After the effector cell has being stimulated by acetylcholine (ACh), what enzyme stop the stimulation and allows the effector membrane to repolarize?

A) Norepinephrine, dopamine, and serotonin:
Depression has been strongly linked to deficiencies in certain neurotransmitters in the brain, specifically norepinephrine, dopamine, and serotonin. These neurotransmitters play significant roles in regulating mood, emotions, and behavior. When their levels are low, individuals may experience symptoms of depression, such as sadness, low energy, anhedonia (inability to feel pleasure), and difficulty concentrating. Antidepressant medications often work by increasing the availability of these neurotransmitters in the brain.

B) Epinephrine, Norepinephrine, and Acetylcholine:
While norepinephrine plays a key role in depression, epinephrine and acetylcholine are not typically highlighted as the primary neurotransmitters involved in depression. Epinephrine (also known as adrenaline) is more associated with the body’s stress response and fight-or-flight reaction. Acetylcholine is involved in memory and learning processes, but it is not the primary neurotransmitter related to depression.

C) Acetylcholine, gamma-aminobutyric acid, and serotonin:
Acetylcholine and gamma-aminobutyric acid (GABA) are involved in many brain functions, but they are not the primary neurotransmitters linked to depression. While GABA may play a role in mood regulation, it is not typically associated with depression in the same way that serotonin, norepinephrine, and dopamine are. Serotonin is the exception in this answer

D) Gamma-aminobutyric acid, dopamine, and epinephrine:
Although dopamine is involved in depression, gamma-aminobutyric acid (GABA) and epinephrine are not the key neurotransmitters associated with the pathophysiology of depression. Epinephrine primarily affects the stress response, and while GABA does influence mood and anxiety, it is not the main neurotransmitter linked to depression itself.

A) Beta 1-receptors:
Beta 1-receptors are primarily found in the heart, and their stimulation leads to increased heart rate and contractility. These receptors are not typically involved in vasoconstriction, pupil dilation, or piloerection.

B) Beta 2-receptors:
Beta 2-receptors are primarily located in smooth muscles such as the bronchi and blood vessels. Their stimulation causes smooth muscle relaxation, leading to bronchodilation and vasodilation. Beta 2-receptors are not responsible for the effects of vasoconstriction, piloerection, or pupil dilation described in the question, making this option incorrect.

C) Alpha 2-receptors:
Alpha 2-receptors are involved in the inhibition of norepinephrine release and play a role in regulating sympathetic tone. They are not primarily responsible for vasoconstriction or the other physiological responses listed in the question. Alpha 2-stimulation typically results in decreased sympathetic activity, not the effects described here.

D) Alpha 1-receptors:
Alpha 1-receptors are located on smooth muscle, including the blood vessels, and their stimulation results in vasoconstriction. They are also involved in other actions such as piloerection (hair standing on end), pupil dilation (mydriasis), and closure of the salivary sphincter. Additionally, they play a role in male sexual emission (ejaculation). The physiological responses described in the question—vasoconstriction, piloerection, pupil dilation, and male sexual emission—are all consistent with alpha 1-receptor stimulation.