drug may prevent the binding of a neurotransmitterto a receptor. b, A drug may increase the amount of neurotransmitter released. A drug may prevent the release of aneurotransmitter, d. A drug may affect the degradation of a neurotransmitter Drugemay affect neurotranemitters usng al of the mechanismslsted. Unanswered

Can you please answer this question and say the correct letter

A drug is called an agonist if it ________.a. blocks a receptorb. interferes with neurotransmitter reuptakec. acts like the endogenous neurotransmitter bybinding to its receptord. blocks the voltage-gated calcium ion channel

Patient in renal failure develops hyperkalemia so that his extracellular [K+] increases from 4.5 mEq/L (normal) to 6.5 mEq/L. What will happen to the resisting membrane potential (RP) of his cardiac myocytes? a. it will depolarizeb. it will hyperpolarizec. there will be no change since K+ channels are freely permeabled. there will be no change since Na+ channels are closede. it will polarize

27.

Conotoxin is produced by marine cone snails. Among its effects is to block voltage-gated Ca2+ channels in n eurons. A. What anatomical part of a neuron would be affected by conotoxin? B. How would the neuron's action potential be affected by conotoxin? Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis C. If conotoxin affected a somatic motor neuron, would this toxin cause muscle weakness or increased muscle tension? Explain why.

Expression of which of the following lowers the threshold for firing action potentials? O A. Voltage-dependent K* channels OB. Na+, K+-ATPase OC. GABAA receptors OD. CI channels O E. Voltage-dependent Na* channels