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Pharmacology test 1 > Membrane-Bound Receptors > Flashcards

Membrane-Bound Receptors Flashcards

1
Q

What are receptors

A

a way in which cells can communicate with each other and gain information about the area around them

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2
Q

2 types of receptors

A

ligand-gated ion channels and G protein coupled receptors

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3
Q

What binds to the receptor

A

ligands, which are a chemical messenger

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4
Q

What does a ligand do when it binds

A

induces a conformational change in the receptor tell the cell something about its environment. The receptor changes shape and tells downstream to do something.

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5
Q

what cells produce Action Potentials

A

neurons, muscle cells, and cardiac cells

-how these cells communicate with each other

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6
Q

How does the AP communicate and what starts in and keeps it going

A

the AP propagates down the axon of a neuron and jumps from the end of on neuron to the beginning of the next. -the ligand-gated ion channel starts the AP
-Voltage-gated ion channels propagate the signal

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7
Q

Excitatory

A

the inside of the cells charge approaches 0mV getting less negative
-Depolarization

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8
Q

Inhibitory

A

the inside of the cells charge becomes more negative, further away from creating an AP
-Hyperploarization

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9
Q

Resting membrane potential

A

inside of the cell has an overall negative charge of -70mV

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10
Q

Agonist

A

a ligand that binds to a receptor, thereby activating it

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11
Q

Antagonist

A

a ligand that binds to a receptor that prevents it from activating

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12
Q

Orthosteric Antagonist

A

Acts on the main binding site of the receptor, blocks the agonist from the binding site

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13
Q

Allosteric antagonist

A

acts on an accessory binding site of the receptor

-changes the receptor shape so the agonist can’t bind, doesn’t fit

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14
Q

Pore blocker

A

physically obstructs the channel

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15
Q

Ligand-Gated Ion Channel

A
  • fast transmission
  • composed of several subunits arranged around a central ion pore
  • agonist binding opens pore
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16
Q

Ligand-Gated Ion channel families

A
  • cys-loop receptors

- Ionotropic Glutamate Receptors

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17
Q

Cys-loop receptor types

A
  • nicotinic ACh receptor
  • glycine receptor
  • 5HT-3 receptor
18
Q

Ionotropic Glutamte receptor types

A
  • AMPA receptor
  • NMDA receptor
  • Kainate receptor
19
Q

Cys-Loop receptors

A
  • have a loop thats formed by a disulfide bond between two cysteine near the N-terminus
  • Made of 5 subunits arranged around a central pore: alpha, beta, gamma, delta, epsilon
20
Q

cys-loop excitatory

A

Nicotinic-ACh

Serotonin

21
Q

Cys-loop inhibitory

A

Glycine and GABAa

22
Q

Gating

A

This is what causes the ion pore to be closed

  • the second transmembrane of the alpha subunit is what forms the gate
  • agonist binding changes the conformation, moving the obstruction (gate) allowing ions to flow through
23
Q

drugs that act on cys-loop receptors

A
  • nicotinic-ACH: nicotine, Carenicline (chantix)

- Barbituates, benzos, alcohol, ambien

24
Q

drugs that act on Glutamate receptor

A

NMDA receptors: Ketamine

AMPA receptors: Aniracetam (cognition-enhancer)

25
Q

Nicotinic-ACH receptor

A

exist at the neuromuscular junction (NMJ) and in the CNS

  • composed of 5 subunits
  • NMJ nAChR contains alpha, beta, gamma, and delta
  • Neuronal nAChRs contain only alpha and Beta subunits
  • in the brain nAChRs upregulate in response to chronic nicotine like smoking
26
Q

nAChR excitatory

A

pass Na, K, and some Ca ions

27
Q

Iontropic Glutamate Receptors

A
  • AMPA
  • NMDA
  • Kainate
  • composed of 4 subunits
  • -each subunit has 4 transmembrane domains and the 2nd transmembrane forms the ion pore
  • each subunit has a binding site-not all binding sites are for glutamate
28
Q

Iontropic Glutamate Receptors, excitatory

A

pass Na and K ions

NMDA receptors can also pass Ca ions

29
Q

NMDA receptor binding sites

A

2 binding sites for glutamate, 2 binding sites for glycine

-all 4 binding sites must be occupied for the channel to open.

30
Q

long term potentiation

A

the more often a neuron fires the stronger the synapse gets

31
Q

NMDA receptors at resting membrane, and what happens when activated

A

NMDAr are blocked by Mg

  • Mg is voltage dependent
  • depolarization of neuron relieves the block, allows NMDAr to open
  • When open Ca can pass which activates Ca calmodulin Kinase II
  • which leads to AMPARs being inserted into the synapse
  • more AMPARs=stronger synapse
  • NMDARs are “coincidence detectors”
32
Q

G-Protein-Coupled receptors (GPCR)

A

slower signaling that ligand-gated ion channels

  • relay on 2nd messenger
  • 3% of our genome dedicated to GPCR coding
  • *target for more than 1/2 of current drugs
33
Q

GPCR classes

A

A:adrenergic receptors, muscarinic acetylcholine receptors
B:Parathyroid Hormone receptor
C: metabotropic glutamate receptors, GABAB receptors

34
Q

G-Proteint activation

A
  • ligand binds to receptor
  • GDP is traded for a GTP on the alpha subunit
  • Beta/gamma break off
  • Alpha and GTP activate target protein
  • activation is terminated when GTP is hydrolyzed to GDP
35
Q

G alpha S

A

activation of adenylyl cyclase and increase in cAMP

36
Q

G alpha I

A

inhibition of adenylyl cyclase and decrease in cAMP

37
Q

G alpha Q

A

activation of phospholipase C, phosphoinositol hydrolysis, increase in IP3 and DAG, and release of Ca2+ from intracellular stores

38
Q

Downstream targets of GPCR

A
  • Target enzymes: Adenylate cyclase and phospholipase C
  • 2nd messengers: cAMP, IP3, DAG
  • Protein kinases: PKG, PKA, PKC
  • Effectors: enzymes, transport proteins, contractile proteins, Ion channels
39
Q

GPCR desensitization

A

if a ligand is bound onto a GPCR for a prolonged time it is phosphorated by a specific kinase

  • Beta-Arresting binds to the receptor,
  • causing it to loose its ability to associate with G-protein, which tags it for internalization
  • undergoes endocytosis which removes its receptor fro the membrane.
  • -this contributes to drug tolerance
40
Q

GPCR-beta arrestin

A

can act as a protein scaffold inside the cell. Contains the GPCR
-this is independent of G protein signaling

41
Q

Cholera Toxin Mechanism

A
  • cholera toxin is internalized by the cell
  • disrupts conversion of GTP to GDP (blocks GTPase activity preventing inactivation)
  • increases level of GTP leads to abnormally high cAMP levels
  • -this activates Cl ion pumps which release more Cl into the investing lumen
  • -Na, K and bicar ions follow–leading to more water being held in the intestine to balance osmolarity

Pharmacology test 1 (4 decks)

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