excitable cells Flashcards
action potential
rapid change in membrane potential
from -70 to 60 mV
how is the resting membrane potential maintained?
high permeability to K+
active transport of Na+ across membrane
transmembrane proteins (K+ leak channel and Na+ pump)
electrogenic
creating slight positive charge outside of cell
equilibrium potential
voltage at which the electrical gradient is equal and opposite to that of K+ concentration gradient
K+ therefore stops moving
how is equilibrium potential determined?
the nernst equation
nernst equation
(-RT/zF)Ln (conc (ion in)/conc(ion out))
equilibrium potential of K+
-86 mV
equilibrium potential of Na
+60mV
equilibrium potential of Cl
-70mV
resting membrane potential
-70mV
what equation determines resting membrane potential?
the Goldmann equation
why is RMP closer to Ek than ENa?
biggest weighting given to most permeable ion
V-gated Na+ channel
potential reaches -55mV
Na+ rushes through activation gate of channel
sodium activation gate
voltage and time dependent
sodium inactivation gate
time-dependent
sodium gate open to inactivated
fast and automatic
sodium gate inactivated to closed
slow automatic
sodium gate closed to open
fast
voltage-gated
voltage gated K+ channel
opens at membrane depolarisation slower than Na+
closes slowly in response to repolarisation
K+ gate open to closed
slow
voltage-gated
K+ closed to open
slow
voltage gated
absolute refractory period
period in which membrane can’t generate another action potential despite stimulus size.
sodium channels are inactivated
relative refractory period
period in which membrane can generate another a.p, only if stimulus is bigger than normal
some Na+ recovered
some K+ still open
where does a.p start
axon hillock
refractory period function
prevents a.p. being set off backwards
velocity of action potential
proportional to sqrt (diameter*membrane resistance)
consequence of diameter on neuron transmission
more room for local current flow in loops
consequence of resistance on neuron transmission
lower resistance = less current lost by leaking
what affects a.p velocity in a myelinated neuron
resistance
diameter
distance between nodes of ranvier
multiple sclerosis
demyelinating disorder causing gradual loss of motor function
a.p. unable to jump between nodes of ranvier
what happens when a.p invades neuron terminal?
membrane is depolarised and voltage-gated calcium ion channels open
what happens when voltage-gated calcium ion channels open?
Ca2+ rushes into axon terminal, causing vesicle fusion with the presynaptic membrane
what happens when vesicles fuse to the pre-synaptic membrane?
vesicles release ACh into the synaptic cleft so that they diffuse across and bind to postsynaptic receptors
what happens when ACh binds to post-synaptic receptors?
ligand-gated Na+ channels open and rush into postsynaptic cell and K+ out, reaching endplate potential of -15mV
endplate potential
1/2 total equilibrium potentials of sodium and potassium ions
a.p at junction folds
none as there’s no voltage-gated Na+ channels
what happens when EPP reaches -15mV?
EPPs in junctional folds trigger a.p’s nearby, propagating deep to trigger contraction
smallest EPP generated
when
0.5mV
occurs at random when nerve is at rest
1mEPP
1 vesicle fusion =1 quantum=10000ACh
1EPP
100mEPP therefore 100 vesicles
safety factor of neurones
margin of 200-300 vesicle releases for normal a.p at NMJ
what does acetylcholine break down into?
choline + acetate
reforms via acetyl coA
acetylcholinesterase location
junctional folds in the synaptic cleft
acetylcholinesterase function
cleaves ACh so action potentials aren’t transient
curare
South American arrow poison causing paralysis by blocking ACh receptor
also used as muscle relaxant by anaesthetists
botulinum toxin
inhibits exocytosis so ACh release is blocked
used in botox
bacteria in tinned food
myasthenia gravis
autoimmune disorder
antibodies destroy ACh receptors
safety factor means many antibodies need to accumulate for NMJ to stop functioning
treated by ACh-ase inhibitors
sarcoplasmic reticulum
protein pumps transport Ca2+ ions into T-tubules
T-tubules
deep infoldings in sarcolemma
get a.p. into parts of muscle that membrane can’t reach
muscle fibre size
roughly 100micrometers
what happens during muscle contraction to muscle
shortens
myosin/ actin don’t change length
actin slides over myosin (thick)
Z-line
vertical line of actin
M-line
vertical line of myosin
H band
length change during contraction?
distance between actin filaments
shortens
A band
length change during contraction?
length of myosin horizontal filaments
no change
I band
length change during contraction?
distance between myosin filaments
shortens
myosin
thick filament
fibrous protein with globular head
held together by M-line
actin
thin filaments
globular protein (G-actin) linked to form chain
2 F-actin strands twist to form double helix
tropomyosin
fibrous protein twisted around actin
troponin
attached to actin at regular intervals
3 sub-units of actin filament
T/I > tropomyosin and actin binding
C> Ca2+ binds to C, uncovering binding site
G-actin number of binding sites
1
sarcolemma
tubular structure surrounding myofibrils
enlarges into terminal cisternae
stores much Ca2+
what happens when there’s an a.p in t-tubules?
triggers Ca2+ release from terminal cistae of sarcoplasmic reticulum, triggering contraction
Ca2+ binds to troponin-C, uncovering myosin binding site on actin to form cross-bridge
excitogen contraction coupling
- myosin in high-energy state, hydrolysing ATP
- myosin heads rotate> powerstroke
- ATP binds to myosin head, breaking actin-myosin bond and releasing ADP+Pi
- ATP split returning myosin to high energy state
number of myosin heads in one muscle fibre
500
how many cycles per second in one muscle fibre
5
muscle relaxation
SR removes Ca2+ via Ca-ATPase pump
ATP binds to myosin
3 types of neurone
motor (efferent)
interneurone
sensory (afferent)
where are interneurones located
CNS
types of sensory neurone
pseudo-unipolar > somatic senses
bipolar> smell and vision
neurone characteristics
don’t divide (foetal neurones lose mitosis ability)
longevity
high metabolic rate
2 types of electrical signal in neurones
action potential
graded potential
action potential characteristics
large, uniform depolarisations travelling rapidly for long distances w/o losing strength
all or none
graded potentials
variable strength signals that travel over short distances, losing strength
can generate a.p’s
where do graded potentials occur?
in dendrites, cell bodies or axon terminals
NOT AXONS
depolarizing graded potential
excitatory post-synaptic potential
EPSP
hyperpolarizing graded potential
inhibitory post-synaptic potential
IPSP
threshold voltage
-55mV
subthreshold vs suprathreshold
below / reachind threshold
pros of frequency encoded signals
digital and therefore less prone to ‘noise’
greater fidelity
divergence
presynaptic neurone branching to affect large number of postsynaptic neurones
convergence
large number of presynaptic neurones converge to affect smaller number of postsynaptic neurones
spatial summation
EPSP’s originating simultaneously at different locations on the neurone to form suprathreshold signal and therefore an a.p.
postsynaptic inhibition
EPSP’s diminished by summation with an IPSP, meaning summed potential is subthreshold and therefore no a.p.
temporal summation
summation occurring from graded potentials overlapping in time
postsynaptic integration/ modulation
evaluation of strength / duration of signals to determine action potential firing
presynaptic modulation characteristics
more precise
excitatory/ inhibitory
presynaptic similarities
action potential
Ca2+ channel opening and Ca2+ increases in concentration to cause exocytosis
neurotransmitter diffuses across cleft
postsynaptic differences
neurotransmitter identity
receptor identity and mechanisms
neurotransmitter examples
ACh
amines
amino acids
polypeptides
purines
gases
2 receptor mechanisms
ligand-gated ion channels (inotropic)
G-protein coupled receptors (metabotropic)
inotropic channel characteristics
example
fast synaptic potential
e.g. nicotinic
metabotropic channel characteristics
example
activates 2nd messenger systems
slow synaptic potential
e.g. muscarinic
advantage of inotropic/ metabotropic receptors
adds diversity to the system
synaptic plasticity
variation of electrical activity, causing rearrangmenets of circuit connections
long-term potentiation
process by which repetitive stimulation at a synapse increases the efficacy of transmission at that synapse
where was LTP first observed?
in the hippocampus
how is LTP prevented?
by Ca2+ removal from extracellular medium
main excitatory transmitter in CNS
glutamate
LTP process
glutamate released and binds to NMDA and AMPA inotropic receptors.
repetitive stimulation results in greater depolarisation, Mg2+ ejected from NMDA receptor so Ca2+ can flow through.
therefore, postsynaptic cell more sensitive to glutamate release from presynaptic cell.
AMPA
Na+ channel triggering EPSP
NMDA
blocked by Mg2+ therefore no effect
