[PCOL] 2.5 Parasympathetic Nervous System (Introduction)

The M1 Muscarinic receptor is coupled to which G-protein type, and what is its effect on the intracellular cascade?

A. Gi; Decreases cAMP

B. Gq; Increases IP3, DAG cascade

C. Gs; Increases cAMP

D. Go; Activates K channels

B. Gq; Increases IP3, DAG cascade

Explanation: The M1 receptor is coupled to the Gq protein, which activates the IP3/DAG second messenger system, leading to its functional effects.

What is the location and major function of the M1 receptor in the gastric system?

A. Heart; Bradycardia and Negative Dromotism

B. Exocrine glands; Increased secretion

C. Gastric gland in the parietal cells; Hyperacidity (HCl secretion)

D. Smooth muscles of the lungs; Bronchospasm

C. Gastric gland in the parietal cells; Hyperacidity (HCl secretion)

Explanation: M1 receptors are located on the nerves supplying the GIT, including the gastric parietal cells, where their activation results in the positive stimulation of the proton pump, causing HCl secretion and hyperacidity.

The M2 Muscarinic receptor is primarily located in the heart, specifically the atria. It is coupled to which G-protein and produces what major cardiac effects?

A. Gq; Positive Chronotropy (tachycardia)

B. Gs; Increased cAMP (Positive Inotropy)

C. Gi; Bradycardia and Negative Dromotism

D. Gq; Increased IP3

C. Gi; Bradycardia and Negative Dromotism

Explanation: M2 is coupled to the Gi protein, which decreases cAMP and activates K+ channels, resulting in slowed heart rate (Bradycardia) and decreased conduction velocity (Negative Dromotism).

The M3 Muscarinic receptor is coupled to the Gq protein, which leads to IP3 and DAG cascade activation. What is the effect of M3 activation on the smooth muscles of the circular muscles of the eye?

A. Relaxation; Mydriasis

B. Contraction; Miosis

C. Contraction; Accommodation

D. Relaxation; Cycloplegia

B. Contraction; Miosis

Explanation: M3 activation causes contraction of the circular muscles (sphincter pupillae) of the eye, resulting in miosis (pupil constriction).

M3 receptor activation causes the contraction of the ciliary muscles in the eye. What is the resulting function of this contraction?

A. Pupillary dilation (Mydriasis)

B. Impaired near vision (Cycloplegia)

C. Accommodation (focusing on near objects)

D. Decreased aqueous humor outflow

C. Accommodation (focusing on near objects)

Explanation: Contraction of the ciliary muscle (cytoplasm) causes the lens to become rounder, which is necessary for accommodation (near vision).

What is the effect of M3 receptor activation on the smooth muscles of the lungs?

A. Bronchodilation

B. Bronchospasm / Bronchoconstriction

C. Cough suppression

D. Increased secretion clearing

B. Bronchospasm / Bronchoconstriction

Explanation: M3 receptors on bronchial smooth muscle cause contraction, leading to bronchospasm or bronchoconstriction.

M3 receptor activation on exocrine glands, such as the lachrymal and salivary glands, results in what major function?

A. Inhibited secretion

B. No effect

C. Increased secretion

D. Decreased fluid absorption

C. Increased secretion

Explanation: M3 activation stimulates the majority of exocrine glands, including salivary, lachrymal, sweat (thermoregulatory), and bronchial/gastrointestinal glands, leading to increased fluid secretion.

The M3 receptor controls movement in the GIT. What are the effects of M3 activation on the GIT walls and the GIT sphincter?

A. Walls (Contraction), Sphincter (Contraction)

B. Walls (Relaxation), Sphincter (Relaxation)

C. Walls (Contraction), Sphincter (Relaxation)

D. Walls (Relaxation), Sphincter (Contraction)

C. Walls (Contraction), Sphincter (Relaxation)

Explanation: M3 activation stimulates the Gut Walls to Contract (bowel movement) and the Gut Sphincter to Relax (opening), collectively promoting defecation (diarrhea).

M3 receptor activation on the urinary bladder leads to Urination / Micturition. What are the specific M3 effects on the Detrusor and Trigone muscles of the bladder?

A. Detrusor (Contraction), Trigone (Relaxation)

B. Detrusor (Relaxation), Trigone (Contraction)

C. Detrusor (Relaxation), Trigone (Relaxation)

D. Detrusor (Contraction), Trigone (Contraction)

A. Detrusor (Contraction), Trigone (Relaxation)

Explanation: M3 activation causes the Detrusor muscle (bladder body) to Contract and the Trigone (bladder neck/exit) to Relax, facilitating the voiding (urination) process.

Nicotinic receptors are classified as what type of receptor based on their transduction mechanism?

A. Gq coupled (Metabotropic)

B. Gi coupled (Metabotropic)

C. Ion Channel (Ionotropic)

D. Gs coupled (Metabotropic)

C. Ion Channel (Ionotropic)

Explanation: Nicotinic receptors are ionotropic receptors, meaning they function as an ion channel. Their activation is described as having STIMULATORY effects.

The Nn (Neuronal) Nicotinic receptor is stimulated by the opening of which ion channel?

A. Outward K Channel

B. Inward Ca

2+

Channel

C. Inward Na Channel

D. Outward Cl Channel

C. Inward Na Channel

Explanation: Nn receptors are Ion Channels that, upon stimulation, open and allow the inward flow of Na ions, which depolarizes the cell.

The Nn Nicotinic receptor is primarily located in the ANS Ganglion and Adrenal Medulla. What is the major function of Nn activation in these locations?

A. Skeletal muscle contraction

B. Synaptic transmission and Epinephrine (Epi) release

C. Bradycardia and Negative Dromotism

D. Hyperacidity (HCl secretion)

B. Synaptic transmission and Epinephrine (Epi) release

Explanation: In the ANS Ganglion, Nn mediates synaptic transmission (stimulating both Parasympathetic and Sympathetic neurons). In the Adrenal Medulla, Nn stimulation triggers Epinephrine (Epi) release.

Which type of Nicotinic receptor is located at the Neuromuscular end plate of the Skeletal muscles?

A. Nn (Neuronal)

B. M1 (Muscarinic)

C. Nm (Muscular)

D. M3 (Muscarinic)

C. Nm (Muscular)

Explanation: The Nm receptor is the muscular subtype of the nicotinic receptor, situated on the somatic neuromuscular end plate.

What is the major physiological function evoked by the depolarization that occurs upon activation of the Nm Nicotinic receptor?

A. Elevation of mood and alerting

B. Adrenal medulla catecholamine release

C. Increased glandular secretion

D. Skeletal muscle contraction

D. Skeletal muscle contraction

Explanation: Nm receptors are found at the neuromuscular junction. Their activation depolarizes the muscle membrane, evokes an action potential, and leads directly to skeletal muscle contraction.

Drugs that complexly stimulate the Nn receptor, such as nicotine, can lead to what behavioral or neurological effects at moderate concentrations?

A. Coma

B. Elevation of mood, alerting, and addiction

C. Paralysis

D. Hyperacidity

B. Elevation of mood, alerting, and addiction

Explanation: The notes describe Nn as having complex stimulatory effects, including elevation of mood, alerting, and addiction. Excessive concentrations may cause coma.

What is the overall effect of Nn receptor stimulation on the ANS?

A. Inhibition of all autonomic activity

B. Stimulation of only Sympathetic neurons

C. Stimulation of only Parasympathetic neurons

D. Stimulation of both Parasympathetic and Sympathetic neurons

D. Stimulation of both Parasympathetic and Sympathetic neurons

Explanation: Since Nn is located in the ANS Ganglion where pre-ganglionic neurons meet post-ganglionic neurons, its stimulation simultaneously activates the post-ganglionic fibers of both the Parasympathetic and Sympathetic systems.

Which of the following is considered the rate limiting step in the biosynthesis of Acetylcholine (ACh) in the pre-synapse?

A. Quantal release of ACh

B. Formation of ACh from Acetyl CoA + Choline

C. Active uptake of Choline into the pre-synapse

D. Vesicular storage of ACh

C. Active uptake of Choline into the pre-synapse

Explanation: The first step, the active uptake of Choline into the presynaptic terminal, is the slowest and most regulated step, making it the rate limiting step for the entire synthesis process.

What drug acts as an inhibitor specifically targeting the active uptake of Choline into the pre-synapse?

A. Vesamicol

B. Botulinum toxin

C. alpha-latrotoxin

D. Hemicholinium

D. Hemicholinium

Explanation: Hemicholinium is the inhibitor that blocks the specific transport mechanism responsible for the uptake of Choline, thereby blocking the entire synthesis pathway.

What is the enzyme responsible for the formation of Acetylcholine (ACh) from the precursors Acetyl CoA and Choline?

A. Dopa decarboxylase

B. Monoamine Oxidase (MAO)

C. Choline acetyltransferase (CAT)

D. Dopamine beta-hydroxylase

C. Choline acetyltransferase (CAT)

Explanation: Choline acetyltransferase (CAT) catalyzes the transfer of an acetate group from Acetyl CoA to Choline to form ACh.

Which inhibitor targets the vesicular storage / uptake of ACh into synaptic vesicles?

A. Hemicholinium

B. Vesamicol

C. Botulinum toxin

D. alpha-latrotoxin

B. Vesamicol

Explanation: Vesamicol is the inhibitor that blocks the Vesicle Associated Transporter (VAT), preventing the newly synthesized ACh from being stored in the vesicles.

The release of ACh into the synaptic cleft is described as quantal. What does the term "quantal release" signify?

A. A slow, continuous release process

B. Release only in response to muscarinic receptor feedback

C. An all or none release process

D. A calcium-independent release mechanism

C. An all or none release process

Explanation: Quantal release means that ACh is released in discrete packets (quanta) corresponding to the contents of a single vesicle, signifying an all or none release event.

Which substance acts as an inhibitor of the quantal release (Exocytosis) of ACh and causes flaccid paralysis?

A. Hemicholinium

B. Vesamicol

C. Botulinum toxin

D. alpha-latrotoxin

C. Botulinum toxin

Explanation: Botulinum toxin is a protease that cleaves proteins required for vesicular fusion (Exocytosis), preventing the release of ACh and resulting in the loss of muscle tone (flaccid paralysis).

Which substance acts as a stimulant for the quantal release (Exocytosis) of ACh into the synaptic cleft?

A. Hemicholinium

B. Vesamicol

C. Botulinum toxin

D. alpha-latrotoxin

D. alpha-latrotoxin

Explanation: alpha-latrotoxin, a component of black widow spider venom, is a potent stimulant that causes massive, indiscriminate release of ACh (Exocytosis).

Which of the following is not listed as a site for the biosynthesis of Acetylcholine (ACh)?

A. Preganglionic fiber

B. Sympathetic post-ganglionic fibers

C. Parasympathetic post-ganglionic fibers

D. Central nervous system

B. Sympathetic post-ganglionic fibers

Explanation: ACh is synthesized at Preganglionic fibers (ANS ganglia), Parasympathetic post-ganglionic fibers, Central nervous system, and Somatic nerves (neuromuscular junctions). The majority of Sympathetic post-ganglionic fibers synthesize Norepinephrine.

After its release into the synaptic cleft, what are the three main fates of Acetylcholine (ACh)?

A. Metabolism by MAO, reuptake, and binding to Alpha receptors

B. Binding to M or N receptors, metabolism by AChE, and reuptake into the synapse

C. Binding to D1 receptors, exocytosis, and storage

D. Conversion to Choline and Acetate, release by VAT, and storage

B. Binding to M or N receptors, metabolism by AChE, and reuptake into the synapse

Explanation: The three fates of released ACh are: 1) binding to its specific Muscarinic (M) or Nicotinic (N) receptors to exert its effect, 2) breakdown (metabolism) by Acetylcholinesterase (AChE), and 3) reuptake into the presynapse.

Acetylcholinesterase (AChE) is described as the true cholinesterase. In which cellular location is it primarily found?

A. Plasma

B. Liver

C. Central Nervous System (CNS)

D. Red Blood Cells (RBCs)

D. Red Blood Cells (RBCs)

Explanation: Acetylcholinesterase (AChE) is the true cholinesterase and is primarily found on the surface of Red Blood Cells (RBCs) and in neural tissues, where it rapidly metabolizes ACh.

Butylcholinesterase (BuChE) is known as pseudocholinesterase. Where is it primarily found, and what is its role?

A. RBCs; Specific hydrolysis of ACh

B. Plasma; Metabolizes all esters (non-specific)

C. Synaptic cleft; ACh reuptake

D. Liver; Conversion of Choline to Acetate

B. Plasma; Metabolizes all esters (non-specific)

Explanation: Butylcholinesterase (BuChE) or plasma Cholinesterase is found in the plasma and liver. It is non-specific, meaning it metabolizes all esters, including certain drugs, not just ACh.

How do Acetylcholinesterase (AChE) inhibitors affect the fate of Acetylcholine?

A. They stimulate the reuptake of ACh into the synapse.

B. They increase the synthesis of ACh from Choline and Acetyl CoA.

C. They prevent the metabolism (breakdown) of ACh, prolonging its effect.

D. They block M and N receptors, preventing ACh from binding.

C. They prevent the metabolism (breakdown) of ACh, prolonging its effect.

Explanation: AChE inhibitors prevent the enzyme Acetylcholinesterase from metabolizing ACh, thus increasing ACh concentration and extending its duration of action at the receptor sites.

What is the key characteristic that distinguishes Acetylcholinesterase (AChE), the true cholinesterase, from Butyrylcholinesterase (BuChE), the pseudo cholinesterase?

A. AChE is non-specific, while BuChE is highly specific to Acetylcholine.

B. AChE is highly specific to Acetylcholine, while BuChE is non-specific.

C. AChE is found only in the plasma, while BuChE is found on RBCs.

D. AChE is the non-specific plasma cholinesterase.

B. AChE is highly specific to Acetylcholine, while BuChE is non-specific.

Explanation: Acetylcholinesterase (true cholinesterase) is highly specific to Acetylcholine (ACh), whereas Butyrylcholinesterase (pseudo cholinesterase) is non-specific and metabolizes all esters, including certain drugs.

After Acetylcholine is degraded in the synaptic cleft, what is the fate of the resulting Choline molecule?

A. It is eliminated from the body.

B. It is metabolized by Butyrylcholinesterase.

C. It undergoes reuptake into the pre-synapse.

D. It binds to post-synaptic receptors.

C. It undergoes reuptake into the pre-synapse.

Explanation: The Choline molecule resulting from the degradation of Acetylcholine is recycled by being taken up back into the pre-synapse to be used again for Acetylcholine synthesis, while Acetate is eliminated.

Which drug is used to interfere with the first step of Acetylcholine biosynthesis by inhibiting the active uptake of Choline into the pre-synapse?

A. Vesamicol

B. Botulinum toxin

C. Hemicholinium

D. alpha-latrotoxin

C. Hemicholinium

Explanation: Hemicholinium acts at the pre-synapse by blocking the specific carrier responsible for the active uptake of Choline, the rate-limiting step of Acetylcholine synthesis.

Which drug interferes with the synthesis of Acetylcholine by being taken up instead of Choline, thereby forming a false neurotransmitter (NT)?

A. Vesamicol

B. Triethylcholine

C. Botulinum toxin

D. alpha-latrotoxin

B. Triethylcholine

Explanation: Triethylcholine is an analog that is actively taken up in place of Choline, leading to the formation of a false neurotransmitter that is less active than true Acetylcholine.

Which drug inhibits the vesicular storage of Acetylcholine, preventing the neurotransmitter from being sequestered and protected prior to release?

A. Hemicholinium

B. Vesamicol

C. alpha-latrotoxin

D. Beta-bungarotoxin

B. Vesamicol

Explanation: Vesamicol is the inhibitor that blocks the carrier mechanism responsible for packing newly synthesized Acetylcholine into synaptic vesicles for storage.

What is the specific target protein for Botulinum toxin's inhibitory action on Acetylcholine release?

A. Choline acetyltransferase (CAT)

B. Synaptobrevin

C. Muscarinic receptor

D. Plasma cholinesterase

B. Synaptobrevin

Explanation: Botulinum toxin, a peptidase, specifically targets and cleaves proteins like Synaptobrevin that are crucial for the fusion of Acetylcholine vesicles with the cell membrane (exocytosis).

What is the clinical effect resulting from the action of Botulinum toxin on the Acetylcholine release process?

A. Excitation and convulsions

B. Hypertensive crisis and tachycardia

C. Progressive parasympathetic and motor paralysis

D. Profound sedation and depression

C. Progressive parasympathetic and motor paralysis

Explanation: By inhibiting the exocytosis of Acetylcholine at the neuromuscular junction and post-ganglionic parasympathetic nerve endings, Botulinum toxin causes flaccid paralysis.

What is the active ingredient/mechanism of action of Beta-bungarotoxin, a component of Cobra family venom?

A. Phospholipase that affects the cell membrane

B. Peptidase that cleaves Synaptobrevin

C. Selective inhibitor of Choline uptake

D. Competitive antagonist at the Nicotinic receptor

A. Phospholipase that affects the cell membrane

Explanation: Beta-bungarotoxin, another inhibitor of Acetylcholine release, acts as a phospholipase, which degrades phospholipids in the nerve terminal membrane, interfering with the release process.

Which agent stimulates the massive exocytosis (quantal release) of Acetylcholine into the synaptic cleft?

A. Vesamicol

B. Botulinum toxin

C. alpha-latrotoxin

D. Triethylcholine

C. alpha-latrotoxin

Explanation: alpha-latrotoxin is a potent stimulant of neurotransmitter release, causing the massive exocytosis of Acetylcholine and other neurotransmitters.

What is the overall effect of Acetylcholinesterase (AChE) inhibitors on the cholinergic system?

A. Inhibits the synthesis of Acetylcholine

B. Causes degradation of Acetylcholine

C. Positively stimulates (enhances) cholinergic transmission

D. Blocks post-synaptic Muscarinic receptors

C. Positively stimulates (enhances) cholinergic transmission

Explanation: By preventing the degradation of Acetylcholine, AChE inhibitors increase the concentration and duration of action of the neurotransmitter, resulting in a positive stimulation of cholinergic effects.

What are the primary neurotransmitters (NT) that activate Muscarinic receptors?

A. Nicotine and Acetylcholine (ACh)

B. Muscarine and Acetylcholine (ACh)

C. Epinephrine and Norepinephrine

D. Dopamine and Serotonin

B. Muscarine and Acetylcholine (ACh)

Explanation: The primary natural agonist is Acetylcholine (ACh), and the receptor is named for the alkaloid Muscarine, which selectively activates it.

What are the primary neurotransmitters (NT) that activate Nicotinic receptors?

A. Muscarine and Acetylcholine (ACh)

B. Nicotine and Acetylcholine (ACh)

C. Histamine and Serotonin

D. Dopamine and Glutamate

B. Nicotine and Acetylcholine (ACh)

Explanation: The primary natural agonist is Acetylcholine (ACh), and the receptor is named for the alkaloid Nicotine, which selectively activates it.

Muscarinic receptors are classified as Type 2 receptors, which are functionally known as what type of membrane receptor?

A. Ion channel / Ligand gated

B. G Protein-linked membrane receptor

C. Kinase-linked receptor

D. Nuclear receptor

B. G Protein-linked membrane receptor

Explanation: Muscarinic receptors are Metabotropic (Type 2) receptors, coupled to G proteins (Gq or Gi), which initiate second messenger cascades upon activation.

Nicotinic receptors are classified as Type 1 receptors, which are functionally known as what type of membrane receptor?

A. G Protein-linked membrane receptor

B. Ion channel / Ligand gated

C. Nuclear receptor

D. Enzyme-linked receptor

B. Ion channel / Ligand gated

Explanation: Nicotinic receptors are Ionotropic (Type 1) receptors that are Ligand-gated ion channels, opening an inward Sodium channel when activated.

Which of the following is not a location for Muscarinic receptors?

A. Heart and VSM (Vascular Smooth Muscle)

B. Exocrine glands and presynaptic nerve terminals

C. Neuromuscular junction

D. Gastric glands

C. Neuromuscular junction

Explanation: Muscarinic receptors are located on effector cells (Heart, VSM, SM, exocrine glands) and presynaptic terminals. The Neuromuscular junction contains Nicotinic (Nm) receptors.

Which specific subtype of Muscarinic receptor is primarily located in the heart?

A. M1

B. M2

C. M3

D. N neural

B. M2

Explanation: The M2 subtype is predominantly located in the heart (atria), where its Gi-coupling mediates negative chronotropic and dromotropic effects (bradycardia).

Nicotinic receptors in the Ganglia are blocked by which specific antagonist?

A. Tubocurarine

B. Hexamethonium

C. Atropine

D. Scopolamine

B. Hexamethonium

Explanation: Nicotinic receptors at the Ganglia (N neural) are blocked by the ganglionic blocker Hexamethonium.

Nicotinic receptors at the Neuromuscular junction are blocked by which specific antagonist?

A. Hexamethonium

B. Tubocurarine

C. Atropine

D. Clonidine

B. Tubocurarine

Explanation: Nicotinic receptors at the Neuromuscular junction (N muscular) are blocked by the skeletal muscle relaxant Tubocurarine.

Which two Muscarinic receptor subtypes are coupled to the Gq protein (Gq cascade)?

A. M1 and M2

B. M2 and M3

C. M1 and M3

D. M1 and N neural

C. M1 and M3

Explanation: M1 (gastric glands) and M3 (exocrine glands and smooth muscles) are both coupled to the Gq protein, which initiates the IP3/DAG cascade. M2 is coupled to Gi.

Nicotinic receptors are divided into which two subtypes?

A. N1 and N2

B. N neural and N muscular

C. N presynaptic and N postsynaptic

D. N cardiac and N vascular

B. N neural and N muscular

Explanation: The two main subtypes of Nicotinic receptors are N neural (found in ganglia and CNS) and N muscular (found at the neuromuscular junction).