Flashcards in Receptors Deck (18):
Excitatory vs. Inhibitory
Excitatory: inside the cell's charge approaches 0 mV, gets more positive, depolarizes
Inhibitory: inside the cell's charge becomes more negative, hyperpolarizes
Agonist vs. Antagonist
Agonist: a ligand that binds and activates a receptor
Antagonist: a ligand that binds to a receptor, preventing it from activating
Orthosteric antagonist vs. allosteric antagonist
Orthosteric: acts on the main binding site, blocks the agonist from binding so it is stuck inactive, competitive ex: changing the key so it doesn't fit the lock
Allosteric: acts on an accessory binding site of the receptor making it hard for anything else to bind, noncompetitve ex: breaking the lock
What is a pore-blocker antagonist?
Physically obstructs the channel (ion channels), ex: put duct tape over the key-hole
What are cys-loop receptors?
Ligand gated ion channel, formed by the disulfide bond between 2 cysteines near the N-terminus
5 subunits/ pentamer arrangement
Types: Nicotinic ACh receptors, barbituates, benzos, alcohol
What are the excitatory and inhibitory cys-loop receptors?
Excitatory: nicotinic acetylcholine receptors (nicotine, chantix) and serotonin receptors
**nicotinic Ach receptors upregulate to chronic nicotine
Inhibitory: glycine and GABA-A
Which specific subunit is responsible for obstructing the ion pore/ blocking the gate?
What are Ionotropic Glutamate Receptors?
Ligand-gated ion channels with 4 subunits/ tetromere arrangement, all 4 sites must be occupied for the gate to open (glutamate and glycine)
Types: AMPA receptors (Aniracetam), NMDA receptors (Ketamine), and Kainate receptors
Excitatory Ionotropic Glutamate receptors pass Na and K ions, which specific receptor can also pass Ca ions?
What is long term potentiation? What does it the application?
The more often a neuron fires, the stronger a synapse gets, used in learning and memory, "exercising the brain"
More specifically, at resting potential, NMDA receptors are blocked by Mg. Depolarization allows NMDA receptors to open and pass Ca which activates CaMKII which leads to AMPA receptors inserted into the synapse. The more AMPA receptors, the stronger the synapse, uses positive feedback.
What speed do ligand-gated ion channels work vs. G-protein coupled receptors?
Ligand-gated are very quick
G-protein are slow, rely on secondary messengers, but it works for a longer period of time
What are the three classes of G-protein coupled receptors?
Class A: adrenergic receptors, muscarinic ACh receptors
Class B: PTH receptor
Class C: metabotropic glutamate receptors, GABA-B receptors
How are G proteins activated?
GTP is hydrolyzed to GDP and that allows downstream effects to occur
What does G-alpha-S do with adenylyl cyclase and cAMP?
Activates adenylyl cyclase and increases cAMP
**This causes smooth muscle relaxation/dilation, increased HR, increased cardiac contractility
What does G-alpha-I do with adenylyl cyclase and cAMP?
Inhibits adenylyl cyclase and decreases cAMP
**This leads to vasoconstriction, increased K conduction which hyperpolarizes
What does G-alpha-Q do with phospholipase C, phosphoinositol hydrolysis, IP3 and DAG, and calcium?
Activation of phospholipase C and phosphoinositol hydrolysis, increase in IP3 and DAG, releases calcium from intracellular stores
**This causes contraction and vasoconstriction
What causes G protein receptor desensitization?
When a ligand binds to a G-protein receptor for a prolonged period of time, beta-arrestin acts as a scaffold inside the cell by binding to the receptor, tagging it for internalization. This contributes to drug tolerance because the body thinks there is too much of the drug, so it down-regulates receptors, with less receptors, you need a higher dosage of the drug to create the same effect