Lecture 6 Physiology of Neurons Flashcards
what are electrical synapses like compared to chemical synapses
faster bidirectional much smaller gap -3.5nm no plasticity (no learning) no amplification coupled via gap junctions
why is there no amplification in an electrical synapse
signal always weakened as transmitted from presynaptic to postsynaptic cell
(signal won’t transmit if postsynaptic cell is too much bigger than presynaptic)
what can’t excitatory presynaptic signal do in post synaptic cells
inhibit
what is spatial summation (of signals)
a neuron determines whether to fire based on amount of signals received from synapsing neurons
can then reach threshold
what is temporal summation of signals
input neuron is firing fast enough so that receiving neuron can add together signals (as can’t recover from small depolarisations fast enough) and reach threshold
what are the steps of an action potential
threshold reached by stimulation depolarisation overshoot repolarisation after-hyperpolarisation with refractory period resting state
what are the important voltages in an action potential
rest -70mV (near Ek)
threshold ~-50mV
Vm>0 overshoot (reaches ~+30mV)
inward rectifiers open -60mV (delayed rectifiers already open- repolarisation)
what does action potentials being ‘all-or-none’ mean?
carry no info about size of stimulus that stimulated them
how do neurons code the intensity of their synaptic input
firing frequency
different neurons for different strength stimuli
how does firing frequency represent the intensity of the activity
increasing threshold lowers firing freq and increasing excitatory synaptic activity increases it
how do lengthy synaptic currents affect firing frequency
when lengthy synaptic currents are small they create higher threshold potential due to accommodation than larger currents
what is accommodation
of Na+
inactivates duding the slower subthreshold depolarisation
first response stronger than later responses
how do different neurons code intensity
light touch receptors vs pain receptors - specific neuron for each stimuli
what is excitability
how easy it is to start nervous signalling
aka sensitivity in sensory cells, irritability in muscle or effector cells
risk of seizure or spasms if too much
how does increased threshold effect excitability
lowers it
what are excitability changes the basis of
psychotropic pharmacology - changes in threshold have profound health and behavioural effects
what are channels made up of
proteins
sometimes they conduct ions, sometimes they don’t
have different conformational states
what controls voltage-gated channels
change states based on transmembrane voltage
open when membrane +ve so can conduct and increase permeability, closing when membrane depolarises
how are inward rectifiers affected by transmembrane voltages
inward rectifiers are the opposite of other channels
close when inside positive and open when negative
why is inactivated not the same as closed
both non conducting, inactivated is when channel stops conducting (after a delay) when membrane positive inside (closed is when negative)
what happens to the membrane when Na+ channels open
positive inside as Na+ high on outside than inside
what is the potential of the extracellular space
electrically joined in all cells so same voltage everywhere
extracellular fluid considered electrical ground
what happens to the membrane when K+ channels open
negative inside as K+ higher on inside than outside
what happens to the membrane when Ca2+ channels open
positive inside as Ca2+ higher on outside than inside
passively goes inward
how do ionic permeabilities affect voltage
increased permeability to K+ makes membrane negative, Na+ opposite
how is the voltage of the cell membrane determined
inter-related feedback loops
at rest Vm=~Ek
as conductance of K+ is greater than that of Na+ or Ca2+
what is lidocaine
local anaesthetic, applied topically
how does lidocaine work
raises the threshold so lowers excitability stopping local action potentials by blocking Na+ channels in pain neurons
what is Carbamazepine
anticonvulsant
how does carbamazepine work
inactivates sodium channels to raise AP threshold and lower excitability
what are examples of other Na+ channel blockers
antiarrythmic drugs (class 1 eg quinidine) work by lowering conduction velocity to extend refractory period fugu fish poison (tetrotoxin (TTX))
how does Glibenclamide work
sulfonylurea to manage type 1 diabetes
increases excitability of pancreatic beta cells leading to increased insulin secretion (inhibit K+ channels)
what is chemical force
force on an ion
aka diffusional force
based on difference in concentration across a membrane
what is electrical force
force on an ion
based on membrane potential (Vm) which varies over time
what is the equilibrium potential
Ek aka reversal potential of K+
voltage when K+ in(electrical)=out(chemical) as electrochemical forces are in equilibrium
same for other ions
what is used to calculate equilibrium potential
Nernst Equation
how do equilibrium potentials differ
the more permeable the cell membrane is to K+ the more the membrane potential approaches the value of Ek
what are the equilibrium potentials of Ena, Ek, Eca, Ecl?
ENa = +60 mV EK = -90 mV ECa = +123 mV ECl = -40 mV (in neurons –65 mV)
how do ion channels control voltage
open channels conducting with little competition - membrane potential to that ion’s equilibrium potential
both open - halfway point between 2 equilibrium potentials
what are action potentials (compared to graded potentials)
stereotyped electrical signal
short-duration
in most neurons, skeletal and cardiomyocytes
a spike
all or none
require time to start due to conformational changes
what are graded potentials (compared to action potentials)
electrically localised - membrane potential last a long time much flatter in shape conducted almost instantly in receptor cells eg cones and rods variable in duration and voltage
how is electricity conducted in axons
passive
all + = - at start, Na+ moves in, increasing flow and -ve charges
all charges move simultaneously in same direction
depolarisation jumps to NofR’s - saltatory conduction
what makes saltatory conduction down an axon faster
large diameter as less resistance
myelinated
what are graded potentials issues with transmitting signals
changes in membrane potential don’t propagate far via passive electrical forces and voltage diminishes further from source - needs help
why do voltage signals in graded potentials decrease further from the source
axon has a finite resistance
how do graded potentials transmit action potentials
transmit along length of axon, the AP re-amplifies the signal but slows down transmission at the nodes due to conformational changes
what is saltatory conduction
when action potential jumps from node to node for faster conduction velocity
what are typical conduction velocities
100 m/s for alpha motor fibres (myelinated, 15 um diam.)
1 m/s for C nociceptive fibres (unmyelinated, 0.2 - 1.5 um)
clinical uses for conduction velocity
Nerve conduction studies are used for evaluation of paraesthesias
numbness, tingling, burning
Evaluation of weakness of the arms and legs
