Quiz On K6 & K7 Pharmacology Sem 2 Session 2018-2019 (Nb 2264)

The correct answer is β2 (Gs). Adrenoceptor subtypes are receptors that respond to adrenaline or noradrenaline. The β2 adrenoceptor subtype is coupled to the Gs protein, which activates adenylyl cyclase and increases the production of cyclic AMP (cAMP). Increased levels of cAMP in liver cells stimulate glycogenolysis, the breakdown of glycogen, and gluconeogenesis, the production of glucose from non-carbohydrate sources. Therefore, activation of the β2 adrenoceptor subtype promotes liver glycogenolysis and gluconeogenesis.

The vesicular ACh-H+ antiporter is a target for vesamicol. This means that vesamicol can specifically bind to and inhibit the activity of the vesicular ACh-H+ antiporter, which is responsible for transporting acetylcholine (ACh) into vesicles for storage and release. This inhibition would result in a decrease in ACh release at the synapse.

Botulinum toxin inhibits the fusion of vesicles to the presynaptic membrane. This toxin can enter nerve terminals and cleave specific proteins involved in vesicle fusion, such as synaptobrevin. By inhibiting the fusion of vesicles to the presynaptic membrane, botulinum toxin prevents the release of ACh into the synaptic cleft, leading to muscle paralysis.

Nicotinic receptors do not belong to the G-protein-coupled receptor superfamily. Instead, they are ligand-gated ion channels that open in response to binding of ACh, allowing the influx of ions and generating an excitatory response.

Acetylcholine in the synaptic cleft is degraded by acetylcholinesterase, not choline acetyltransferase. Acetylcholinesterase breaks down ACh into choline and acetate, terminating its action at the synapse.

Hemicholinium inhibits the reuptake of choline into the nerve terminal, which is necessary for the synthesis of ACh. By blocking choline uptake, hemicholinium reduces the availability of choline for ACh synthesis, leading to a decrease in ACh levels.

Parasympathetic preganglionic fibers are shorter than sympathetic preganglionic fibers because parasympathetic fibers have their ganglia located near or within the target organ, while sympathetic fibers have their ganglia located closer to the spinal cord. The receptors at the postganglionic neuron at the sweat gland are muscarinic, which means they are activated by acetylcholine. All preganglionic autonomic neurons secrete acetylcholine as their neurotransmitter.

The sympathetic nervous system is responsible for the "fight or flight" response in the body. It activates various organs and tissues to prepare the body for action. The renin-secreting cells of the kidney are under the control of the sympathetic nervous system, as they play a role in regulating blood pressure. Similarly, the ejaculatory muscle of the genital organ is also controlled by the sympathetic nervous system, as it is involved in the process of ejaculation.

Noradrenaline binds to receptors located on autonomic ganglia, but this statement is not mentioned in the answer. The correct statements in the answer are: binding to α2-receptors will inhibit noradrenaline release from the nerve ending, its action is mainly terminated by Uptake 1 mechanism, and reserpine may deplete its storage in the vesicles. Binding to β2-receptors actually causes vasodilation, not vasoconstriction.

Tyrosine is an essential amino acid involved in the biosynthesis of catecholamines, such as noradrenaline. Cocaine interferes with the reuptake of noradrenaline into the nerve terminal, leading to increased levels of noradrenaline in the synaptic cleft. Disulfiram inhibits dopamine-β-hydroxylase, an enzyme responsible for converting dopamine to norepinephrine, resulting in increased levels of dopamine in the brain.