nervous coordination Flashcards

1
Q

resting potential

A

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

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2
Q

how is resting potential established

A

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

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3
Q

action potential

A

When the neuron’s voltage increases beyond the -55mV
threshold
nervous impulse generated
generated due to membrane
becoming more permeable to
Na+

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4
Q

action potential stimulus

A

Voltage-gated Na+ channels open - membrane more permeable to Na+
Na+ diffuse (facilitated) into neuron down conc. gradient
voltage across membrane
increases

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5
Q

action potential depolarisation

A

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

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6
Q

action potential repolarisation

A

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

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7
Q

action potential hyperpolarisation

A

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

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8
Q

all or nothing principle

A

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

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9
Q

importance of all or nothing principle

A

Makes sure animals only respond to large enough stimuli rather than responding to every small change in environment
(overwhelming)

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10
Q

refractory period

A

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

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11
Q

importance of refractory period

A

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

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12
Q

factors affecting speed of conductance

A

Myelination (increases speed)
axon diameter (increases speed)
temperature (increases speed)

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13
Q

how myelination affects speed

A

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

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14
Q

how axon diameter affects speed

A

increases speed of conductance
less leakage of ions

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15
Q

how temperature affects speed

A

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

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16
Q

saltatory conduction

A

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

17
Q

synapse

A

Gaps between end of axon of
one neurone and dendrite of
another
impulses are transmitted as
neurotransmitters

18
Q

why are synapses unidirectional

A

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

19
Q

cholinergic synapse

A

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

20
Q

summation

A

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

21
Q

spatial summation

A

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

22
Q

temporal summation

A

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

23
Q

inhibitory synapses

A

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

24
Q

neuromuscular junction

A

Synapse that occurs between a
motor neurone and a muscle
similar to synaptic junction

25
Q

neuromuscular junction vs cholinergic synapse

A

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

26
Q

myofibril

A

Made up of fused cells that share nuclei/cytoplasm
(sarcoplasm) and many mitochondria
millions of muscle fibres make
myofibrils - bringing about movement

27
Q

role of Ca2+ in sliding filament theory

A

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

28
Q

role of tropomyosin in sliding filament theory

A

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

29
Q

role of ATP in myofibril contraction

A

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

30
Q

role of myosin in myofibril contraction

A

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

31
Q

phosphocreatine

A

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

32
Q

slow-twitch fibres

A

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

33
Q

fast-twitch fibres

A

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