Receptors

Question 0

Agonist vs. Antagonist

Answer 0

Agonist: a ligand that binds and activates a receptor
Antagonist: a ligand that binds to a receptor, preventing it from activating

Question 1

Excitatory vs. Inhibitory

Answer 1

Excitatory: inside the cell’s charge approaches 0 mV, gets more positive, depolarizes
Inhibitory: inside the cell’s charge becomes more negative, hyperpolarizes

Question 2

Orthosteric antagonist vs. allosteric antagonist

Answer 2

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
“Allosteric.. Accessory”

Question 3

What is a pore-blocker antagonist?

Answer 3

Physically obstructs the channel (ion channels), ex: put duct tape over the key-hole

Question 4

What are cys-loop receptors?

Answer 4

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

Question 5

What are the excitatory and inhibitory cys-loop receptors?

Answer 5

Excitatory: nicotinic acetylcholine receptors (nicotine, chantix) and serotonin receptors
**nicotinic Ach receptors upregulate to chronic nicotine
Inhibitory: glycine and GABA-A

Question 6

Which specific subunit is responsible for obstructing the ion pore/ blocking the gate?

Answer 6

Alpha subunit

Question 7

What are Ionotropic Glutamate Receptors?

Answer 7

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

Question 8

Excitatory Ionotropic Glutamate receptors pass Na and K ions, which specific receptor can also pass Ca ions?

Answer 8

NMDA receptors

Question 9

What is long term potentiation? What does it the application?

Answer 9

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.

Question 10

What speed do ligand-gated ion channels work vs. G-protein coupled receptors?

Answer 10

Ligand-gated are very quick

G-protein are slow, rely on secondary messengers, but it works for a longer period of time

Question 11

What are the three classes of G-protein coupled receptors?

Answer 11

Class A: adrenergic receptors, muscarinic ACh receptors
Class B: PTH receptor
Class C: metabotropic glutamate receptors, GABA-B receptors

Question 12

How are G proteins activated?

Answer 12

GTP is hydrolyzed to GDP and that allows downstream effects to occur

Question 13

What does G-alpha-S do with adenylyl cyclase and cAMP?

Answer 13

Activates adenylyl cyclase and increases cAMP

**This causes smooth muscle relaxation/dilation, increased HR, increased cardiac contractility

Question 14

What does G-alpha-I do with adenylyl cyclase and cAMP?

Answer 14

Inhibits adenylyl cyclase and decreases cAMP

**This leads to vasoconstriction, increased K conduction which hyperpolarizes

Question 15

What does G-alpha-Q do with phospholipase C, phosphoinositol hydrolysis, IP3 and DAG, and calcium?

Answer 15

Activation of phospholipase C and phosphoinositol hydrolysis, increase in IP3 and DAG, releases calcium from intracellular stores
**This causes contraction and vasoconstriction

Question 16

What causes G protein receptor desensitization?

Answer 16

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

Question 17

What does the cholera toxin do?

Answer 17

When internalized by the cell, it disrupts conversion of GTP to GDP. Increased GTP leads to higher cAMP levels which activates Cl ion pumps, releasing more Cl into the intestines. Then Na, K, and bicarb ions follow, leading to increased water reabsorption