Changing The Membrane Potential Flashcards
(17 cards)
Give 5 examples of cell signalling by changes in membrane potential
- Action potentials in nerve and muscle cells (next week)
- Triggering and control of muscle contraction (next week)
- Control of secretion of hormones and neurotransmitters
- Transduction of sensory information into electrical activity by receptors
- Postsynaptic actions of fast synaptic transmitters (later)
What is depolarisation?
A decrease in the size of the membrane potential from its normal value. Cell interior becomes less negative e.g. a change from – 70 mV to – 50 mV
What is hyperpolarisation?
An increase in the size of the membrane potential from its normal value. Cell interior becomes more negative e.g. a change from – 70 mV to – 90 mV
How is membrane ion permeability changed?
Membrane potentials arise as a result of selective ionic permeability Changing the selectivity between ions will change membrane potential
Increasing membrane permeability to a particular ion moves the membrane potential towards the Equilibrium Potential for that ion
Opening K+ or Cl- channels will cause hyperpolarization Opening Na+ or Ca2+ channels will cause depolarization
Thus, changes in membrane potential are caused by changes in the activity of ion channels
Describe the selectivity of real cell membranes
Real cell membranes have channels open for >1 type of ion. How do we deal with membranes that are not perfectly selective for one ion species? The contribution of each ion to the membrane potential will depend on how permeable the membrane is to that ion (this is known as ‘conductance’)
What is the GHK equation
A theoretical treatment that fits real membranes quite well is: The GHK (Goldman-Hodgkin-Katz) equation PK, PNa, PCl are relative permeabilities to K+, Na+, Cl- Depends on number of open channels for each ion
When opened by mechanical/extricated forces Flap opens Ions move in Only about 1000 Then fully opens more move in Na ions
Give an example of a less selective channel
At the neuromuscular junction, motor neurone terminals release acetylcholine (Ach) that binds to receptors on the muscle membrane
Nicotinic Acetylcholine Receptors
1. Have an intrinsic ion channel
2. Opened by binding of acetylcholine (x2)
3. Channel lets Na+ and K+ through, but not anions
4. Moves the membrane potential towards 0 mV - intermediate between ENa and EK
describe 3 types of gating
- Ligand Gating
Channel opens or closes in response to binding of a chemical ligand
- e.g. Channels at synapses that respond to extracellular transmitters (ACh, Serotonin)
Channels that respond to intracellular messengers - Voltage Gating
a. Channel opens or closes in response to changes in membrane potential
- e.g. Channels involved in action potentials - Mechanical Gating
a. Channel opens or closes in response to membrane deformation
- e.g. Channels in mechanoreceptors: carotid sinus stretch receptors, hair cells in inner ear, etc.
Give an example of mechanical gating
Hair cells in the inner ear
1. K+ channel closes in cuticular plate - increase in +ve charge on inside
2. Membrane depolarises
3. Ca2+ channel opens - Ca2+ enters cell, passes through to basoelectric surface of cell
4. Vesicles containing neurotransmitter (dopamine or dynorphin) fuse with basement membrane close to afferent nerve
5. Neurotransmitter binds to receptor on post-synaptic plate and
generates action potential that goes to CNS for interpretation
Where can synaptic connections occur between?
Synaptic connections occur between: nerve cell – nerve cell nerve cell – muscle cell nerve cell – gland cell sensory cell – nerve cell At the synapse, a chemical transmitter released from the presynaptic cell binds to receptors on the postsynaptic membrane
Dscribe fast synaptic transmission
In fast synaptic transmission, the receptor protein is also an ion channel
Transmitter binding causes the channel to open
Describe excitatory synapses
Excitatory transmitters open ligand-gated channels that cause membrane depolarization Can be permeable to Na+, Ca2+, sometimes cations in general (nAChR)
The resulting change in membrane potential is called an
Excitatory post-synaptic potential (EPSP)
1. Longer time course than an Action Potential
2. Graded with amount of transmitter
3. Transmitters include: Acetylcholine, Glutamate, Dopamine
Describe inhibitory synapses
Inhibitory transmitters open ligand-gated channels that cause hyperpolarization Permeable to K+ or Cl-
Inhibitory post-synaptic potential (IPSP)
Transmitters include: Glycine, γ-aminobutyric acid (GABA)
Describe slow synaptic transmission
1. Direct G-protein gating Localised Quite rapid Ligand binding to gpcr G protein released GDP>GTP travels across inner of cell Activates an ion channel Since ion channel has intrinsic gtpase Dephosphorylates gtp Localised Rapid in relation to second one
2. Gating via an intracellular messenger Throughout cell Amplification by cascade Ligand binding to receptor Cd2 not cd1 G protein released Alone inner of membrane Until hits enzymeeg adenylyl cyclase Protein kinase a Then act on channel Phosphorylation channel Opens channel Slowe because enzyme and cascade system involved Activate second messenger Effect throughout cell Amplification by cascade A lot of activity
What are 2 other factors that can influence membrane potential?
- Changes in ion concentration
- Most important is extracellular K+ concentration (~4.0 mM normally)
- Sometimes altered in clinical situations
- Can alter membrane excitability, e.g. in heart - Electrogenic pumps
Na/K- ATPase - 3 NA out for 2 K+ in
One positive charge is moved out for each cycle
In some cells, this contributes a few mV directly to the membrane potential, making it more NEGATIVE Indirectly, the active transport of ions is responsible for the entire membrane potential, because it sets up and maintains the ionic gradients that generate the resting membrane potential
Explain insulin secretion
Glucose enter Metabolised ATP dependant k+ channel K+ leaves Vg calcium channel open calcium flood in Vesicles containing insulin fuse with plasma membrane Type 2 Diabetic Sulphanylurea receptor - shuts k+ channel Rewatch this part
What happens when membrane potential changes in anterior pituitary?
When trh added to system Causes a hyperpolarisation Decrease in memb potential Even more hyperpolarisation Trh bindsto gpcr Activated gq Phospholipids c activity Increased ip3 Binds to receptor on earth Increased intracellular ca conc Allows ca to leave Only when hyperpolarised Erg l+channel is shut Depolarisation - opens a vg ca2+ channel Influx of calcium Second round of secretion of prolactin
