411Section 2: Drug Receptors and Pharmacology – Vocabulary FLASHCARDS

A set of vocabulary-style flashcards covering core concepts from receptor pharmacology, including ligand-receptor interactions, signal transduction, autonomic receptor subtypes, adenosine and opioid systems, and basic pharmacokinetics/pharmacodynamics.

Ligand

A substance that binds to a biomolecule (e.g., a receptor) to produce a biological effect; binding often alters the receptor's conformation.

Receptor

A cellular component that binds drugs/hormones and initiates a biochemical signaling cascade, often changing receptor shape and cellular metabolism.

Lock and Key mechanism

Concept describing specific fit between a ligand and its receptor, producing a conformational change that triggers signaling.

Ion channel receptor

A receptor that forms a pore in the cell membrane; ligand binding opens the pore, changing membrane permeability (example: acetylcholine receptor at the NMJ; GABA-A/C channels).

Nicotinic acetylcholine receptor

Ligand-gated ion channel at the neuromuscular junction and autonomic ganglia; activation increases Na+ permeability leading to depolarization.

GABA-A receptor

Ligand-gated chloride channel in neurons; activation increases Cl− influx causing hyperpolarization.

GABA-B receptor

G-protein-coupled receptor that increases K+ efflux, leading to hyperpolarization.

Tyrosine-kinase receptor

A receptor with an extracellular ligand-binding domain and an intracellular tyrosine kinase domain; ligand binding activates phosphorylation and signaling.

Catalytic receptor proteins

Receptors that act as enzymes or recruit enzymatic activity (e.g., receptor tyrosine kinases) upon ligand binding.

G protein

A membrane-associated regulatory protein that transduces signals from activated receptors by binding GDP/GTP and activating effector proteins.

First messenger

The extracellular ligand that binds a surface receptor to initiate signaling.

Second messenger

Intracellular signaling molecules that relay and amplify signals from receptors (e.g., cAMP, Ca2+).

Cyclic AMP (cAMP)

A second messenger produced by adenylyl cyclase that activates protein kinase A and downstream signaling.

Calcium (Ca2+) as a second messenger

A versatile intracellular signal that activates kinases and regulates various cellular processes.

Cyclic GMP (cGMP)

A second messenger with regulatory (often inhibitory) roles in signaling pathways.

Protein kinase

Enzymes that transfer phosphate groups from ATP to target proteins, amplifying signaling cascades.

Second messenger amplification

A single receptor activation can generate many second messengers and downstream responses (amplification).

Affinity

The degree of attraction between a drug and its receptor.

Selectivity

The preference of a drug for a particular tissue or receptor subtype.

Efficacy

The ability of a drug to activate a receptor and produce a cellular response.

Agonist

A drug that binds to a receptor and initiates a cellular response.

Partial agonist

A drug that produces a less-than-maximal response even when occupying all receptors.

Antagonist

A drug that binds to a receptor but produces no receptor activation (no efficacy).

Competitive antagonist

Antagonist that binds the same site as the agonist and can be displaced by higher concentrations of agonist.

Non-competitive antagonist

Antagonist that binds to a different site or irreversibly inactivates the receptor.

Allosteric regulation

Regulation where a molecule binds to a site other than the active site to modulate receptor/enzyme activity.

Desensitization

Brief, temporary decrease in receptor responsiveness due to over-stimulation (tolerance).

Down-regulation

Prolonged decrease in receptor number/function from excessive exposure to ligand.

Up-regulation

Increase in receptor number/sensitivity due to reduced exposure to ligand.

Nicotinic receptor

Cholinergic receptor; ligand-gated; located at NMJ and autonomic ganglia; activated by nicotine.

Muscarinic receptor

Cholinergic G-protein-coupled receptor; five subtypes (M1–M5); mediates parasympathetic effects at effector tissues.

Adrenergic Alpha-1 receptor

Postsynaptic receptor; located in smooth muscle/vascular tissue; stimulation causes contraction of vascular smooth muscle and other responses.

Adrenergic Alpha-2 receptor

Presynaptic/inhibitory receptor; reduces neuronal excitability and inhibits sympathetic outflow.

Adrenergic Beta-1 receptor

Predominant in heart and kidney; increases heart rate, contractility, and renin release.

Adrenergic Beta-2 receptor

Located in smooth muscle (bronchioles, vasculature), uterus; causes bronchodilation and smooth muscle relaxation; also affects metabolism.

Adrenergic Beta-3 receptor

Located mainly in adipose tissue; stimulates lipolysis; also present in heart/smooth muscle.

Adenosine receptor

G-protein-coupled receptor with four subtypes; generally Gi-coupled; mediates inhibitory effects including heart rate reduction and coronary dilation; A1 activates K+ channels and inhibits Ca2+ channels.

Mu opioid receptor

Primary receptor for analgesia; activation produces analgesia but also respiratory depression, constipation, and potential addiction.

Kappa opioid receptor

Opioid receptor that provides analgesia with less respiratory depression but can cause sedation and dysphoria.

Delta opioid receptor

Opioid receptor involved in analgesia and modulation of mu effects.

ORL-1 receptor

Opioid receptor-like-1; distinct receptor in the opioid family.

Morphine

Prototype opioid analgesic with high affinity for mu receptors; used as a standard for opioid analgesia.

Endogenous opioids

Body’s own opioid-like peptides (endorphins, enkephalins, dynorphins) that activate opioid receptors.

Pharmacokinetics

What the body does to a drug: absorption, distribution, metabolism, and excretion (including first-pass effects).

Pharmacodynamics

What the drug does to the body: mechanisms of action and the relationship between drug concentration and effect.

Endosome signaling in opioids

Opioid receptor activation can involve endosome signaling that may alter adenylyl cyclase activity via intracellular pathways.

Non-receptor drug mechanisms

Drug actions not mediated by receptor binding (e.g., antimetabolites interfering with DNA/protein synthesis; antacids neutralizing stomach acid).