ion channels n ionotropic receptors Flashcards

1
Q

why is phosolipid bilyer called as parallel capacitor and resistor

A

ions are unable to penetrate the lipid bilayer of the cell membrane(resistor)

and phospholipid bilayer (insulator ) separates the intracellular space from the extracellular space

the intrinsic electivcal conducted of this structure is very poor(resistor function)

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2
Q

presence of ion channel effect on resistance

A

since the ion channel act as conduits, allow fro flow of ions across the phospholipid bilayer

  • decreased resistance
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3
Q

what is membrant potential

A

generated by the differential distribution of ions, particularly Na+, K+ and Cl-

unequal distribution is maintained by ionic pumpus and exchanges

usually -60–75 (diff resting potential for. iff cells )
can also change while the cells are at different level of activity

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4
Q

what are important ions in resting potential and where are they present at higher conc

A

na -outisde
k-inside
ca-outside
cl-outside

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5
Q

what are the propertioes of ion channel

A

rate and direction of ion movemnr thru the pores is governed by electrochemical gradient of the ions in question, which is a function of its concentrations on either side of the membrane , and of the membrane potential

  • selectivity( selective to specific ions)
  • gating properties (type of control of the ion channel)
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6
Q

ion channels protein

A

transmembrane protein
- pore domain
have voltage sensing domain
ligand binding domain
span across the membrane

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7
Q

what are the different type of gatinf of the ion channels

A

passice (kk + leak channel)
voltage gated (Na, ca, k voltage gated channel)
mechnically gated(baroreceptors and hair cells)
ligand gated (nicotinic acetylcholine, GABA receptor )

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8
Q

what s action potential mechanism

A
  1. resting potenital (with ligand gat are closed )
  2. stimulus cause some channel to open
  3. when the threshold is reached, the action potential occue, more gated channel opens
  4. depolarization occcuer: sodium rush into the cell
  5. when the voltage is more than 30mv, voltage channel NA+ closes
  6. k+ channel opens
  7. repolarisation occur where k rush out of the cell
  8. voltage will decrease below -70
  9. k + channel clsoes
  10. an + and k+ pump restore the resting potential of the cell
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9
Q

how does signalling happen in one direction only?

A

when is it depolarsing the behind is repolarising, allowing for signal to only move in one direction

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10
Q

two different type of refracotry period an what they do

A

absoulte and relative
absolute means that another action potential cannot be triggered during this time
Na+ channel are briefly inactviated
and membrane need to be hyper polarised before depolarisation can happen

for relative refractory period,
a stong stimular can cause Ap
- Since membrane is below the resting potential, strong EPSP can trigger the threshold

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11
Q

what improves the AP propogation

A

myeline shealths which are rich in lipids, they are made of oligodendrocytes in CNS and svuann cell in PNS

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12
Q

what happens when AP reaches the end

A

depolarisaion trigger voltage gaterd channel
ca2+ channel open
ca2+ enetr
exocytosis of vesicles
neurotransmitters released into synaptic cleft
neurotransmitters bind to receptor on post synaptic neurons
EPSP/IPSP
Trigger another AP

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13
Q

what happens when sodium channel is clocked

A

increase in threshold for excitation
slow impulse conduction
decreased rate of rise of AP
decreased amplitude of AP
when blocked at critical length, propagation across the blcojed area is impossibl

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14
Q

what are drugs used as sodium blocker

A

local anaestheitc agents , cocaine, lidocaine

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15
Q

what are channels that regulate the calcium in and out

A

ligand gated ca channle
voltage gated ca channel
ryanodine receptor
store operated calcium channels
NA ca exchange

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16
Q

state the calcuim effect on cardiac/skeletal msucle

A

AP travel down the sacolemma

causes openong of the ryanodine and voltage gated ca channel

ca rush into the cell

ca diffuse with cytoplasm towards active filaments(g actin monomers)

ca bind to troponin

confirmation change in troponin

tropomyosin move

g actin active site is exposed, myosin bind to g actin

form cross bridge that causes muscular contraction

17
Q

state the calcium effect on smooth muscles

A

when there is a increase in free intracellular calcium

increase in calcium influx into the cell
or by release of calcukm from internal stores

free calcium bind to the calmodulin

calcium calmodulin activates myosin light chain kinase
this phosphorylates the myosin light chains in the presence of ATP

myosin light chains are found on the myosin heads

myosin light chains phsophorylation leads to smooth muscle contraction

18
Q

what is the effect of the L type calcium blockade in the heart

A

reduced in contractility
decreases sinus node pacemaker rate
decrease atrioventricular node condition velocity
use In the treatment of angina and supraventricular tachyarrhythamias

19
Q

what is the effect of the L type calcium blockade in the smooth muscles

A

losg lasting relaxation
dilate peripheral arterioles and reduce blood pressure
use in the treatment of hypertension

20
Q

list other ligand gated channels

A

glutamate
acetylcholine
GAB
5HT
ATP

21
Q

List the calcium channel blockers

A

amiodpine
verapamil

22
Q

what are the molecules for GABA receptor

A

benzoidiazepines and zolpidem

23
Q

what do GABA regualte

A

it is a gab RECEPTOR CHOLORIDE CHANNEL COMPLEX

24
Q

what does GABA do ?

A

postsynaptic
increse the cl- influx from outside

25
Q

what are the selective agnoist and antagosit of GABA

A

agonist : isoguvacine and antagonist :biuculline

26
Q

what are the regulatory sites on the GABA

A

benzodiazepine and barbiturate sites

27
Q

what do benzodiazepines do ?

A

potentiate GABA action by increasing the frequency of GABA induced channel opening

28
Q

what does phenobarbital do?

A

increases the frequence and duration of opening

29
Q

what are the clincial application of benzodiazepines

A

anti anxity agenst
sedative agents
anti-epileptic drugs
general anaesthetic agents

30
Q

what are nicotinic acetylcholine receptors

A

extensive projection out of the membrane
chaneel pore with a narrow spot
closed intracellular end of the channel with laterally places outlets for ions

  • subtype found in the skeletal muscles, neurons and autonomic ganglia
31
Q

what are the seletive agonist and antagonist of nicotinic acetylcholine receptors

A

nicotine is the agonist
a bengartoxin is the antagonist

32
Q

what do neuromuscular blocking drugs

A

block nitonic receptors function resulting in skeletal muscle paralysis
- used during surgical procedures as muscles relaxants

33
Q

how are neuromuschlar blocking drugs divided?

A

non depolarising drugs - act as antagonist at the nicotinic receptors

depolarising drugs- act as agnosit at the nicotinic receptors : causing persisten depolarising following by desensitization of the nictonic receptors

34
Q

what are non depolarizing neuromuscular blocking drugs

A

pancuronium, atracurium and tubocurarine

35
Q

what are depolarizing neuromuscular blocking drugs

A

succinylcholine

36
Q

name 2 dieases due to defective ino channel functions

A

function 1: cystic fibrosis
function 2: long qt syndrome

37
Q

what is cyctsic fibrosis

A

mutation in the epithelial chloride channel cftr(transmembrane conductance regulator)
- deletion of the phenylalanine at position 508, the defective protein cannot reach the surface membrane
- causes impaired cl, conductance in the membrane of the secretory epithelial cells
— in the lungs, this loss of CFTR activity leads to the dehydration in the airway epithelia, thickening mucus, build up of thick mucus promotes bacterial growth and potentially serious lunch infection

38
Q

what is long qt syndrome

A

mutation in the cardiac potassium channels(HERG, KCNQ1, KCNE1, KCNE2)
loss of function and reduced potassium currents
long AT intervals in the electrocardiogram, reflecting the delayed repolarization of the caridia action potential

– results in irregular heart beat — and muscle weakness

39
Q
A