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Cell physiology and pharmacology > Lecture 13- Intracellular signalling and calcium homeostasis > Flashcards

Lecture 13- Intracellular signalling and calcium homeostasis Flashcards

(43 cards)

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1
Q

how much calcium in the body

A

1kg

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2
Q

where is most calcium found

A

in bones (99%)

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3
Q

concentration of calcium in the blood serum

A

8-10 mg/dL (50% free calcium)

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4
Q

whole body calcium homeostasis is regulated via

A

• Intestinal calcium uptake • Ca2+ reuptake by the kidney • Bone calcium regulation

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5
Q

how is calcium homeostasis controlled hormonally

A

• Ca2+ sensing receptors in the parathyroid (GPCR) • Parathyroid hormone receptor • Calcitonin receptors • Vitamin D3- nuclear receptors

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6
Q

concentration of calcium in the cytoplasm

A

low 1 x 10^-7 M

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7
Q

concentration of calcium outside the cell

A

high (same conc as blood) 1-2 x10^-3M

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8
Q

concentration of calcium outside in the endoplasmic reticulum/ SR

A

high 2-3 x 10^-4

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9
Q

why is calcium important

A

• Muscle contraction • NT/ stimulus-secretion coupling • Fertilisation • Cell death (apoptosis) • Regulation of metabolism • Learning and memory

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10
Q

plasma membrane is

A

impermeable to calcium

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11
Q

specific pumps and transporters

A

move calcium in and out of the cell

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12
Q

what decrease the free level of calcium

A

buffer proteins within the cytoplasm

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13
Q

channels which decrease intracellular [calcium]

A
  1. PMCA 2. SERCA 3. NXC
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14
Q

PMCA

A

plasma membrane calcium ATPase uses ATP to pump calcium out of the cell

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15
Q

SERCA

A

sarcoplasmic reticulum calcium ATPase Uses ATP to pump calcium in the SR from the cytoplasm

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16
Q

NCX

A

sodium calcium exchanged calcium exchanged for sodium

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17
Q

channels which increase levels of calcium in the cell (Influx)

A

• Ligand gated ion channel • Voltage gated channels

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18
Q

how is calcium moved out of the SR

Study These Flashcards
A
  • Calcium induced calcium release (CICR)- ryanodine receptors - IP3R receptors (think Gq)
19
Q

effectors stimulated by GPCR G protein can be

Study These Flashcards
A

enzymes (2nd messengers) or ionic channels

20
Q

example of ionic channels

Study These Flashcards
A

• Voltage gated calcium channels (VOCCs) • G-proteins evaluated inwardly rectifying K+ channels (GIRKs)

21
Q

example of 2nd messengers

Study These Flashcards
A

• Adenylyl cyclise (ATP —> cyclicAMP) • Phospholipase C (PIP2–> IP3 + DAG) • Phosphoinositide 3-kinase (P13K) • cGMP phosphodiesterase (cyclic GMP —> 5’-GMP)

22
Q

outline agonist binding to Gs GPCR

Study These Flashcards
A
  1. Agonist binds to GPCR
  2. Causes GDP for GTP exchange in G-protein
  3. AlphaS and BY subunits dissociate
  4. AlphaS-GTP activates AC
  5. AC converts ATP to cAMP
  6. cAMP activates PKA
23
Q

cAMP exerts the majority of its effects via

24
Q

PKA structure

Study These Flashcards
A
  • x2 C subunit contain protein kinase subunit
  • x2 R subunit is where CAMP binds
25
how many cAMP bind to each regulatory region
2 (4 in total)
26
when cAMP binds to PKA
this causes it to release the catalytic subunit (covalent change) , so it can act as a PK and phosphorylate other proteins to activate them (usually phosphorylation serine or threonine residues) - Therefore when CAMP increases so does the activity of PKA
27
outline agonist binding to Gi GPCR
1. Agonist binds to GPCR 2. Causes GDP for GTP exchange in G-protein 3. AlphaI and BY subunits dissociate 4. AlphaI inhibits adenyl cyclase 5. No production of cAMP 6. No activation of second messengers- no signal transduction
28
which G protein is activated to regulate phospholipase C (PLC)
Gq
29
outline agonist binding to Gq GPCR
1. Agonist binds to GPCR 2. GDP for GTP exchange in G protein 3. Alphaq – GTP activates phosoholipase C (PLC) 4. PLC catalyses the hydrolysis of PIP2 5. PIP2  DAG (still associated with membrane)+ IP3 6. IP3 diffuses through cytoplasm and binds to IP3 receptros and causes them to open 7. Allows movement of calcium out of SR/ER 8. DAG has its own PK and phosphoryklates PKC
30
IP3 binds to
IP3R
31
IP3R activation can
increase cytoplasmic [CA2+] by 5-10fold within a few seconds of agonist addition
32
key feature of signalling pathways
signal amplification
33
signal amplification
- allows small amount of ligand e.g. hormone to cause a relatively large response within the cells • E.g. For a few molecules of adrenaline binding to surface of B-adrenoreceptors may cause a massive cellular response
34
inotropy
strength of contraction
35
chronotrophy
heart rate
36
outline how B1- adrenoreceptors can be stimulated to cause positive inotropy
1. Adrenaline binds 2. Activates alphas (can also directly activate VOCC) activates AC 3. AC produces cAMP 4. cAMP activates PKA 5. PKA phosphorylates VOCC (voltage gated calcium channels) 6. Increases intracellular calcium 7. Increase contractility of the heart
37
sympathetically released noradrenaline interacts with alpha1 adrenoreceptors of smooth muscle
vasoconstriction
38
parasympathetic ally release ACh can interact with bronchiolar smooth muscle M3 receptors causing
bronchoconstriction
39
smooth muscles all utilise
Gq- Phospholipase C (PLC)
40
smooth muscle utilisation of Gq
Phospholipase C (PLC) • IP3 causes release of calcium from SR (triggers contraction) • PKC activated (sustained contraction) • Leads to prolonged contraction of the smooth muscle
41
At the presynaptic neurone, GPCRs
can regulate NT release
42
BY subunit of G inhibits specific types of
Can VOCCs reducing calcium influx and NT release at the synaptic cleft
43
U-opiod reeptor
1. Morphine binds to U-opioid receptor 2. Gi protein 3. Activates GI (GDP for GTP exchange) 4. Causes release of both alpha and BY subunits 5. BY binds to VOCC and inhibit VOCC 6. This means that the next time there is a depolarisation, the VOCC is inhibited 7. Meaning less NT is released into synaptic cleft 8. Reduced transmission of AP from neurone to neurone • 80-90% of inhibition

Cell physiology and pharmacology (20 decks)

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