biophysics Flashcards

1
Q

ohm’s law

A

current, voltage, conductance and resistance
current = conductance x voltage
conductance = 1 / resistance
current = voltage / resistance

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2
Q

equilibrium

A

state of system where no further changes are possible

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3
Q

Nernst equation at 37 degrees Celsius for monovalent cations

A

Ex = (RT/zF)log([X]o/[X]i)

simplified - Ex = 61.5log([X]o/[X]i)

the inside and outside ion cons are switched for anions (invert the ratio)

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4
Q

ion equilibrium potentials (skeletal muscles)

A

potassium - -98mV, sodium - 67mV, chloride - -90mV, calcium - 110mV

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5
Q

Goldman-hodgkin-katz equation

A

resting membrane (Vm) is calculated using the Nernst equation where the difference is, is that all the concentrations of ions are added together where outside are added on top of the ration (opposite for anions) and the inside concentrations are added on the bottom of the ration ( opposite for anions), P is 1 combined

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6
Q

ion channels

A

conduct small ionic current along electrochemical gradient, selective permeability, open/close in milliseconds underlying rapid membrane potential changes, when closed generates resistance, when open generates conductance

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7
Q

transporters/exchangers

A

transport or exchange along electrochemical gradient, bind/ release ions, don’t normally conduct ionic current

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8
Q

ion pumps

A

transport ions agains electrochemical gradient, requires ATP (sodium potassium ATPase, plasma membrane calcium ATPase

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9
Q

voltage-gated ion channels

A

ion conducting pore and gates controlling the pore, pore has selectivity filter region allows permeable ion to move through easier than others, gate coupled to voltage sensor - moveable portion of protein molecule sensitive to to voltage changes across membrane movement of voltage sensor controls ion channel gate, important in action potential generation, each channel contains 4 domains/subunits each made of 6 transmembrane helices

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10
Q

potassium channel selectivity filter

A

potassium channel pore mimics hydration of potassium ion but sodium is too small so oxygens will be too far away from normal hydration shell of sodium, energetically unfavourable for it to lose water and gain nothing in potassium channel pore the T V G Y G residues that are conserved and create the selectivity filter in the pore have oxygens that are at the same distance are the water surrounding potassium so these are easy to swap out

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11
Q

sodium channel gate

A

activation gate (m gate) opens rapidly on depolarisation allowing sodium to flow, inactivation gate (h gate) responds to depolarisation by plugging channel pore after brief delay (5ms), h gate remains in place for short time - refractory period, further sodium influx not possible

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12
Q

membrane potentials and ions roles

A

potassium brings the cell membrane towards hyperpolarisation whereas sodium and calcium bring it towards depolarisation

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13
Q

neuronal ion channel activity

A

potassium (-90mV) - hyperpolarises membrane and increases voltage needed to reach action potential firing threshold, sodium (+65mV) - depolarises membrane, calcium (+110) - depolarises membrane, cations (~0mV) - non selective cation channels (don’t discriminate between small cations) depolarises membrane, chloride (varies ~-90mV) - inhibitory

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14
Q

driving force of ion

A

Vm-Eion

+ve = outward driving force
-ve = inward driving force

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15
Q

reversal potential

A

membrane potential at which direction of current flow reverses

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16
Q

voltage clamp

A

feedback system, allows voltage control (voltage clamp) across plasma membrane, essential for analysis of channels who’s activation is voltage dependant, voltage controlled and current across membrane recorded - directly tests properties of active ion channels

17
Q

current clamp

A

feedback system, allows current control (current clamp) across plasma membrane, essential for recording membrane potentials, controls current flowing through cell and voltage responses recorded - mimic action potentials and synaptic input

18
Q

role of sodium channels in action potential

A

voltage gated, open on membrane depolarisation, influx of sodium into cell, influx causes more depolarisation - more sodium channels open, sodium influx drives membrane too and past 0 mV towards Esodium, explosive sodium influx only occurs if threshold reached (~55-50 mV), channels inactivate rapidly - no new action potentials possible - absolute refactor period

19
Q

role of potassium channels in action potential

A

voltage gated, open in response to depolarisation at more positive potential then sodium channels (delayed), small fraction of specific voltage gated and non gated potassium channels open at rest (leak channels) - maintain rising membrane potential near potassium equilibrium, delayed opening main factor responsible for depolarisation phase, potassium ions flow out cell (+ flow out) cell becomes more negative, repolarisation creates a temporary more negative membrane potential than rest (afterhyperpolarisation) - voltage gated potassium channels deactivate and resting membrane potential restored

20
Q

calcium activated potassium channels

A

some neurones, internal calcium trigger specific family of potassium channels, contribute to action potential repolarisation, respond to activation of voltage gated calcium channels which contribute to depolarisation similar to sodium channels, calcium-gated potassium channels often open longer than voltage gated potassium channels and can prolong the afterhyperpolarisation, create a ‘shoulder’ on action potential readings

21
Q

action potential propagation

A

action potential originates at axon initial segment, in myelinated axons action potential jumps from one node of ranvier tot he next

22
Q

channel recordings

A

single channel recordings - current through single ion channel, scrutinise io channel property
whole cell recording - gating properties of ion channels can be revealed

23
Q

M current (excitatory effect on cell by acetylcholine binding to M1)

A

depolarisation activated noninactivating potassium channel, M channel activity defines firing patterns, muscarinic acetylcholine receptor excites sympathetic neurones by inhibiting M channels, acetylcholine binds to M - hetrotrimeric G protein activates enzyme PLC beta - PIP2 broken down into DAG which activates PKC and Ins(1,4,5)P2 which activates calcium release both pathways inhibit Kv7/ M channel, PIP2 all inhibits it

24
Q

GIRK channels (inhibitory effect on cell by acetylcholine binding to M2)

A

muscarinic acetylcholine receptors inhibit cardiac muscle cells by activating GIRK channels, acetylcholine binds to M2 - beta gamma unit of G protein binds to GIRK channel opening it and allowing potassium to enter