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Quizzes > Quizzes for Business > Healthcare

Take the Neurotransmitter Function Knowledge Test

Challenge Your Neurochemistry and Synaptic Function Knowledge

Difficulty: Moderate
Questions: 20
Learning OutcomesStudy Material
Colorful paper art depicting brain and quiz elements for Neurotransmitter Function Knowledge Test.

This neurotransmitter function quiz helps you practice how neurons send signals at synapses and how receptors work. Work through 15 multiple-choice questions to check gaps before a class or exam and learn a few facts as you go. When you finish, try the anatomy quiz or the IT basics quiz .

Which neurotransmitter is the primary excitatory transmitter in the central nervous system?
Glutamate
Dopamine
Serotonin
GABA
Glutamate is the major excitatory neurotransmitter in the CNS, mediating fast synaptic transmission. It acts on ionotropic and metabotropic receptors to depolarize postsynaptic neurons. Other transmitters like GABA, dopamine, and serotonin serve different roles.
Which neurotransmitter is the main inhibitory transmitter in the adult mammalian brain?
Glycine
Glutamate
GABA
Acetylcholine
GABA (gamma-aminobutyric acid) is the principal inhibitory neurotransmitter in the adult brain, causing hyperpolarization of postsynaptic neurons. Glycine also inhibits but primarily in the spinal cord and brainstem. Glutamate and acetylcholine are generally excitatory.
Acetylcholine is primarily degraded in the synaptic cleft by which enzyme?
Choline acetyltransferase
Catechol-O-methyltransferase
Monoamine oxidase
Acetylcholinesterase
Acetylcholinesterase breaks down acetylcholine into acetate and choline in the synaptic cleft, terminating its action. Choline acetyltransferase synthesizes acetylcholine in the presynaptic terminal. MAO and COMT degrade monoamines, not acetylcholine.
Which amino acid is the precursor for serotonin synthesis?
Tryptophan
Tyrosine
Glutamate
Glycine
Tryptophan is hydroxylated and decarboxylated to form serotonin (5-HT) in serotonergic neurons. Tyrosine is the precursor for dopamine and norepinephrine. Glutamate and glycine serve as neurotransmitters themselves.
During an action potential, which event triggers neurotransmitter release at the presynaptic terminal?
Opening of voltage-gated calcium channels
Potassium efflux through leak channels
Membrane hyperpolarization
Sodium influx through ligand-gated channels
Depolarization opens voltage-gated calcium channels in the presynaptic terminal, and calcium influx triggers synaptic vesicle fusion and neurotransmitter release. Hyperpolarization would inhibit release. Sodium and potassium movements are critical for the action potential but not the direct trigger for release.
Which glutamate receptor subtype is ionotropic and mediates fast synaptic transmission?
mGluR5
GABA-B receptor
D2 receptor
AMPA receptor
AMPA receptors are ionotropic glutamate receptors that allow sodium influx and rapid excitatory postsynaptic currents. mGluR5 is metabotropic, D2 is a dopamine receptor, and GABA-B is an inhibitory metabotropic receptor.
Which enzyme converts L-DOPA to dopamine in catecholaminergic neurons?
Catechol-O-methyltransferase
Monoamine oxidase
Tyrosine hydroxylase
Aromatic L-amino acid decarboxylase
Aromatic L-amino acid decarboxylase (also called DOPA decarboxylase) catalyzes the decarboxylation of L-DOPA to dopamine. Tyrosine hydroxylase is the rate-limiting step converting tyrosine to L-DOPA. MAO and COMT degrade monoamines.
Which transporter is primarily responsible for serotonin reuptake in the synaptic cleft?
VGLUT
EAAT
DAT
SERT
The serotonin transporter (SERT) clears serotonin from the synaptic cleft back into presynaptic terminals. DAT serves dopamine, EAAT is for glutamate, and VGLUT is the vesicular glutamate transporter.
Activation of GABA-A receptors typically causes which effect on the postsynaptic neuron?
Potassium efflux and depolarization
Calcium influx and excitation
Sodium influx and depolarization
Chloride influx and hyperpolarization
GABA-A receptors are ionotropic chloride channels. Their activation allows Cl❻ influx, leading to hyperpolarization and inhibition of the postsynaptic neuron. The other options describe excitatory receptor actions.
In Parkinson's disease, loss of which neurotransmitter-producing neurons contributes to motor symptoms?
Dopamine
GABA
Acetylcholine
Serotonin
Parkinson's disease is characterized by degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to dopamine deficiency in the striatum and resulting motor deficits. Serotonin, GABA, and acetylcholine are less directly involved in those core motor symptoms.
Which neurotransmitter receptor uses a Gs protein to activate adenylate cyclase and increase cAMP?
Nicotinic acetylcholine receptor
NMDA receptor
GABA-A receptor
Beta-adrenergic receptor
Beta-adrenergic receptors are G protein - coupled receptors that couple to Gs, stimulating adenylate cyclase and increasing cAMP. GABA-A and NMDA are ionotropic, and nicotinic acetylcholine receptors are also ligand-gated ion channels.
Which enzyme mainly degrades catecholamines in the synaptic cleft?
Choline acetyltransferase
Catechol-O-methyltransferase
Glutamic acid decarboxylase
Acetylcholinesterase
Catechol-O-methyltransferase (COMT) methylates catecholamines like dopamine and norepinephrine, aiding their inactivation. Acetylcholinesterase and choline acetyltransferase deal with acetylcholine, and glutamic acid decarboxylase synthesizes GABA.
What is the rate-limiting step in catecholamine synthesis?
L-DOPA decarboxylation to dopamine
Norepinephrine methylation to epinephrine
Tyrosine hydroxylation to L-DOPA
Dopamine hydroxylation to norepinephrine
The conversion of tyrosine to L-DOPA by tyrosine hydroxylase is the rate-limiting step in catecholamine synthesis. Subsequent steps proceed more rapidly. The other steps are not rate limiting.
Excessive release of glutamate can lead to which pathological process?
Hyperpolarization
Cholinergic blockade
Excitotoxicity
Reduced neural firing
Excitotoxicity refers to neuronal injury or death caused by excessive glutamate receptor activation and calcium influx. This process is implicated in stroke and neurodegenerative diseases. The other choices do not describe this damage mechanism.
Which receptor interaction is a classic example of a metabotropic signaling mechanism?
GABA-A receptor chloride influx
AMPA receptor sodium influx
mGluR activation leading to IP3 production
Nicotinic receptor sodium influx
Metabotropic glutamate receptors (mGluRs) activate G proteins, leading to second messenger cascades like IP3 production. AMPA, GABA-A, and nicotinic receptors are ionotropic, mediating direct ion flux.
Impaired GABAergic inhibition in which brain region is most directly associated with increased anxiety?
Amygdala
Striatum
Cerebellum
Hippocampus
The amygdala plays a central role in fear and anxiety regulation, and GABAergic inhibition here dampens excitatory circuits. Reduced GABA function in the amygdala is linked to heightened anxiety. Other regions have different primary functions.
Which neurotransmitter imbalance is most closely linked to major depressive disorder?
Increased dopamine
Decreased serotonin
Decreased GABA
Increased glutamate
Major depressive disorder is often associated with decreased serotonergic function in key brain regions. While glutamate and GABA alterations can play a role, serotonin imbalance is most directly linked to classic antidepressant mechanisms.
Activation of which presynaptic receptor subtype decreases neurotransmitter release via Gi/o-mediated inhibition of adenylate cyclase?
AMPA receptor
NMDA receptor
GABA-B receptor
Nicotinic receptor
GABA-B receptors are metabotropic and couple to Gi/o proteins, which inhibit adenylate cyclase and reduce cAMP, decreasing neurotransmitter release. NMDA, AMPA, and nicotinic receptors are ionotropic and do not use Gi/o signaling.
Lithium's mood-stabilizing effects in bipolar disorder involve the inhibition of which intracellular enzyme?
Inositol monophosphatase
Tyrosine hydroxylase
Phosphodiesterase
Monoamine oxidase
Lithium inhibits inositol monophosphatase, depleting inositol and dampening phosphatidylinositol signaling pathways implicated in mood regulation. This mechanism is distinct from PDE inhibition or neurotransmitter synthesis/degradation.
In Alzheimer's disease, loss of which neurotransmitter system in the basal forebrain correlates with memory deficits?
GABA
Acetylcholine
Serotonin
Dopamine
Cholinergic neurons in the basal forebrain degenerate in Alzheimer's disease, leading to reduced acetylcholine levels and memory impairment. Dopamine and serotonin systems are affected differently, and GABA changes are secondary.
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Learning Outcomes

  1. Identify key neurotransmitters and their physiological roles
  2. Analyze synaptic transmission mechanisms in neural circuits
  3. Evaluate effects of neurotransmitter imbalances on behavior
  4. Apply knowledge of receptor interactions in signaling pathways
  5. Demonstrate understanding of neurotransmitter synthesis and degradation
  6. Master distinctions between excitatory and inhibitory neurotransmitters

Cheat Sheet

  1. Understand the role of neurotransmitters in neuron communication - Neurotransmitters are chemical messengers zooming across tiny gaps called synapses, making sure your neurons can chat nonstop. They're the reason you can react to a hot stove in a blink or remember your best friend's birthday. Buckle up to see how these microscopic mail carriers keep your brain buzzing!
  2. Identify key neurotransmitters and their functions - Meet the all-stars: glutamate fires up your neurons with excitatory pep, while GABA calms things down by inhibiting overexcited signals. Other VIPs like dopamine and serotonin help regulate mood, motivation, and reward pathways. Knowing who does what is like learning the lineup of your brain's dream team!
  3. Learn the mechanisms of synaptic transmission - Synaptic transmission is a three-act play: release of neurotransmitters, binding to receptors, and signal propagation down the next neuron. This precise choreography ensures messages travel swiftly and accurately across neural highways. Dive into the molecular drama that keeps your thoughts and actions in sync!
  4. Explore the impact of neurotransmitter imbalances - When neurotransmitter levels stray from the norm, your brain's harmony can hit a sour note - think depression from low serotonin or tremors from dopamine misfires. Even small shifts can ripple outward, affecting mood, sleep, and behavior. Investigate how balance (or imbalance) shapes mental health and well-being!
  5. Understand receptor interactions - Neurotransmitters bind to specific receptors on the receiving neuron like keys in locks, triggering different cellular responses. Acetylcholine, for example, fits into nicotinic and muscarinic receptors to regulate muscle action and memory. Grasp these lock-and-key dynamics to unlock how signals get interpreted!
  6. Study neurotransmitter synthesis and degradation - Your neurons are busy factories, crafting neurotransmitters from raw materials and then recycling or breaking them down once they've delivered their message. Enzymes like monoamine oxidase keep levels in check, preventing overactivity. Explore these manufacturing and cleanup crews that maintain synaptic balance!
  7. Differentiate between excitatory and inhibitory neurotransmitters - Excitatory neurotransmitters ramp up neuron firing, pushing signals forward, while inhibitory ones put the brakes on excess activity. It's like having an accelerator (glutamate) and a brake pedal (GABA) to control your brain's traffic. Mastering this push-and-pull keeps neural circuits running smoothly!
  8. Recognize the role of neuromodulators - Neuromodulators such as serotonin and dopamine tweak the strength and duration of other neurotransmitter signals, shaping mood, attention, and reward. They're the behind-the-scenes directors fine-tuning your brain's performance. Delve into how these modulators orchestrate complex behaviors!
  9. Understand the criteria for classifying neurotransmitters - Neurotransmitters can be grouped by chemical structure - like amino acids, monoamines, or peptides - and by function. This classification helps predict how they're made, stored, and interact with receptors. Sorting them into families reveals patterns in brain chemistry and drug design!
  10. Learn about the removal of neurotransmitters from the synaptic cleft - After duty calls, neurotransmitters are either reabsorbed through reuptake channels, broken down by enzymes, or simply drift away by diffusion. These cleanup processes prevent overstimulation and prepare the synapse for the next message. Study these removal methods to see how your brain resets for round two!
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