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These flashcards review key concepts about receptors, signaling molecules, GPCRs, ligand-gated ion channels, second messengers, receptor regulation, and clinical correlations such as diabetes.
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What are the two main classes of signaling molecules discussed in the lecture?
Hormones and neurotransmitters.
From which tissues are hormones and neurotransmitters released, respectively?
Hormones are released from endocrine (glandular epithelial) tissue, while neurotransmitters are released from neurons.
Why do signaling molecules require receptors on target cells?
Without receptors to bind and initiate downstream responses, the molecules would have no functional effect.
What is receptor specificity?
The property that only certain signaling molecules (sometimes just one) can bind to a given receptor.
Which receptor type functions as both a receptor and an ion channel?
Ligand-gated ion channels.
Describe the immediate cellular effect of a ligand-gated sodium channel opening.
Sodium influx depolarizes the cell.
Give one classic example of a ligand-gated ion channel and its ligand.
Cholinergic nicotinic receptor with acetylcholine as its ligand.
What primary structural components make up most receptors?
Proteins that span the plasma membrane.
Why do polar (lipophobic) signaling molecules need surface receptors?
They cannot cross the hydrophobic lipid core of the plasma membrane on their own.
Define a G-protein coupled receptor (GPCR).
A membrane receptor linked to an intracellular G-protein that triggers a cascade when activated by a ligand.
What nucleotide switches a G-protein from inactive to active form?
GDP is exchanged or phosphorylated to GTP.
Name two common second messengers generated through GPCR cascades.
Cyclic AMP (cAMP) and calcium ions (Ca²⁺).
Which cholinergic receptor subtype is GPCR-linked?
Muscarinic receptors.
What are the two broad categories of adrenergic receptors for norepinephrine/epinephrine?
Alpha (α) receptors and beta (β) receptors.
Define receptor saturation.
The state in which all available receptors on a cell are occupied by ligand.
What is receptor upregulation and when might it occur?
Insertion of additional receptors into the membrane; occurs when cells need more signaling (e.g., muscle during exercise).
Explain receptor downregulation.
Removal or decrease of receptors when ligand levels are chronically high, reducing cellular response.
How is type 2 diabetes related to receptor downregulation?
Chronic high insulin causes insulin-dependent cells to remove insulin receptors, diminishing glucose uptake.
Why can uncontrolled diabetes impair brain glucose uptake?
The blood-brain barrier downregulates glucose transporters in response to prolonged high blood glucose, risking shortages when glucose later falls.
Differentiate agonists and antagonists.
Agonists mimic the natural ligand and trigger the same response; antagonists bind but block receptor activation.
How do some bacterial toxins (e.g., cholera, botulism) cause disease in relation to receptors?
They interfere with GPCR signaling, blocking or misregulating downstream events.
Where are receptors for non-polar (lipophilic) signaling molecules typically located?
Inside the cell, in the cytoplasm or nucleus, because these molecules cross the membrane easily.
What intermediate role does depolarization play in neurons and pancreatic β-cells?
In neurons it triggers neurotransmitter release; in β-cells it triggers insulin release.
Why don’t circulating hormones activate every cell they encounter?
Only cells that express specific receptors for the hormone will respond.