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Cell Communication Flashcards

1
Q

Order of bonds from weakest to strongest :
Hydrogen, Ionic, Van der Waals, Covalent, Hydrophobic

A
  1. Van der Waals
  2. Hydrophobic
  3. Hydrogen
  4. Ionic
  5. Covalent
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2
Q

Order of GCPR signaling (5)

A
  1. first messenger (ligand)
  2. GCPR
  3. Effector
  4. Second messenger
  5. Cellular response
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3
Q

What does Adenylyl Cyclase stimulate/inhibit?

A

Cyclic AMP (cAMP)

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4
Q

What does Phospholipase C stimulate?

A

Inositol Triphosphate (IP3)
& Diacylglycerol (DAG)

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5
Q

What is the function of adenylyl cyclase?

A

to convert ATP to cAMP

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6
Q

What GCPR turns on adenylyl cyclase?

A

Gs

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7
Q

What GCPR turns off adenylyl cyclase?

A

Gi

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8
Q

Stimulatory GCPRs

A

Gs & Gq

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9
Q

Inhibitory GCPR

A

Gi

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10
Q

What GCPR stimulates more cAMP?

A

Gs

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11
Q

What GPCR inhibits the release of cAMP?

A

Gi

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12
Q

What is the function of Phospholipase C?

A

Converts PIP2 to IP3 & DAG

PIP2 - phospha-tidyl-inositol, 4-5 biphosphate
IP3 - Inositol triphosphate
DAG - Diacylglycerol

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13
Q

What GPCR stimulates Phospholipase C?

A

Gq (G11)

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14
Q

What enzyme liberates arachidonic acid from the cell membrane?

A

Phospholipase A2

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15
Q

What does increased cAMP in cardiac monocytes result in?

A

Enhanced contractility (beta-1 effect)

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16
Q

What does increased cAMP in the smooth muscle of the airways and vessels cause?

A

Relaxation & Dilation (beta-2 effect)

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17
Q

What does increased cAMP in platelets result in?

A

Increased platelet aggregation

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18
Q

What does increased cAMP do in the principal cells of the nephron?

A

increase in aquaporin-2 water channels

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19
Q

What enzyme produces IP3 and DAG from PIP2?

A

Phospholiapase C

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20
Q

What is the primary NT in the peripheral efferent (motor) neural pathway?

A

Acetylcholine

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21
Q

What does Acetylcholine control peripherally vs centrally?

A

peripherally- motor function
centrally - sleep, wakefulness (RAS), learning and memory

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22
Q

How is Acetylcholine eliminated?

A

By Acetylcholinesterase (AChE) in the synaptic cleft

-it hydrolyzes ACh into acetate and choline
-Choline is taken back up to the pre-synaptic terminal for recycling

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23
Q

Why can magnesium cause muscle weakness or potentiate neuromuscular blockade?

A

Because magnesium antagonizes calcium at the presynaptic nerve terminal. Without calcium going into the presynaptic nerve terminal, acetylcholine can’t be released from the vesicles.

-No ACh release, decrease in skeletal muscle contraction

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24
Q

Which cholinergic receptor is the ion-gated one?

A

Nicotinic

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25
Q

Which cholinergic receptor is the GPCR?

A

Muscarinic

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26
Q

What must happen for the nicotinic ion channel to open?

A

Acetylcholine must bind simultaneously to the two alpha subunits on the receptor

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27
Q

Which cholinergic receptor type is inhibitory and which is excitatory?

A

Excitatory: Nicotinic (N1/N2, Nm/Nn), M1, M3, M5
Inhibitory: M2, M4

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28
Q

Where are NmAChR’s found?

A

NMJ of skeletal muscles

29
Q

Where are NnAChR’s found? (3)

A

Autonomic ganglia
CNS
Adrenal Medulla

30
Q

What 4 things can bind to the NMDA receptor?

A
  1. Glutamate
  2. Glycine
  3. Ketamine
  4. Magnesium
    (Tylenol, nitrous)
31
Q

What specific receptor does Propofol target?

32
Q

What is the primary excitatory NT in the brain?

33
Q

Where is Glycine the primary inhibitory NT? (2)

A

In the spinal cord and lower brainstem.

34
Q

Are GABA receptors ionotropic or metabotropic?

A

GABA-A is ionotropic
GABA-B is metabotropic

35
Q

What 6 things is GABA-A a receptor for?

A
  1. Propofol
  2. Benzos
  3. Volatile Anesthetics
  4. Etomidate
  5. Barbiturates
  6. Alcohol
36
Q

What is the primary inhibitory NT in the brain?

37
Q

Where are NMDA and AMPA receptors found to be most prevalent?

A

Hippocampus & Cerebral Cortex

38
Q

All catecholamines are synthesized from what?

A

Tyrosine (Amino acid)

39
Q

Serotonin is synthesized from what?

A

Tryptophan

40
Q

Histamine is synthesized from what?

41
Q

What is the primary NT in the SNS?

A

Norepinephrine

42
Q

What is the rate-limiting step in catecholamine synthesis?

A

Tyrosine hydroxylase converting Tyrosine to L-DOPA

43
Q

What 2 enzymes are catecholamines metabolized by?

A

MAO & COMT

Monoamine oxidase &
Catechol-O-Methyltransferase

44
Q

What are the 5 biogenic amine neurotransmitters?

A
  1. Dopamine
  2. Norepinephrine
  3. Epinephrine
  4. Serotonin
  5. Histamine
45
Q

5 Steps in catecholamine synthesis

A
  1. Tyrosine > DOPA (tyrosine hydroxylase*)
  2. DOPA > Dopamine (Dopa decarboxylase)
  3. Dopamine transported into vesicles
  4. Dopamine > NE (dopamine Beta hydroxylase)
  5. NE > Epi (Phenyl-ethanolamine N-methyltransfersase (PNMT)
46
Q

What’s the most important method of removal of catecholamines from the synaptic cleft?

A

REUPTAKE

(diffusion happens first, but it’s mainly removed via reuptake)

47
Q

What is the end product of dopamine metabolism and how is it excreted?

A

Homovanillic acid

Excreted in urine

48
Q

Where is the largest concentration of dopaminergic neurons in the brain?

A

The substantia nigra

Located in the midbrain
-coordination of motor movements + fine motor control via basal ganglia

49
Q

What are dopaminergic neurons in the substantia nigra crucial for?

A

coordinating motor movements

50
Q

Degeneration of dopaminergic neurons in the substantia nigra leads to what?

A

Parkinson’s Disease

51
Q

Where is the largest concentration of non-adrenergic (NE) receptors in the CNS?

A

Locus Coeruleus (in the pons)

52
Q

Adrenergic (Epi) receptors in the CNS can be found in what main two places?

A
  1. Rostral Ventrolateral Medulla
  2. Nucleus Tractus solitarius
53
Q

Activation of which receptor inhibits further release of NE?

A

Pre-synaptic Alpha 2

54
Q

5-HT3 antagonists work by blocking receptors in which two locations?

A
  1. Area postrema
  2. Vagus nerve
55
Q

What is the substrate for nitric oxide synthase (NOS)?

A

L-arginine

56
Q

Nitric oxide synthase (NOS) catalyzes the oxidation of L-arginine to what two end products?

A
  1. L-citrulline
  2. Nitric Oxide
57
Q

What is the substrate for guanylyl cyclase?

A

Guanosine Triphosphate (GTP)

58
Q

What converts GTP to cGMP (2nd messenger)?

A

Guanylyl cyclase

59
Q

What are the 3 pureinergic NTs?

A
  1. ATP
  2. ADP
  3. Adenosine
60
Q

What are two ligands for receptor tyrosine kinases (RTKs)?

A
  1. Insulin
  2. Growth factors
61
Q

T4 in the cell is converted to T3 by what?

A

Deiodinase

(de)iodine-ase

62
Q

What syndrome is associated with congenital hypothyroidism?

63
Q

In the presynaptic nerve terminal, opioid-activated G-protein (beta,gamma) subunits block what kind of voltage-gated ion channels?

64
Q

What are the 4 types of opioid receptors?

A
  1. Mu (MOR)
  2. Delta (DOR)
  3. Kappa (KOR)
  4. Nociceptin (NOR, OR1)
65
Q

What type of GPCRs are opioid receptors?

66
Q

Do Opioid receptors exhibit inhibitory effects on pre or postsynaptic neurons?

67
Q

How do opioids inhibit the presynaptic neuron?

A

The beta/gamma subunit blocks voltage-gated calcium channels, reducing NT release into the synaptic cleft

68
Q

How do opioids inhibit the postsynaptic neuron?

A

Gi alpha subunit inhibits adenylyl cyclase, cAMP, and PKA –> modulation of sodium gated ion channels

*ANS (4 decks)

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