Membrane Potential Flashcards
What is the membrane potential of a cell?
The magnitude of an electrical charge (mV) that exists across a plasma membrane.
Negative at rest in all mammalian cells.
Give examples of resting cell membrane potentials.
- Cardiac and skeletal muscle cells have largest resting potentials: -80mV to -95 mV.
- Nerve cells: -50mV to -75mV.
- Erythrocytes have the smallest: -9mV.
How is MP measured?
Using a voltmeter and microelectrode.
What are the 2 minimum essential factors in generation of the MP?
- Asymmetric distribution of ions across the PM (i.e. Ion conc gradients)
- Selective ion channels in the PM: K+, Na+ and Cl- channels are the most important for most cells
Describe the selective permeability of the plasma membrane.
Phospholipid bilayer has a hydrophobic interior so
- is permeable to small uncharged molecules (O2, CO2, H2O, benzene)
- but very impermeable to charged molecules (ions) - requires ion channels
What are the properties of ion channels?
Have an aqueous pore through which ions flow by diffusion in both directions down their chemical gradient.
- Selectivity: for one (or a few) ions species
- Gating: pore can open or close by a conformational change in the protein
- Rapid ion flow (microsecs)
Describe the ionic concentrations for a typical mammalian cell.
Intracellular Extracellular (plasma)
Na+ 10mM. Na+ 145mM
K+ 160mM. K+ 4.5mM
Cl- 3mM. Cl- 114mM
A- 167mV. A- 40mM
What dominates the membrane inonic permeability at rest?
- Open K+ channels
- When the K+ chemical gradient and electrical gradient are equal and opposite, there will be no net movement of K+ but there will be a negative charge across the membrane - the resting MP.
- So resting MP arises due to selective permeability to K+.
What does the Nernst equation calculate?
- The MP at which an ion will be in equilibrium, given the extracellular and intracellular concentrations of the ion.
- E.g. Ek = K+ equilibrium potential = -95mV
What are depolarisation and hyperpolarisation?
- Depolarisation: decrease in the size of the MP from its normal value - cell interior becomes less negative.
- Hyperpolarisation: increase in the size of the MP from its normal value - cell interior become more negative.
What causes changes in MP?
- Changes in the activity of ion channels - move the MP towards the equilibrium potential of those ions.
In which cells do K+ channels have an important effect on MP?
- Cardiac muscle cells (-80mV) and nerve cells (-70mV): resting MP quite close to Ek but not exactly as membrane not perfectly selective for K+.
- Skeletal muscle: many Cl- and K+ channels open in resting membrane so resting potential = 90mV, close to both Ek and Ecl.
- Cells with lower resting MPs have lower selectivity for K+ - increased contribution from other channels. E.g. Smooth muscle cells (-50mV), erythrocytes have virtually no K+ selectivity (-9mV).
Opening of which channels leads to hyperpolarisation and depolarisation?
- Opening Na+ or Ca2+ channels - depolarisation (Ena = +70mV, Eca = +122 mV).
- Opening K+ or Cl- channels - hyperpolarisation (Ek = -95mV, Ecl = -96mV).
What is membrane conductance?
How permeable a membrane is to specific ions (i.e. The number of open channels for that ion).
Which equation describes the imperfect selectivity of membranes?
Goldman-Hodgkin-Katz equation (involves relative permeabilities to K+, Na+ and Cl-).
How can channel activity be controlled?
- They are gated:
1. Ligand gating - open/close in response to binding of a chemical ligand.
2. Voltage gating - open/close in response to changes in MP.
3. Mechanical gating - open/close in response to membrane deformation (e.g. Hair cells of the inner ear).
What do ligand-gated channels give rise to?
Synaptic potentials
Where do synaptic connections occur?
Between:
- nerve cell - nerve cell
- nerve cell - muscle cell
- nerve cell - gland cell
- sensory cell - nerve cell
What is the difference between fast and slow synaptic transmission?
- Fast (microseconds): the receptor protein is also an ion channel - transmitter binding causes channel to open.
- Slow (milliseconds): the receptor and channel are separate proteins.
Describe fast synaptic transmission at excitatory synapses.
- Excitatory transmitters (e.g. ACh, glutamate, dopamine) open ligand-gated ions channels that cause membrane depolarisation (excitatory post-synaptic potential).
- Channel can be permeable to Na+, Ca2+ or sometimes cations in general (e.g. nAChR).
- Longer time course than an AP (1/2 msec) and graded by transmitter amount).
How are the actions of inhibitory transmitters different to those of excitatory transmitters at synapses?
Inhibitory transmitters (e.g. Glycine, GABA) open ligand-gated channels that cause hyperpolarisation - more permeable to K+ or Cl-.
What is summation?
Process that determines whether an AP will be triggered by the combined effects of excitatory and inhibitory signals from:
- multiple simultaneous inputs (spatial summation)
- repeated inputs (temporal summation)
What are the 2 types of slow synaptic transmission?
- Direct G-protein gating: localised and relatively rapid (as G-protein doesn’t move far to get to channel). Involves GTP to GDP hydrolysis.
- Gating via an intracellular messenger: acts throughout the cell and can be amplified by an enzyme cascade. Requires more time as several intermediates, culminating in intracellular messenger or protein kinase activating channel.
Which 2 additional factors can influence membrane potential?
- Changes in ion concentration - sometimes altered in clinical situations, can alter membrane excitability, e.g. In heart. Most important is extracellular K+ concentration.
- Electrogenic pumps (e.g. Na+/K+ ATPase) - in some cells, this contributes a few mV directly to MP, making it more negative (e.g. In erythrocytes).
