Lecture 8- Changing membrane potential Flashcards
depolarisation
Depolarization
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
hyperpolarisation
An increase in the size of the membrane potential from its normal value
- *Cell interior becomes more negative
e. g. a change from–70mVto–90mV**
how do membrane potentials arise
as a result of selective ionic permeability
changing selectivity to ions
will change membrane potential
increasing membrane permeability to a particular ion moves the membrane potential
towards the equilibirum potential for that ion
list the equilibrium potential for :
K+
Cl-
Na+
Ca2+
opening of K+ or Cl- (moving eqilibrium potential towards Ek and Ecl)
will hyperpolarise
opening Na+ or Ca2+ (moving equilibrium potential towards ENa or ECa
channels will depolarise
The contribution of each ion to the membrane potential will depend on
how permeable the membrane is to that ion
some channels are less selective e.g.
nACHr at the NMJ
- allows both Na+ and K+ to enter (not anions)
equation that can be used to understand selective permeability
GHK (Goldman-Hodgkin-Katz) equation
nAChR at the NMJ
- Have an intrinsic ion channel
- Opened by binding of acetylcholine
- Channel lets Na+ and K+ through, but not anions
- Moves the membrane potential towards 0 mV, intermediate between ENa and EK
- = depolarisation
channels are often..
gated
controlling gated channels
- ligand gated
- voltage gated
- mechanical gated
ligand gated channel
responds to binding of a chemical ligand (ACh)
Channels at synapses that respond to extracellular transmitters and intracellular messengers
Voltage gate
responds to change in membrane potential
- Channels involved in AP
mechanical gated
response to membrane deformation
- Mechanoreceptors e.g. hair cells
synaptic conenction occur between (4 types of tissue)
- Nerve cell – nerve cell
- Nerve cell – muscle cell
- Nerve cell – gland cell
- Sensory cell – nerve cell
how does a synapse work
a chemical transmitter released from the presynaptic cell binds to receptors on the postsynaptic membrane.
two types of synaptic transmission
fast and slow
example of fast synaptic transmission
Receptor protein is also an ion channel
Transmitter binding causes the channel to open
E.g. nicotinicACh
example of slow synaptic transmission
GPCRs
- direct G-protein gating
- gating via an intracellular messenger
fast synaptic tranmission can be separated into 2 branches
excitatory
inhibitory
excitatory synapes
Open ligand gated channels that cause membrane depolarisation (e.g. permeable to sodium and calcium)
i. Ach binding
ii. Glutamate binding
Inhibitory synapes
Open ligand gated channels that cause hyperpolarisation (permeable to potassium and chloride)
Membrane taken further away from action potential
i. Glycine binding
ii. GABA binding
direct G-protein gating
G protein directly linked to channel- when ligand binds to G protein the channel will open
- Localised
- Quite rapid
GPCR- gating via intracellular messenger
G protein causing enzyme to signal intracellular messages or protein kinases which activate channels to open
what other factors can influence membrane potential?
- change in ion concentration
- electrogenic pumps
Changes in ion concentration influencing membrane potential
Most important is extracellular K+ concentration (~4.5 mM normally)
Sometimes altered in clinical situations
Acute hyperkalaemia-
brings resting potential closer to threshold- initially more excitable
In chronic hyperkalaemia, cells become less excitable
- Cannot reactivate sodium. Channels to keep opening- no AP
- Can alter membrane excitability, e.g. in heart – arrythmias
electrogenic pumps (Na/K ATPase) influence on membrane potential
tiny affect
- One positive charge moved out for each cycle
- Contributes a few mV directly to the membrane potential, making it more negative
Indirectly active transport of ions (Na/K ATPase) is responsible for
entire membrane potential, because it sets up and maintains the ionic gradient
