Other channels Flashcards

1
Q

What are hERG channels

A

human ether a-go-go related gene
alpha subunit of Kv1.1
the rare mutation and drugs can cause long QT syndrome

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2
Q

What is QT syndrome and what can it cause

A

extended duration in ventricular action potentials

causing arrhythmias because decreased repol of heart ap, therefore the inward current can trigger early depol

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3
Q

list the hERG drug interactions

A

anti psychotics, some antibiotics and antiarrhythmic drugs

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4
Q

describe hERG regular function

A

its a voltage gated channels that is activated by depol
it has slow activation and deactivation bc the probability of moving s$ is low
it has rapid recovery from inactivation so it doesnt interfere with ca2+ plateau

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5
Q

What do TRP channels do in flies

A

mediate light perception = PLC -> IP3 + CA -> channel opening

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6
Q

why are TRP channels called transient receptor potential channels

A

because a mutation in TRP causes a transient response

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7
Q

describe the structure of TRP channels and how they are activated

A

tetrameric with 6 transmembrane domains per subunit
act with depol at Ca entry
linked to PLC
temperature and ligands are activators

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8
Q

what are the functional roles of TRPs

A

somatosensation = mechano, propriom thermo

TRPV1, TRPM8, TRPA1 = noci

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9
Q

describe TRPV1

A

venoms modulate receptor channels function
shock, paralysis, death
acute pain, neurogenic inflammation
irreverisble agonists

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10
Q

Describe TRPM8

A

activated by menthol + cold stimuli
deficiency = no preference for hot or cold
antagonists could become analgesics

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11
Q

Describe TRPA1

A

detects chemical irritants and inflammatory + pungent agents

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12
Q

Describe the therapeutic potential of TRPs

A

block sensitising actions of inflam agents without altering heat sensitivity
TRP channels are needed for the detection of noxious substances and are implicated in cancer development, asthma, cardiac hypertrophy

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13
Q

Describe the CFTR cl channel

A

decrease in cl and bicarbonate secretion from submucosal glands because of viscous acidic surface liquid
promotes bacterial colonisation

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14
Q

describe mutation of CLC-1 CL- channel

A

myotonia = inherited CL- chan mutation

conductance in skeletal muscle = exaggerated contraction and increase in muscle excitability

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15
Q

Describe CaCls

A

activated slowly by depol ca entry
control fertilisation, olfaction, epithelium secretion, smooth muscle contraction
regulated by CA and CA modulated kinases

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16
Q

What are gap junctions and their main functions

A

electrical synapses to allow bidrectional flow
can be gated and show recitification in current flow
they pull together neurons for uniform spread of smooth, wave-like depol
present in early development, glial + muscle cells
6 subunits per channel

17
Q

how are gap junctions involved in early development

A

interconnectivity between immature neurons shown by dye coupling
development of uncoupling overlaps with the formation of chemical synapses

18
Q

how are gap junctions involved in CNS injury

A

send pro-survival signals or pathological death signals through glial cells

19
Q

describe the features of inward rectifiers

A

act downstream of GPCRs
nicotinic + muscarinic
M1 M2 M3 couple with Gq to activate PLC

20
Q

what does signal cascade of PLC do

A

alters Kir activation

21
Q

Describe the structure of inward rectifiers

A

2 transmembrane domains with tetramic channels
equivalent to 5th and 6th transmembrane domain and intervening KV pore loop
lack S4

22
Q

how are Kirs related to EPSPs and IPSPs

A

GPCR -> EPSPS by decreases Kir to increase excitability

GPCR -> IPSPs by increasing Kir to decrease excitability