nervous coordination Flashcards
resting potential
the difference between electrical charge inside and outside the axon when a neuron is not conducting an impulse
more positive ions outside axon than inside
inside the axon -70mV
how is resting potential established
Sodium potassium pump actively transports 3 Na+ out of the axon, 2 K+ into the axon membrane more permeable to K+
K+ diffuses out down conc. gradient - facilitated diffusion
membrane less permeable to Na+ (closed Na+ channels)
higher conc. Na+ outside
action potential
When the neuron’s voltage increases beyond the -55mV
threshold
nervous impulse generated
generated due to membrane
becoming more permeable to
Na+
action potential stimulus
Voltage-gated Na+ channels open - membrane more permeable to Na+
Na+ diffuse (facilitated) into neuron down conc. gradient
voltage across membrane
increases
action potential depolarisation
When a threshold potential is reached, an action potential is
generated
more voltage-gated Na+ channels open
Na+ move by facilitated diffusion down conc. gradient into axon
potential inside becomes more
positive
action potential repolarisation
Na+ channels close, membrane less permeable it Na+
K+ voltage-gated channels open, membrane more permeable to K+
K+ diffuse out neuron down
conc. gradient
voltage rapidly decreases
action potential hyperpolarisation
K+ channels slow to close -> overshoot in voltage
too many K+ diffuse out of neuron
potential difference decreases to
-80mV
sodium-potassium pump returns neuron to resting potential
all or nothing principle
If depolarisation does not exceed -55 mV threshold, action potential is not produced
any stimulus that does trigger depolarisation to -55mV will always peak at the same maximum voltage
importance of all or nothing principle
Makes sure animals only respond to large enough stimuli rather than responding to every small change in environment
(overwhelming)
refractory period
After an action potential has been generated, the membrane enters a period where it cannot be stimulated
because Na+ channels are recovering and cannot be opened
importance of refractory period
Ensures discrete impulses produced - action potentials separate and cannot be
generated immediately
unidirectional - cannot generate
action potential in refractory
region
limits number of impulse
transmissions - prevent
overwhelming
factors affecting speed of conductance
Myelination (increases speed)
axon diameter (increases speed)
temperature (increases speed)
how myelination affects speed
With myelination - depolarisation occurs at Nodes of Ranvier only -> saltatory conduction
impulse jumps from node-node
in non-myelinated neurones,
depolarisation occurs along full
length of axon - slower
how axon diameter affects speed
increases speed of conductance
less leakage of ions
how temperature affects speed
Increases speed of conductance
increases rate of movement of
ions as more kinetic energy
(active transport/diffusion)
higher rate of respiration as
enzyme activity faster so ATP is
produced faster - active
transport faster
saltatory conduction
Gaps between myelin sheath are nodes of Ranvier
an action potential can “jump”
from node to node via saltatory
conduction - action potential
travels faster as depolarisation
across the whole length of the axon not required
synapse
Gaps between end of axon of
one neurone and dendrite of
another
impulses are transmitted as
neurotransmitters
why are synapses unidirectional
Receptors only present on the post-synaptic membrane
enzymes in the synaptic cleft break
down excess-unbound
neurotransmitter - concentration gradient
established from pre-post synaptic neurone
neurotransmitter only released from the pre-synaptic neurone
cholinergic synapse
The neurotransmitter is acetylcholine
enzyme breaking down
acetylcholine = acetylcholine-esterase
breaks down acetylcholine to
acetate and choline to be
recycled in the pre-synaptic
neurone
summation
Rapid build-up of neurotransmitters in the synapse to help generate an action potential by 2 methods:
spatial or temporal
required because some action
potentials do not result in
sufficient concentrations of
neurotransmitters released to
generate a new action potential
spatial summation
Many different neurones collectively trigger a new action
potential by combining the
neurotransmitter they release
to exceed the threshold value
e.g., retinal convergence for
rod cells
temporal summation
When one neurone releases
neurotransmitters repeatedly
over a short period of time to
exceed the threshold value
e.g., 1 cone cell signalling 1
image to the brain
inhibitory synapses
Causes chloride ions (Cl-) to move into post-synaptic neuron and K+ to move out
makes membrane hyperpolarise
(more negative) so less likely an
action potential will be propagated
neuromuscular junction
Synapse that occurs between a
motor neurone and a muscle
similar to synaptic junction
neuromuscular junction vs cholinergic synapse
NMJ -
unidirectional
only excitatory
connects motor neurons to muscles
end point for action potential
CS-
unidirectional
excitatory or inhibitory
connects 2 neurons
new action potential generated in next neuron
myofibril
Made up of fused cells that share nuclei/cytoplasm
(sarcoplasm) and many mitochondria
millions of muscle fibres make
myofibrils - bringing about movement
role of Ca2+ in sliding filament theory
Ca2+ enters from sarcoplasmic
reticulum and causes tropomyosin to change shape
myosin heads attach to exposed
binding sites on actin forming
actin-myosin cross bridge
activates ATPase on myosin
ATP hydrolysed so energy for
myosin heads to be recocked
role of tropomyosin in sliding filament theory
Tropomyosin covers binding site on actin filament
Ca2+ bind to tropomyosin on
actin so it changes shape exposes binding site
allows myosin to bind to actin,
forming cross bridge
role of ATP in myofibril contraction
Hydrolysis of ATP -> ADP + Pi releases energy
movement of myosin heads pulls actin - power stroke
ATP binds to myosin head causing it to detach, breaking cross bridge
myosin heads recocked
active transport of Ca2+ back to
sarcoplasmic reticulum
role of myosin in myofibril contraction
Myosin heads (with ADP attached) attach to binding sites on actin.
form actin-myosin cross bridge
power stroke - myosin heads
move pulling actin
requires ATP to release energy
ATP binds to myosin head to
break cross bridge so myosin
heads can move further along
actin
phosphocreatine
A chemical which is stored in muscles
when ATP concentration is low,
this can rapidly regenerate ATP
from ADP by providing a Pi group.
for continued muscle contraction
slow-twitch fibres
Specialised for slow, sustained contractions (endurance)
lots of myoglobin
many mitochondria - high rate
aerobic respiration to release
ATP
many capillaries - supply high
concentrations of glucose/O2 &
prevent build-up of lactic acid
e.g. thighs/calf
fast-twitch fibres
Specialised in producing rapid,
intense contractions of short duration
glycogen -> hydrolysed to glucose -> glycolysis
higher concentration of enzymes involved in anaerobic
respiration - fast glycolysis phosphocreatine store
e.g., eyelids/biceps
