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bio membranes Flashcards

1
Q

The major interaction responsible for stabilising the plasma membrane

A

Hydrophobic interactions

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2
Q

What structural features of the plasma membrane are major contributors to its selective permeability?

A

Phospholipid bilayer

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3
Q

what type of movement is least possible for a phospholipid in the membrane

A

Flip-flop

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4
Q

If the temperature in the cellular environment is lowered, the cell responds metabolically to maintain the fluidity of its membrane by

A

A: Introducing more double bonds into fatty acyl chains of fatty acids.

B: Reshuffling the chain between different phospholipid molecules to produce lipids with two unsaturated fatty acids.

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5
Q

Glycolipids are usually located at the

A

Outer leaflet of the membrane

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6
Q

The best method for study the properties of integral membrane proteins in the plasma membrane is

A

Freeze fracture and electron microscopy

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7
Q

Cholestrol what portion is facing the external to the membraen

A

The polar portion

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8
Q

what dose cholestrol to to the flexiability of the lipid membrane

A

reduces it interfering with the lipid hydorcarbon chain meaing that it gives stiffness to the membrane

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9
Q

Is cholestrol absent in the plasma membrane of plants

A

no

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10
Q

to increase fludity of the plamsa membrane

A

Increase the unsaturated fatty acids in the membrane

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11
Q

what kind of compositions occour at the leaflets of the membrane lipids

A

diffrent ones

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12
Q

list the compents of the membrane that are amphipathic (hydrophilic/phobic parts)

A

Integral membrane proteins
Phospholipids
Glycolipids
Membrane steroids such as cholesterol, sitosterol and ergosterol

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13
Q

Diffusion involves the movement of………. molecules.

A

all states of matter

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14
Q

What is the definition of Selective Permeability?

A

The ability of the cell membrane to allow some things to pass through while preventing other things from passing through.

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15
Q

what 5 things indicate passive membrane souliblity

A 
Unstirred layer
Molecular shape
Membrane viscosity
Oil/water partition coefficient
Solute charge
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16
Q

what is important in determing the rate of solute diffusion

A

The competitive presence of other solutes

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17
Q

What will happen to animal cell when it is placed in an isotonic solution?

A

Remain at same size

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18
Q

in a hypertonic soultin a cell will shrink becasue

A

The concentration of solute is greater outside of the cell so water rushes out of the cell. Osmotic gradient favours water movement out of the cell

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19
Q

An animal cell placed in a hypotonic solution will

A

Take on water

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20
Q

Gases such as Oxygen and Carbon Dioxide cross cell membranes by the process of

A

Passive Diffusion

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21
Q

What does diffusion and active transport have in common

A

They both move molecules across the cell membrane

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22
Q

what are some propities of pores be that channels of transporters

A

Solute flux&raquo_space;> predicted by passive diffusion
Stereospecific
Inactivated by drugs/inhibitors

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23
Q

what are some exmaples of primary active transport

A

Glutamine/Leucine exchange
Na+/Glutamine transport
Na+/Ca2+ exchange

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24
Q

Specific transport mechanism, limited capacity and transport affected by competition describes

A

Facilitated diffusion

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25
Q

What type of membrane transporter moves two species in opposite directions across the membrane

A

Symporter

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26
Q

What is the definition of the Michaelis constant, Km

A

Km is the concentration of substrate at half Vmax.

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27
Q

When [S] =Km, then v = ?

A

1/2 Vmax

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28
Q

what is exocytosis used for

A

Is used to deliver material into the extracellular space

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29
Q

what is an exmaple of regulated secreation by cells

A

exocytosis

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30
Q

The Na+/K+ ATPase belongs to the P-type family of ATPases

true/ false

A

true

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31
Q

how many modes dose Na/K have

A

5

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32
Q

Na,K-ATPase transport has the binding site for NA,K, ATP and ouabain where

A

The catalytic subunit

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33
Q

The Na,K-ATPase possesses a …….. stimulated phosphatase activity

A

K

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34
Q

what dose the Na+/K+ ATPase help to maintain

A

a stable membrane potential

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35
Q

wherer is the gamma phosphate of ATP transfered to

A

an aspartyl residue on the catalytic subunit

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36
Q

The Na+/K+ ATPase can utilise para-nitrophenyl phosphate as substrate
true false

A

True

The ATPase activity can split para-nitrophenyl phosphate to generate para-nitrophenol

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37
Q

The Na+/K+/ATPase is an electrogenic transport protein.

true false

A

True

The charge imbalance means that the Na pump is electrogenic

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38
Q

For every ATP molecule hydrolyzed by the Na+/K+ ATPase (also referred to as the Na+ pump) what is the ratio of K to NA

A

3 Na+ ions are transported out of the cell and 2 K+ ions are transported into the cell

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39
Q

Ouabain binds to

A

To the alpha subunit of the Na pump

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40
Q

why is the beta Na/K ATPase subunit needed

A

The beta subunit is required for Na pump assembly and stability

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41
Q

beta Na/K ATPase subunit is not glycosylated

true false

A

false it is heaviely glycosylated

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42
Q

how many isforms of the alpha subinut are there for Na/K ATPase

A

4

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43
Q

how are alpha subinut Na/K ATPase typically expressed

A

Alpha subunits are developmentally regulated and expressed in a tissue-specific manner

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44
Q

The alpha subunit of the Na,K-ATPase is phosphorylated by which amino acid residues

A

Serine
Threonine
Tyrosine

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45
Q

C-peptide induces what

A

phosphorylation of Na,K-ATPase in an ERK-dependent manner

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46
Q

Phosphorylation of ERK kinase in response to C-peptide is blocked by what

A

PD 98059

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47
Q

C-peptide increases the abudence of what in the basolateral membrane of renal tubular cells

A

alpha 1 and beta 1 subunits

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48
Q

Insulin will casue the tranlocation of what in skeltal musceles

A

Na,K-ATPase subunits to the plasma membrane

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49
Q

in what manner are Beta 1 and Beta 2 subunits expressed in skeletal muscle

A

fibre type specific manner

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50
Q

what effect dose high-fat feeding have on the alpha 1 and alpha 2 subints

A

increases the abundance of alpha 1 and reduces that of alpha 2 subunits in skeletal muscle

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51
Q

Facilitative transporters

are energy …

A

independant

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52
Q

SGLT1 is an example of a

A

Secondary active transporter

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53
Q

what is the stociomestery of glucose uptake by sodium

A

2Na to 1 glucose

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54
Q

in what direction do facillative GLUT transporters uptake

A

in the direction of the solute chemical gradient

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55
Q

SGLT 1 uses what for transport

A

sodium electrochemical gradient

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56
Q

define saturation

A

When a group of carrier proteins is operating at its maximum rate

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57
Q

HCO3–/ Cl– transporter is an example of

A

Antiport

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58
Q

what kind of transporter only carrys one thing

A

Uniport carriers

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59
Q

what transporters are located on the Basolateral membrane of the enterocyte (gut cell)

A

GLUT2

Na,K-ATPase

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60
Q

where is GLUT 4 expressed

A

GLUT4 is expressed in skeletal muscle and adipose tissue

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61
Q

what kind of sensor is GLUT 2

A

GLUT2 is a glucose sensor

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62
Q

Exercise stimualtes what for GLUT4

A

translocatino in skeletal musceles

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63
Q

Bumetanide acts to regulate water balance by

A

Inhibiting the renal Na,K,2Cl cotransporter

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64
Q

Ouabain is a cardiac glycoside. Its effect on heart contraction is due to

A

Inhibition of the Na,K-ATPase, reduced Na/Ca exchange and increased intracellular calcium in heart cells

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65
Q

define the pump leak hypothesis

A

the idea that there is a slow movment of Na and K into and out the cell via diffusion

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66
Q

name evidence for the pump leak hypotheis

A

the use of radiolabbelling Na and K in a soultion

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67
Q

what is the energy source for the Na/K pump

A

ATP as glucose removal did not inhibit the pump ruling out glycolysis and removal of O2 removed krebs

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68
Q

What kind of trnasporter is the Na/K pump

A

it is symport as Na goes one way and K the other

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69
Q

what are the five operantion modes of the pump

A 
Normal
reverse
Na-Na exchange
uncoupled Na efflux
K-K exchange
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70
Q

Look up the mechanism for actoin for Na/K pump

A

thoughts

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71
Q

look up strucutre of Na/K pump

A

thoughts

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72
Q

On the Na/K pump where dose oubain bind

A

the caylylic subunit

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73
Q

In the Na/K pump what is the funtion of beta units

A

unique function for skeletal muscle with b1 or b2 expressed differently if the muscle is contracting properties of the muscle fibre and oxidative properties

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74
Q

where are alpha one and two found

A

alpha one - all issues highest in the kindneys

alpha two - all tissue a lot in the brain and skeletal tissue

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75
Q

What is a basic fact about the Cl ion

A

negative ion with two stable and one unstabel

the third shell of the Cl accepts the electron

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76
Q

in animal cells what is the Cl concentraiton of the ECF compared to the ICF

A

larger in the ICF than in the ECF

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77
Q

normal Cl levels in the ICF

A

5-40 nm depeinding on the tissue

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78
Q

What are the 5 main ClC channel familes

A 
CIC
CFTR
CaCC
VSOAC
MAC-1
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79
Q

What are the members of the CIC family

A

CIC- 1-6 ,CIC-7/Ostm1 as well as hCIC-Ka/barttin and hCIC-Kb/barttin
( barttin and Ostm1 needed for funtion)

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80
Q

what ar the two tpyes of anion channels of the Cl

A

those found at the plamsa membrane (hCIC-Ka/barttin , hCIC-Kb/barttin , CIC-1,2
and the membrane of intracellular organells (CIC-7/Ostm1 . CIC-3-6)

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81
Q

Describe the double barrled idea found in CIC-0 and shown in others

A

that the CIC channels show an exact doulbing indiactes that the channel has two identical channels each indepdant of the other

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82
Q

the gating of the Cl channels can be influenced by what

A

changes in MP with a more + MP increasing the liklehood of the channels opening

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83
Q

What structure do all CICs shows

A

also homodimeric made up of two identical protomers

84
Q

what technique was used to investigate neurotrammiter release

A

high reselution pictures of the nurotransmitter with Taiwan bandit kraits venom

85
Q

What are mepps

A

small depolorisation events when measuring the MP

86
Q

vesamicol was used to investigat mepps how

A

as vesamicol blocks Ach uptake into the vesicels with addition cuasing a reduction in mepps

87
Q

How was black widoe venom used to invesitage vesiceles

A

when measured addition cuased massive relase of mepps then a flatline shows it causes massive release of vesicels

88
Q

look at the digram for the vesicel life cycle

A

thoughts

89
Q

why is Ca essential for neurotransmitter

A

This Ca will trigger vesicle exocytosis of the vesicels

90
Q

what effect dose Mg have on neurotranmitters

A

block the relese of vesicels

91
Q

define the endplate potentiol (EPP)

A

it is a MP change that is made up of diffrent units eg all for one

92
Q

quantal content (QC) is what

A

is the mean epp amplitude divided by the mean mepp. This will represent the number of vesicles released per nerve stimulus

93
Q

How will dendrotoxin effect the QC

A

it will block some K voltage gated channels

causing Ca influx and rasied EPP but not mepps

94
Q

Tubocurarine will change the ….

A

reduced epp as it block the ACh receptors as well as the mepp as ther is less space for the Ach to bind

95
Q

Botulinum acts pre/post synaptically

A

pre and will reduced the number of vesihels released

96
Q

read over vesicular release

A

thoughts

97
Q

What dose patch clamp allow for

A

study of single and populations of receptors

98
Q

name the 4 diffrent types of pacth clamp

A

Cell attachted
whole-cell
outside-out
insude-out

99
Q

explain cell attachted patch clamp and give one pro and con

A

the receptor still attached to the membrane
pro can recrd a singel receptor
con cannot change drug concentratins

100
Q

explain whoel-cell patch clamp and give one pro and con

A

suction is increased and it can break the membrane with the recording solution accessing the cell measuring a population of receptors
pro control of intra & extracellular environment
con biochemical washout of the intracellular environment

101
Q

explain outside-out patch clamp and give one pro and con

A

when pulling away the membrane will snap with the receptors facing towards the cell
pro can change/ control extracellular drug (agonist) concentrations
cons cannot easily change intracellular environment

102
Q

explain inside out patch clamp and give one pro and con

A

cell-attached where it is pulled where the membrane will snap with the receptors facing into the pippete
pro control of intra/extracellular environment
con - cannot easily change concentration of agonist

103
Q

look at the digrams for all the patch-clamp syuff

A

thoughts

104
Q

What did cloning allow for the discovery of

A 
what agonist bind
ion channel postions
cation vs anion conductence 
binding site of new drugs
shows how releated they were
105
Q

look up the diffrent subunits for the ACh recepotr

A

thoughts

106
Q

what are the two ways to identify Ach receptor subunits

A

Oocyte expression system (frog)
use epethial cell in culture that do not normally have nAChR
using cDNA to modify them the GFP to ideitfy the nAChR containing cells

107
Q

describe what α7 5HT3A chimeras have found

A

allows for the identification of singel channel conductence region on the receptor as well as agonsit binding site

108
Q

what dose loop C do in ACh binding

A

binding of ACh stabalies loop C casuing it to close resulting in the confomraitonal change

109
Q

describe the watering can model

A

Argaine loops in the 5HT were seen to decrease Na passage happens as 5HT last section Na passes through seen model picture

110
Q

what sites wil GABBA effect

A

GABBAa

GABBAb

111
Q

what is the GABBAa receptor

A

transmitter gated ion channels with 5 subunits

112
Q

what is the GABBAb receptor

A

a hetrodimer with GABBA binding to the B1 and B2 for GPCR coupiling

113
Q

where is GABBAa located

A

postsynaps

114
Q

where is GABBAb located

A

the post and pre synaps

115
Q

what is Tonic inhibition

A

where the extra-synaptic GABBAa receptors that are activated by lower GABBA levels and are constantly being activated resulting in a slow tonic current in response to the GABBA

116
Q

what is phasic inhibition

A

When GABBA triggers them (GABBAa receptors) most will open simultaneously but will stay open for different times this causes a curve to the graph this is called phasic inhibition this is often found in the synaptic cleft

117
Q

What is the effect of glycine and GABBA on MP

A

Glycine will casue depolorisation and an AP to fire through glutamate cartion channels. GABBA will cause a flow of anion channels to open reducing the depolorisation

118
Q

what is feed-forawrd inhibiton

A

after stimulation by the glycine the GABBA will reach the neuron 1-5 msec after casuing the depolorising effect to be reduced

119
Q

what is feed back inhibtion (GABBA)

A

the AP from a glutamte will trigger the GABBA internuoron activating the GABBAa and repolorising the membrane

120
Q

what kind of protein are GABBAb

A

G protiens receptors coupled to Gαi and Gαo

121
Q

what dose actvation of GABBAa do

A

causing Cl channels to open causing an IPSP(inhibitory post-synaptic potential)

122
Q

What dose GABBA in the synaptic cleft do

A

then activate the GABBAB receptors causing the βy complexes to disassociate and lower probability for Ca channels to open. This reduces the IPSP

123
Q

Post synaptic GABBAb activation will casue what

A

GABBAB post-synaptic causing K+ channels to open causing further & prolonged hyperpolarisation and so a longer IPSP

124
Q

what effects do Benzodiazepines have on GABBA receptors

A

increase likleyhood of the receptors opening

125
Q

pentobarbital (barbituate) dose what to GABBA receptors

A

increase time of the receptors opening

126
Q

how many diffrent alpha GABBAa subunits are there

A

6

127
Q

Which GABBAa subunits are enchced by diazepam

A

α1,2,3 & 5

128
Q

What diffrent in AA was seen in the α1,2,3 & 5 compared to the α4,6 of GABBAa

A

one AA with H in the α1,2,3 & 5 and a R in the α4,6

129
Q

what method was used to identify the diffrent effects of the GABBAa a subtypes

A

knock out mice

130
Q

what GABBAaR a subypes corrolate to what effect

A 
α1-sedation
α2,3- anxiolytic/analgesic (anxiety /painkiller)
α5- cognition
B3 - immobility/anesthesia
B2- sedation/anesthesia
131
Q

what is a enhancer of GABBA

A

5α-pregnan-3α-ol-20-one (5α-3α)

132
Q

5α-3α is found to be synthesised where

A

in the brain meaing they are called neurosteroids

133
Q

what conditions casue neurosteroids release

A

to pregnancy, puberty , stress and epilepsy

134
Q

what effects to neurosteroids have

A

anxiolytic (anti-axiety), sedative , hypnotic (get to sleep), analgesic (painkiller), anticonvulsant and antidepressant

135
Q

what evidence is ther that neurosteroids act through the a2 GABBAaR subunit

A

konckout mice of the a2 showed increased speed in synaptic events

136
Q

what are the three diffrent gene familes that act for the glutamate receptor

A

AMPA, kainite and NMDA

137
Q

what will the glutamate recepotr trigger

A

will open causing the flow of Na into the cell resulting in an inward current

138
Q

What is the NMDAR key propites

A

conducts NA and is permeable to CA as well as K out the cell and will be blocked by MG needs the co-agonsit glycine

139
Q

How is the NMDAR blocked by Mg

A

the Mg will be attracted to the open receptor and bind to its center blocking the flow

140
Q

What will happen to NMDAR when Mg is at high doses

A

Chattering will happen with the channel rapdiley opening and shutting as when the Mg binds the depolorisation effect is reduced

141
Q

What is NMDAR co agonist

A

agonist glycine or D-serine

142
Q

How are NMDAR and AMPAR linked

A

after glutamte stimulation and the NMDAR opening and blockage by Mg. The increased Na will activate the AMPAR causing a depolorisatin of the cell and the Mg to be expelled

143
Q

What are the effects of NMDAR and AMPAR linkage

A

casue more NMDAR activation as Mg is removed so a slower depolorisation assosiated with learning

144
Q

where is the glutamte binding site

A

S1&S2 domain

145
Q

look up the way that glutamte receptors are moved to the synaps

A

thoughts

146
Q

what can efffect the translocaiton of glutamate receptors

A

be neuronal activaty, acute/chronic stress, Alzheimer’s and neurodegenerative disorders and drugs eg coke, ket

147
Q

Long term potentiation (LPT) is assosiated with learning how is glutamte receptor assosiated with this

A

the stimulation causes depolarisation the spine causing Mg blocking to be removed on the NMDA and more intracellular Ca and this then causing translocation of CaMKII to spines that cause phosphorylation of AMPA receptors causing them to increasing bind to the post-synaptic through diffusion trapping allowing for more LPT

148
Q

what GLu subunits are related to spacial memory

A

the GluA1 & 2 subunits for the AMPA

149
Q

what do mice with huntingtons express

A

express impaired LTP with AMPAkine (AMPA agonist) improves cognitive performance

150
Q

define gap junitons

A

array of intracellular channel that allow for cell to cell communication and comprise of a large number of cells directly and allow for them to “taste” the others cytoplasm as well as with the extracellular space

151
Q

what are gap juntions made of

A

connexions

152
Q

what is an effect of gap juntions

A

they can alter resistance between cells through the flow of ions

153
Q

how many connexions make up a gap juntion

A

6

154
Q

what are gap juntions peramble to

A

to inorganic ions K, NA, CL, HCO3 as well as small inorganic signalling molecules (cAMP,IP3), dyes and Glucose

155
Q

what do gap juntnions do in neurons

A

they do not generate current fluxes but will pass ions from one to another along the electro-chemical gradient

156
Q

what is eltrical synpases between juntions mediated by

A

Cx36 but only 0.1% actually conducts

157
Q

How were eletrical synapes discovered

A

through the meauring of escape synapses in shrimp with a MP generated much faster than GABBA or a chemical interface could allow

158
Q

what is the diffrence in arragment of eletrical and chemical gap juntions

A

chemical is non-reversible and omnidirectional while the electrical can act in both directions

159
Q

Gap juntions can be mapped with dye but ..

A

they are non-reversible so cannot be repeated and the connexions may show specificty

160
Q

what it the most common way to measure gap juntions

A

Dual cell electrophysiolog with two neurons placed with the current measured between them

161
Q

read over all the diffrnces in gap juniotns

A

thoughts

162
Q

what are improtant propities of the eltrical networks

A

Bidirectionally, shorter synaptic delay, sign preservation, mediates hyper and depolrazing responses, helps with generating AP and synchrony( similar responses), coordinates activity of large cell populations

163
Q

what allows for brain rythmes

A

gap juntions will only form between similar neuonrs with climbing fibers linking the rest allows for large scale linkage

164
Q

why do Cx36 knockout mice show night blindess

A

In the eyes the rods and cone have connexions that connect the cells together with the cones using Cx36 in the KO mice this connection was not longer there meaning that the signal could not be transmitted down to the brain via the electrical synapse and the Cx36

165
Q

how do Cx36 knockout mice cerabellum differ

A

the inferior olive of the cerebellum the eletrical synapses that go to the purkinje cells with linkage by the gap juntions. Allows for wave form to be seen normally with KO mice not showing it and impared muscelse with that

166
Q

what are the two facrotrs that effect K efflux/influx

A

concentration gradient

eletrical gradient

167
Q

Why is the MP of a resting cell + than the EP of K

A

as while K reguatles MP other cahrged ions exist in the cell Na, Cl . The larger + stop K from leaking out and causing changes in flwo of Ca, Cl

168
Q

How is the effect of an ion determined on a membrane

A

its permability as changes in permaiblty will casue efflux/influx and a change in the MP

169
Q

define gating

A

is wjen the TM S4 with its + charge will be repelled out of the cell casuing a conformational change in the a subunit and the pore to open means that the pore only open when needed eg specific MP

170
Q

define channel inactivation

A

causes the blockage of a channel after sustained depolorisation by an IFM see diagram to ensure that there is ont an unctorlled flow

171
Q

define ion selectivity

A

it is found at the top of the pore with a collectin of + or - AA as well as a set size acts as a filter to make sure the right things get through

172
Q

Look at digrams for ion selctivilty channel inacitvaiton and gating

A

thoughts

173
Q

How dose Glu account for the gating in CIC

A

as it is in a + ,- or neutral charge it will bind in three ways with the + charge allowing for conductence this gating can be altered by Ca levels ph

174
Q

myotonia congenita is what

A

mutation in the CIC-1 that causes relaxation of skeletal muscele to be hard

175
Q

A mutation in the CIC-1 will cause what at the transverse tubules

A

causes the accumilation of K and a depolorising effect that is usally contered by CIC but causes autonomous AP friing

176
Q

Look at the double barreled structure

A

thoughts

177
Q

what are the three tpyes of K channel

A

6TM 2TM and 4TM

178
Q

what are the Kv channels responsible for

A

shaping of the AP

179
Q

Describe how maxi-K channels are inacivated

A

20 amino acids that are a hydrophobic “ball” that is at the head of a 50-60 chain of AA blocking the channel

180
Q

What are the two ways that maxi-K channels are contorlled

A

through MP and Ca concentration

181
Q

How dose in maxi-K channels Ca concentration lead to acitvation

A

Ca will gather in the Ca bowl casuing RCK to undergo conformational change and push on the S4

182
Q

Look at the diagram for maxi-K

A

thoughts

183
Q

TREK and KATP are what kind of channel

A

TM4 and TM2 K channels Cav channels

184
Q

What do TREK and KATP help control

A

they allow for stablisaiton of MP as they are always open so are trying to reach GHK equilibrium -80 in cells repolorises the cells

185
Q

What do TREK and KATP KO mice show

A

decreased anaesthetic sensitivity, increased epilepsy and ischemia , increased pain as well as the having anti-depressant qualities

186
Q

What are two things that maxi-K channels helpl do

A

for hypertension regulation as well as timing of bursts of AP and contributes to afterhyperpolarisation or the refractory period. It also balances the effect of excess vasoconstriction as it will open due to the excess Ca and then stop the flow of Ca into the cell

187
Q

How do KATP TM2 channel blockers help in type 2 diabetes

A

As they are the channel for insulin release via K excoytosis. inhibitors of this channel will causes the ATP to not be released and Ca to flow into the cell casuing insulin release see diagram

188
Q

define whole cell depolorisatoin

A

made up of a collection of single channel currents that have the same average current happen at the same time but have different duration and are only open for a short time

189
Q

why do Na channels and K channels open at diffrent times

A

to allow for depolorisation to occour

190
Q

what is cord conductence

A

the relationship between the voltage current and Ena . flows a vally shape with current increasing as MP increases then drop again as it gets closer to the Ena

191
Q

how many Nav a subunits are there

A

Nav1.1-1.9

192
Q

what is the role of beta subunits in Nav

A

They help to modulate channel opening for rapid activation/inactivation with a β1 mutation seen in epileptics with the immunoglobulin domains binding to extracellular proteins that help with channel localisation in cells. The Na channels are located at the node of Ranvier

193
Q

How dose TTX have an effect on Nav channels

A

It block them form the outside of the channels where it binds to AA residues on the outer mouth of the channel. TTX acts on the glutamate of the P domain as well as for cardiac Na channels on cysteine on the P domain

194
Q

how do anasthetics lignocaine have an effect

A

LAs are small lipid molecules that cross the neve sheath and cell membrane to reach the site of action from there they will block the Na from the intieor binding to the - inside Na channels

195
Q

differential sensitivity of cardiac, CNS and PNS sodium channels to tetrodotoxin happens becauses ..

A

the diffrent subuints are present in eacjh of the diffrent tiissues as they regulate diffrently meaing there is a altered effect

196
Q

What is diffrent about Ca to most ions

A

acts as a chemical signal as well as an eltrical

197
Q

list the diffrent subunits of the Cav channel

A

alpha 1, beta , a glycosolated alpha 2 , alpha 2 delta and a gamma

198
Q

what is the role of the P HVA type subtype in a Ca channe

A

neurotrasnmitter release

199
Q

what is the role of the N HVA type subtype in a Ca channel

A

neurotrasnmitter release

200
Q

what is the role of the L HVA tpye subtype in a Ca channel

A

E-C coupling hormone secreation and muscel contraction

201
Q

what is the role of the Q HVA type subtype in a Ca channel

A

neurotrasnmitter release

202
Q

what is the role of the R H/LVA type subtype in a Ca channel

A

Ca-actin potetniols neurotrasnmitter release

203
Q

what is the role of the T LVA type subtype in a Ca channel

A

repetative firing

204
Q

What effect do GPCRs have on the Ca channel

A

inhibit the the Ca current PKA will also cuases an increase in the current via phosphoralaytion

205
Q

name 3 muations in the Ca and effect in the Cav1

A

hypokalemic periodic paralysis in Cav1.1 in the S4 regions that causes a reduced Ca current and muscle weakness

Timothy syndrome where a Cav1.2 mutations causes loss of channel inactivation with increased Ca entry and with that server cardiac dysregulation

. Night blindness found in the Cav1.4 with reduced transmitter released from the retinal photoreceptor

206
Q

name 3 muations in the Ca and effect in in Cav2,3

A

. Autism associated with Cav3.2 mutations

Migraines a Cav2.1 mutation causing increased channel activity and transmitter release and migraines

Ataxia causing attacks of motor dysfunction caused by Cav2.1 mutations that prevent normal channel formation and loss of Ca current

Regulatory (2 decks)

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