Physiology of Neurons Flashcards
how are electrical synapses different from chemical synapses?
faster always excitatory bidirectional smaller gap no plasticity no amplification coupled via gap junctions used for defensive reflexes, retina and brain
what does ‘no amplification’ mean?
signal is always weakened as it is transmitted from pre to post-synaptic cell
signal will not transmit if post-synaptic cell is much bigger than presynaptic cells
what is spatial summation?
a neuron determines whether to fire based on ‘addition’ of all tiny signals from several neurons synapsing on it
hence many small depolarisations can reach threshold
what is temporal summation?
when input neuron is firing fast enough, receiving neuron can ‘add’ many tiny signals to reach threshold
neurons ability to recover from tiny input is slow enough that when next signal arrives, neuron is still slightly depolarised
action potential summary
- at rest - K+ leaving the cell clamps the membrane potential negative (-70mV)
- an external factor (eg synaptic activity) causes membrane to depolarise slightly possibly reaching threshold
- Na+ conductance shoots up, Na+ goes into cell - membrane depolarises and voltage becomes positive
- with time delay, Na+ conduction diminishes, K+ conductance increases - K+ leaves the cell, voltage returns to resting potential
what is permeability?
how easy it is for a particle to move through the membrane
what is conductance?
how easy it is for charge to move across the membrane
what happens at initial depolarisation?
cells start at rest (-70mV), resting membrane potential is near Ek
inward rectifier K+ channels are open - K+ flowing out is dominant current
something occurs, causing cell to become less negative
what can cause a cell to become less negative?
nearby cell depolarising
synaptic transmission where neurotransmitter opens a ligand-gated channel
what is depolarisation?
inside the cell the voltage becomes less negative/more positive
describe the positive feedback of depolarisation
initial depolarisation causes a few Na+ channels to open
Na+ permeability increases, so Na+ current flows through channels into cell
additional current of Na+ entering cell causes greater depolarisation - membrane moves closer to 0mV
when voltage surpasses threshold (-50mV), cell is committed to AP
positive feedback of increasing Na+ conductance and increasing voltage until membrane becomes quite positive (+30mV)
what is repolarisation?
voltage becomes less positive/more negative inside the cell
what happens during repolarisation?
2 delayed-action events occur
Na+ channel inactivation: Na+ current going in decreases
delayed rectifier K+ channels open - K+ going out increases
what is the refractory period?
period of time in which a neuron is incapable of reinitiating an AP
occurs mostly during after-hyperpolarisation
amount of time t takes for membrane to be ready for a second stimulus, once it has returned to resting state following excitation
what is after-hyperpolarisation?
at the end of an AP, the voltage temporarily goes slightly more negative than at rest, followed by the return to resting membrane potential
why does after-hyperpolarisation occur?
when voltage drops below -60mV, inward rectifier K+ channels open, clamping voltage towards Ek
delayed rectifier K+ channels are still open (slow to close)
almost all Na+ channels are inactivated
coding of intensity by neurons
action potentials are ‘all or none’ - carry no information about size of stimulus
firing frequency represents intensity of activity
+ different neurons for different strength stimuli (light tough vs pain receptors)
what can affect firing frequency?
increasing threshold (more positive) lowers firing frequency
increasing excitatory synaptic activity increases firing activity
when lengthy synaptic currents are small, there is a greater threshold than there is for larger currents
this is due to Na+ current accommodation (channels are inactivated during slower, subthreshold depolarisation)
what is excitability?
how easy it is to start nervous signalling
‘sensitivity’ in sensory cells
‘ irritability’ in muscle/effector cells
changes in excitability are the basis of psychotropic pharmacology
what is threshold?
voltage above which an action potential fires
increased threshold lower excitability
changes have profound health and behavioural effects
what are channels?
proteins
sometimes conduct ions, sometimes don’t
have different conformational states
voltage-gated channels
change states based on transmembrane voltage
open when membrane becomes positive inside (increased permeability)
channels close when membrane repolarises
(inward rectifier channels are opposite)
what is the difference between an inactivated and a closed channel?
inactivated = when a channel stops conducting when membrane is positive inside closed = when a channel stops conducting when membrane is negative inside
what happens when Na+ channels open?
Na+ enters the cell
the membrane becomes more positive inside
([Na+] is higher outside the cell)
what is membrane voltage?
described in terms of what happens to the intracellular face of the membrane
when inside is positive with respect to extracellular face, membrane is positive
extracellular space of all cells it electrically joined, thus voltage is the same everywhere (=electrical ground)
what happens when K+ channels are open?
K+ ions travel from inside to outside the cell
([K+] is higher outside the cell)
membrane becomes more negative inside
what happens when Ca2+ channels open?
Ca2+ passively goes inward
([Ca2+] is higher outside the cell)
membrane becomes more positive inside
how does voltage depend on ion permeabilities?
increased permeability to K+ makes membrane more negative
increased permeability to Na+ makes membrane more positive
voltage is determined by inter-related feedback loops
what is lidocaine/lignocaine?
local anaesthetic, applied topically
raises threshold and lowers excitability
stops local APs
specifically blocks Na+ channels in inactivated state (Na+ cannot enter to depolarise cell)
what is carbamazepine?
anticonvulsant
blocks Na+ channels (+ other actions)
raises action potential threshold, lowers excitability
used to treat seizure disorders and neuropathic pain
other Na+ channel blockers
antiarrhythmic drugs (class 1) eg quinidine
lowers conduction velocity
refractory period is extended
tetrodoxin: pufferfish poison
which two forces act on each ion?
chemical and electrical force
what is the chemical force?
diffusional force
based on difference in concentration across the membrane
what is the electrical force?
based on Vm (membrane potential)
varies over time
what is the equilibrium potential?
Ek - also called reversal potential of K+
voltage where K+ flowing out = K+ flowing in
electrochemical forces on K+ are in equilibrium
diffusional forces pushing K+ out (chemical) = voltage forces pushing K+ in (chemical)
the more permeable the cell is to K+, the more Vm approaches Ek
what is the Nernst equation?
used to calculate equilibrium potential
equilibrium potential values
ENa = +60mV EK = -90mV ECa = +123mV ECl = -40mV (-65mV in neurons) different tissues have slightly different values
how to open ion channels control voltage?
if many Na+ channels are conducting, with no other currents, Vm will tend towards +60mV
if may K+ channels are conducting, with no other currents, Vm will tend towards -90mV
If K+ and Na+ channels are open, and cell was equally permeable to both, Vm would tend towards to the average of their equilibrium potantials, -15mV
what are action potentials?
stereotypes electrical signals
short duration
in more neurons, skeletal and cardiomyocytes
a spike
‘all-or-none’
require time to start, due to conformational changes
what are graded potentials?
ordinary changes in electrical potential
describes transmembrane electrical changes in cells which do not have action potentials
how are graded potentials different to action potentials?
decrease as they move along electrically localised last a long time much flatter in shape are conducted almost instantly in receptor cells (eg rods and cones) variable in duration and voltage
how do graded potentials transmit signals?
changes in membrane potential do not propagate very far via passive electrical forces
voltage signals diminish as distance from source increases (axon has finite resistance)
signal is transmitted along length of an axon
AP is a way to reamplify the signal
what is saltatory conduction?
when AP ‘jumps’ from node to node
net effect is a faster conduction velocity
jumps are very fast, initiating an AP at each node is slower (requires conformational change of ion channels)
what is conduction velocity affected by?
myelination diameter size (large has less resistance)
clinical uses of conduction velocity
nerve conduction studies in evaluation of paraesthesis (numbness, tingling, burning)
evaluation of weakness in arms and legs
