Which of these is a neurotransmitter?
Monoamine oxidase
Cholinesterase
Acetylcholine (ACh)
Calcium
The Correct Answer is C
A) Monoamine oxidase:
Monoamine oxidase (MAO) is an enzyme, not a neurotransmitter. It is responsible for breaking down certain neurotransmitters, such as dopamine, serotonin, and norepinephrine, in the brain and other parts of the body. While it plays a crucial role in regulating neurotransmitter levels, it is not itself a neurotransmitter.
B) Cholinesterase:
Cholinesterase is also an enzyme, not a neurotransmitter. It breaks down acetylcholine (ACh) at synaptic junctions to terminate its action after it has transmitted a nerve impulse. This enzyme is important for the proper functioning of cholinergic synapses but does not function as a neurotransmitter.
C) Acetylcholine (ACh):
Acetylcholine (ACh) is a neurotransmitter. It is released by nerve cells at cholinergic synapses and plays a key role in both the peripheral and central nervous systems. ACh is involved in transmitting nerve impulses to muscles (muscle contraction) and is also important in cognitive functions like memory and learning in the brain.
D) Calcium:
Calcium is a vital ion involved in many cellular processes, including muscle contraction and neurotransmitter release. However, it is not a neurotransmitter. It plays a role in the function of neurotransmitters but does not act as one itself.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
A) Reversal of bronchoconstriction: Narcotic antagonists are not used to reverse bronchoconstriction. Bronchoconstriction is typically managed with bronchodilators (such as beta-agonists) or corticosteroids. Narcotic antagonists, such as naloxone, specifically counteract the effects of opioids, not respiratory conditions like bronchoconstriction.
B) Reversal of tachycardia: Narcotic antagonists do not have an effect on reversing tachycardia. Tachycardia may result from various conditions, including stimulant use, dehydration, or heart conditions. Treatment for tachycardia typically involves addressing the underlying cause, such as using beta-blockers for cardiac issues, but not narcotic antagonists.
C) Treatment of alcohol dependence: While certain medications, like disulfiram or acamprosate, are used to treat alcohol dependence, narcotic antagonists are not typically indicated for alcohol dependence. Narcotic antagonists, such as naloxone, are primarily used for opioid overdose or dependence, not for alcohol use disorders.
D) Treatment of narcotic dependence: Narcotic antagonists, such as naloxone, are prescribed in the treatment of narcotic (opioid) dependence. These medications work by blocking the effects of opioids at the receptor sites, thereby preventing the "high" associated with opioid use. They are particularly useful in treating opioid overdoses and can also be used in the management of opioid addiction as part of a comprehensive treatment plan.
Correct Answer is A
Explanation
A) Increased intraocular pressure: Sympathomimetic drugs stimulate the sympathetic nervous system and promote "fight or flight" responses, often resulting in vasoconstriction and other effects. Some sympathomimetics, especially those that affect alpha-adrenergic receptors, can lead to increased intraocular pressure, which is a concern in conditions like glaucoma.
B) Decreased blood pressure: Sympathomimetic drugs generally increase blood pressure by stimulating alpha and beta receptors that cause vasoconstriction and increased heart rate. In contrast, drugs that would decrease blood pressure are usually parasympathomimetics or other agents designed to block sympathetic responses.
C) Decreased heart rate: Sympathomimetic drugs typically increase heart rate by stimulating beta-1 adrenergic receptors in the heart. These drugs are used in situations requiring increased cardiac output or to counteract bradycardia. Decreased heart rate would typically occur with parasympathomimetic drugs or medications that block sympathetic activity (e.g., beta blockers).
D) Increased respiration: Sympathomimetic drugs can increase respiratory rate by promoting bronchodilation through beta-2 adrenergic receptor activation in the lungs. However, "increased respiration" as a general effect is not as specific or consistent as the other cardiovascular and ocular effects of these drugs. The primary and most prominent physiological change would be related to the cardiovascular effects.
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