Exam 1: Membrane-Bound Receptors Flashcards Preview

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Flashcards in Exam 1: Membrane-Bound Receptors Deck (56):
1

Two types of gated ion channels:

Voltage-gated
Ligand-gated

2

Resting membrane potential:

-70mV

3

Define depolarization/excitation:

Membrane potential moves from -70mV towards 0mV

4

Define hyperpolarization/inhibition:

Membrane potential moves away from -70mV (becomes more negative)

5

How each type of channel contributes to AP propagation:

Ligand-gated ion channels begin AP
Voltage-gated continue it

6

Define agonist:

Ligand that binds to receptor and activates it

7

Define antagonist:

Ligand that binds to receptor that prevents it from activating

8

Three types of antagonists:

Orthosteric
Allosteric
Pore blocker

9

Define orthosteric antagonist:

Acts on the main binding site of the receptor

10

Define allosteric antagonist:

Acts on accessory binding site of receptor

11

Define pore blocker antagonist:

Physically obstructs the ion channel

12

Two main types of membrane-bound receptors:

Ligand-gated ion channels
G-protein coupled receptors

13

Relative transmission speed of ligand-gated ion channels:

Very fast

14

Structure of ligand-gated ion channels:

Several subunits around a central ion pore

15

Two major families of ligand-gated ion channels:

Cys-loop receptors
Ionotropic glutamate receptors

16

Examples of cys-loop receptors:

Nicotinic ACh
Glycine
5HT-3

17

Examples of ionotropic glutamate receptors:

AMPA receptor
NMDA receptor
Kainate receptor

18

Structure of cys-loop receptors:

Pentameric

19

Structure of ionotropic glutamate receptors:

Tetrameric

20

Cys-loop receptors are named for:

The loop formed by a disulfide bond between two cysteines

21

Five types of cys-loop subunits:

Alpha, beta, gamma, delta, epsilon

22

Excitatory cys-loop receptors:

Nicotinic ACh
Serotonin

23

Inhibitory cys-loop receptors:

Glycine
GABAa

24

Subunit that obstructs cys-loop receptor pore:

Transmembrane domain of the alpha subunit

25

Mechanism by which agonist binding activates cys-loop receptor:

Changes conformation to move obstructing part of alpha subunit

26

Drugs that act on cys-loop receptors:

Nicotine
Varenicline (Chantix)
Barbiturates
Benzos
ETOH
Ambien

27

Drugs that act on glutamate receptors:

Ketamine (NMDA)
Aniracetam (AMPA)

28

Nicotinic ACh receptors (nAChRs) are found:

Neuromuscular junction
CNS

29

Difference between NMJ and neuronal nAChR subunits:

NMJ receptors have α, β, δ, γ subunits
Neuronal only have α, β

30

Ions that pass through nAChRs:

Na+
K+
Some Ca++

31

Define desensitized state:

Ligand is bound, but gate is closed

32

Glutamate receptors are excitatory/inhibitory?

Excitatory

33

Ions that pass through glutamate receptors:

Na+
K+
Ca++ (NMDA only)

34

Composition of glutamate receptor subunits:

Binding site
Four transmembrane domains
Second TM domain is what forms ion pore

35

Binding sites on NMDA receptor:

Two glutamate
Two glycine

36

# of binding sites required to be occupied for glutamate receptor channel to open:

All four

37

Define long term potentiation:

More often a neuron fires, the stronger the synapse gets

38

Long term potentiation is critical for:

Learning and memory

39

NMDA receptors are normally blocked by _____ and this block is relieved by ______.

Mg++; voltage (depolarization)

40

Potentiation occurs in the neuron via addition of:

AMPA receptors

41

Relative speed of G-protein coupled receptors:

Much slower than ligand-gated

42

% of genome dedicated to GPCR coding:

3%

43

Class A GPCRs:

Adrenergic receptors
Muscarinic ACh receptors

44

Class B GPCRs:

Parathyroid hormone receptors

45

Class C GPCRs:

Metabotropic glutamate receptors
GABAb receptors

46

Alpha subunit action upon GPCR activation:

Binds to GPCR, GDP gets phosphorylated, binds to target protein, GTP gets hydrolysed

47

Three main types of G proteins:

GαQ
GαS
Gαi

48

Gαq activation causes:

PIP2 --> IP3 + DAG + PKC
Release of Ca++ from stores

49

IP3 + DAG are:

Lipid messengers

50

Gαq activation causes:

ATP --> cAMP + PKA

51

PKC and PKA are important because:

Small enough to enter the nucleus

52

Gαi activation causes:

Inhibition of receptor

53

Molecule that "tags" GPCRs that have been bound too long:

β-arrestin

54

What happens to GPCRs 'tagged' with β-arrestin:

Vesicle forms around GPCR and internalizes it

55

Cholera toxin works by:

Disrupting hydrolysis of GTP to GDP

56

Increased GTP from cholera toxin interference causes:

High cAMP levels
Activation of Cl- pumps
Cl- release into the intestinal lumen
Na+, K+, bicarb follow Cl-
Osmosis draws water into lumen