Week 32/Nervous System 3 Flashcards
Q: What is a receptor?
A: A receptor is a protein molecule that receives chemical signals from outside a cell, and it can lead to various physiological responses.
Q: How can receptors vary despite having the same endogenous ligand?
A: The same endogenous ligand can bind to a large number of receptor subtypes, and these subtypes are widespread throughout the nervous system, providing a diversity of functions.
Q: What are the two main types of receptors based on their mechanism of action?
A: Receptors can be either ligand-gated or G-protein coupled.
Q: What is a ligand?
A: A ligand is a substance that forms a complex with a biomolecule (such as a receptor) to serve a biological purpose.
Q: What is a prodrug?
A: A prodrug is a chemical compound that must undergo chemical conversion by metabolic processes before it becomes an active pharmacological agent.
Q: How does diamorphine (heroin) work as a prodrug?
A: Diamorphine enters the brain and is converted into morphine, which then binds to mu (μ) opioid receptors to exert its effects.
Q: What does bioavailability refer to?
A: Bioavailability refers to the extent and rate at which the active drug or metabolite enters systemic circulation.
Q: What is affinity in the context of drug-receptor interactions?
A: Affinity describes how tightly a drug binds to its receptor.
Q: What does efficacy mean in pharmacology?
A: Efficacy refers to the capacity of a drug to produce a change in a target cell or organ after binding to its receptor.
Q: What is potency in terms of drug activity?
A: Potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity.
Q: What does an agonist do to the post-synaptic neuron?
A: An agonist can produce either excitation or inhibition of the post-synaptic neuron.
Q: What is an agonist?
A: An agonist is a neurotransmitter or drug that mimics the action of a neurotransmitter and binds to its cognate receptor, producing a response. A neurotransmitter itself is an agonist, with high affinity for its own receptor.
Q: What is a partial agonist?
A: A partial agonist is a ligand that produces a lower response than a full agonist after binding to the same number of receptors.
Q: What is an inverse agonist?
A: An inverse agonist is a ligand that selectively binds to the inactive state of a receptor and reduces its constitutive activity, producing the opposite effect of an agonist.
Q: What is constitutive receptor activity?
A: Receptors can be active without an activating ligand, displaying “constitutive activity.”
Q: How can a partial agonist act as a competitive antagonist?
A: A partial agonist can act as a competitive antagonist when in the presence of a full agonist, because it competes for the same receptor sites but produces a weaker response.
Q: How does an inverse agonist affect receptor activity?
A: An inverse agonist decreases receptor activity below the basal level, suppressing spontaneous receptor signaling when present.
Q: How do agonists and inverse agonists differ in their effects?
A: - An agonist increases receptor activity above its basal level.
An inverse agonist decreases receptor activity below its basal level.
Q: Can inverse agonists and agonists be blocked?
A: Yes, the effects of both agonists and inverse agonists can be blocked by antagonists.
Q: What type of receptors commonly display constitutive activity?
A: Most, if not all, G-protein-coupled receptors (GPCRs) can display constitutive receptor activity.
Q: What is the main pharmacological effect of inverse agonists?
A: Receptor antagonism.
Q: When do inverse agonists behave as antagonists?
A: In the absence of constitutive receptor activity, inverse agonists function as antagonists.
Q: What is constitutive receptor activity?
A: The activation of receptors and production of a second messenger without the binding of an agonist.
Q: When is the effect of inverse agonists on constitutive activity relevant?
A: Only if the system is spontaneously active.
Q: What is an antagonist?
A: A drug that has affinity for a neurotransmitter receptor and prevents the action of the neurotransmitter.
Q: What is physiological antagonism?
A: When a drug binds to a different receptor and produces a physiological response that opposes the effect of the agonist-bound receptor.
Q: What is an inhibitor?
Q: How does an inhibitor affect enzymes?
Q: How can a neurotransmitter or drug inhibit neuronal activity?
A: Any substance that interferes with a chemical reaction, growth, or other biological activity.
A: It binds to an enzyme and decreases its activity.
A: Through (1) hyperpolarization of the neuron or (2) blockade of neurotransmitter binding to its receptor.
Q: What is disinhibition?
A: Disinhibition results from the inhibition of an inhibitor.
Q: How can endorphins or enkephalins augment excitatory synaptic transmission?
A: By disinhibiting GABAergic inputs.
Q: Describe the process of disinhibition involving opioids and dopamine release.
A:
An opioidergic neuron is depolarized.
This releases endorphins or enkephalins, which bind to opioid receptors on a GABA neuron.
Activation of opioid receptors leads to hyperpolarization of the GABA neuron.
The GABA neuron stops exerting inhibitory control over the dopamine neuron.
The dopamine neuron is now free to fire and release dopamine.
Q: What role do enzymes play in neurotransmitter termination?
A: Enzymes degrade neurotransmitters either intracellularly or in the synaptic cleft.
Q: How is the action of a neurotransmitter terminated?
A: It can be terminated by enzymatic degradation, reuptake into the presynaptic neuron, uptake by glial cells, or binding to autoreceptors.
Q: What is neurotransmitter reuptake?
A: The removal of neurotransmitter molecules from the synaptic cleft back into the nerve terminal that released them.
Q: What is an autoreceptor?
A: A receptor on the presynaptic neuron that regulates neurotransmitter release.
Q: How do glial cells contribute to neurotransmitter termination?
Q: Which neurotransmitters are terminated via reuptake into glial cells?
A: They participate in neurotransmitter reuptake, along with presynaptic nerve terminals.
A: GABA and Glutamate.
Q: What enzyme converts tyrosine into DOPA?
Q: What enzyme converts DOPA into dopamine (DA)?
Q: How is dopamine (DA) converted into noradrenaline (NA)?
Q: What is the primary mechanism for terminating the action of NA and DA in the synaptic cleft?
Q: What enzymes degrade DA and NA?
Q: Where does enzymatic degradation of DA and NA occur?
A: Tyrosine hydroxylase.
A: DOPA decarboxylase.
A: Dopamine beta hydroxylase (DBH) converts DA into NA.
A: Reuptake into the presynaptic neuron.
A: Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).
A: Either intracellularly or in the synaptic cleft.
Q: What is the precursor for glutamate (Glu) synthesis?
Q: What enzyme converts glutamine to glutamate?
Q: Where is glutaminase present?
Q: How is glutamate removed from the synaptic cleft?
Q: Can glutamine activate glutamate receptors?
Q: How is glutamate regenerated in nerve terminals?
A: Glutamine.
A: Glutaminase.
A: In mitochondria.
A: It is taken up by astroglia cells and converted into glutamine.
A: No, glutamine is inactive.
A: Nerve terminals take up glutamine and convert it back to glutamate.
Q: What is the precursor for serotonin (5-HT) biosynthesis?
Q: What enzyme converts tryptophan into 5-hydroxytryptophan?
Q: Can 5-hydroxytryptophan cross the blood-brain barrier (BBB)?
Q: What enzyme converts 5-hydroxytryptophan into serotonin (5-HT)?
Q: How is serotonin (5-HT) primarily removed from the synaptic cleft?
Q: What enzyme deactivates serotonin in the synaptic cleft?
A: Tryptophan.
A: Tryptophan hydroxylase.
A: Yes, it increases central levels of serotonin (5-HT).
A: DOPA decarboxylase.
A: Through reuptake into the presynaptic neuron.
A: Monoamine oxidase A (MAO-A), converting it to 5-hydroxyindoleacetic acid.
Q: What are the precursors for acetylcholine (ACh) synthesis?
Q: What enzyme synthesizes ACh from choline and acetyl-CoA?
Q: Where does choline come from?
Q: Where is acetyl-CoA produced?
Q: How is ACh action terminated in the synaptic cleft?
Q: What happens to choline after ACh is broken down?
A: Choline and acetyl-CoA.
A: Choline acetyltransferase (ChAT).
A: Dietary and intraneuronal sources.
A: From glucose in the mitochondria of neurons.
A: By acetylcholinesterase (AChE), which breaks it down into acetate and choline.
A: It is taken back into the presynaptic terminal and reused to form ACh.
Q: What is the precursor for GABA synthesis?
Q: What enzyme converts glutamate to GABA?
Q: What cofactor does GAD require?
Q: How is GABA removed from the synaptic cleft?
Q: What enzyme degrades GABA?
Q: What does GABA degradation regenerate?
A: Glutamate.
A: Glutamate decarboxylase (GAD).
A: Vitamin B6 (pyridoxine).
A: It is rapidly taken up by surrounding astrocytes and neurons.
A: GABA transaminase.
A: Glutamate and glutamine.
