Nervous coordination and muscles Flashcards
How do nerve cells stimulate their target cells
by secreting neurotransmitters directly on to them
what does secreting neurotransmitters directly on to target cells result in
rapid communication between specific parts of an organism
response produced by nerve cells
-short-lived
-restricted to a localised region of body
how does hormonal system transport chemicals (hormones)
in blood plasma to target their cells
what do target cells have
specific receptors on their cell surface membrane
what does a change in conc of hormones stimulate
specific receptors on cell surface membrane
results of hormonal system
-slower
-less specific form of communication between parts of an organism
response of hormonal system
long lasting
widespread
cell body
-contains usual organelles
-RER > production of proteins and neurotransmitters
what are neurones specialised to do
specialised cells adapted to rapidly carry electrochemical changes (nerve impulses) from one part of body to another
dendrons
-extensions of cell body which divide into dendrites
-carry nerve impulses TOWARDS cell body
axon
single long fibre that carries nerve impulses away from cell body
Schwann cells
-surround axon > protecting it and providing electrical insulation
-carry out phagocytosis
-play part in nerve regeneration
-wrap themselves around axon many times > layers of their membrane build up around it
myelin sheath
-made of membranes of Schwann cells
-membranes are rich in lipid (myelin)
what are neurones with myelin sheath called
myelinated neurones
nodes of Ranvier
-constrictions between adjacent Schwann cells where there’s no myelin sheath
um of constrictions of nodes of Ranvier
- 2-3 um long
-occur every 1-3mm in humans
sensory neurone
-transmit nerve impulses from receptors to an intermediate or motor neurone
structure of sensory neurone
-1 dendron thats often very long
-carries the impulse towards cell body and 1 axon that carries it away from cell body
motor neurone
transmit nerve impulses from an intermediate or relay neurone to effector
structure of motor neurones
-long axon
-many short dendrites
intermediate neurone
-transmit impulses between neurones eg sensory > motor
-have numerous short processes
define resting potential
potential difference across an axon membrane at rest (inside -65mV compared with outside)
How does phospholipid bilayer control Na+ and K+ across axons membrane
-phospholipid bilayer of axons plasma membrane prevents Na+ and K+to diffuse across it
How do proteins control Na+ and K+ across axons membrane
-channel proteins span this phospholipid bilayer
-some channels have ‘gates’ that can be open/closed so Na+ / K+ can move through them via facilitated diffusion
-some gates however remain open all the time so Na+ and K+ move unhindered through them by facilitated diffusion
how does sodium-potassium pump control Na+ and K+ across axons membrane
actively transport potassium ions into axon and sodium ions out axon
How a resting potential is established in neurone
-sodium potassium pump actively transport 3 Na+ out axons membrane and 2 K+ into axons membrane
-1 K+ moved via diffusion from high conc to lower conc through gated K+ channels that open
-Na+ channels remain firmed closed so Na+ cant move onto axon thus remain outside axon’s membrane tissue fluid
-tis makes inside less positive than outside > electrochemical gradient
-membrane more permeable to K+ than Na+ so they diffuse back out of axon further increasing potential difference across the membrane
-inside of axon less positive than outside to the value of -65mV
-polarisation of axon is created
Why is resting potential negative?
as there are more positive ions outside the cell, making the inside comparatively more negative
difference in membrane permeability in resting potential
-MORE permeable to K+ (somove out by facilitated diffusion
-LESS permeable to Na+ (closed channels)
What co-transport protein is involved in the maintenance of resting potentials?
Na-K pump
How many of each ion are transported each time by the Na-K pump?
2 x K+ INTO the cell
3 x Na+ OUT OF the cell
what does the Na-K pump create?
electrochemical gradient
Why is resting potentially end up negative, if both ions diffuse in/out?
because the membrane is more permeable to K+ ions
Why is the axon membrane more permeable to K+ ions?
-most K+ channels stay open (compared to Na+ ions which only open due to change in voltage)
-there are more K+ channels
How is resting potential maintained?
membrane more permeable to K+ ions and less permeable to Na+ ions
Na+ ions are actively pumped out and K+ ions in
What is an action potential?
an increased voltage beyond a set point, generating a nervous impulse
What is depolarisation and why does it occur?
an increase in voltage, which occurs as the membrane becomes more permeable to Na+
What protein channels are voltage dependent?
voltage-gated Na+ channels
How might a stimulus cause depolarisation?
as it may allow voltage-gated Na+ channels to open, allowing Na+ ions to diffuse in, meanwhile K+ ions still diffuse out
What happens if the voltage is raised above the threshold?
More Na+ ions can move into the cell, so voltage increases further
What is the maximum voltage an axon can reach?
+40mV
What happens at +40mV?
more K+ channels are opened, and voltage-gated Na+ channels close. This causes voltage to decrease
What is the refractory period?
where voltage goes temporarily below the resting potential
What are the different stages in generating an action potential?
resting, depolarisation, repolarisation, hyperpolarisation, resting
Why do action potentials move across an axon like a mexican wave?
as one part reaches +40mV, the voltage is enough to trigger the next part (nodes of Ranvier) of the axon to start depolarisation
What happens if the voltage does not pass -55mV?
nothing, the action potential and impulse are not produced
Why does a depolarisation that does not reach the threshold not cause an action potential?
not enough energy to open voltage gated Na+ channels
What does a bigger stimuli cause?
a greater frequency
Why is the all or nothing principle important?
makes sure animals only respond to large enough stimuli, rather than the animal becoming overwhelmed
what does the refractory period mean
action potential cannot be stimulated, as the Na+ channels are recovering
Why is the refractory period important?
-only discrete impulses are produced
-only travel forwards in one direction
-limits the number of impulse transmission
Why is it important that impulses are discrete?
so each action potential is separate and therefore information can be processed in more detail
Why is it important that action potentials only travel forwards?
if it wasn’t, Na and K+ ions would spread out, preventing the threshold from ever being met and therefore preventing a response
Why is it important that the number of action potentials are limited?
it prevents over reaction to a stimulus which could result in overwhelming the sense, hindering survival
process of acton potential
-axon is polarised Na+ channels closed and K+ channels open
-Na+ diffuse into axon by sodium-gates channels which depolarised the axon by energy from stimulus
-reversal of electrochemical gradient causes the potential to increase to +40mV
-axon is depolarised and and increase in electrochemical gradient leads to hyperpolarisation > potential of -75mV
-axon eneters refractory period
nature and importance of refractory period
-refractory period = time to restore axon at resting potential when no further action potential can be generated because Na+ channels are closed so will not happen
-ensures discrete impulses are produced (actions potentials don’t overlap)
-limits high frequency impulse transmission
changes in membrane permeability lead to depolarisation and the generation of action potential
-STIMULUS > Na+ channels open, membrane permeability to Na+ increases > Na+ diffuse into axon down electrochemical gradient (causing depolarisation)
-DEPOLARISATION > if threshold potential reached, an action potential is generated > as more voltage-gated channels open (positive feedback effect) > more Na+ diffuse in rapidly
-REPOLARISATION > voltage-gated Na+ channels close> voltage-gated K+ channels open and K= diffuse out of axon
-HYPERPOLARISATION > K+ channels slow to close so there’s straight overshoot - too many K+diffuse out
-RESTING potential - restored by Na+/K+ pump
passage of action potential in unmyelinated axon
1) at resting potential conc of Na+ outside axon is higher than inside and conc of K+ higher inside than outside > causes polarisation of the membrane as overall conc of + ions is greater on outside than inside
2) stimulus causes sudden influx of Na+ into axon > leading to reversal of charge > action potential and membrane is depolarised
3) localised electrical current established by influx of Na+ causes voltage-gated sodium channels to open little further along axon for new area of axon becoming depolarised > behind this new region of depolarisation Na voltage-gated channels close so K opens > K+ leave axon along electrochemical gradient so depolarisation moved along membrane
4)action potential (depolarised area) is propagated further along the axon > K+ continues to move out until axon membrane behind action potential has returned to its original charged state ( + outside, - inside) > leading to repolarisation
5)repolarisation of axon allows Na+ to actively move out again, once again returning the axon to its resting potential in readiness for new stimulus
passage of action potential along myelinated axon
-fatty sheath of myelin along axon acts as electrical insulator, preventing action potential from forming
-intervals of 1-3mm there’s nodes of Ranvier where action potentials can occur
-localised circuits therefore arise between adj nodes of Ranvier and action potentials in effect jump from node to node in process of saltatory conduction
why is an action potential passed along myelinated neurone faster than along the axon of an unmyelinated one of same diameter
-in an unmyelinated neurone, the events of depolarisation have to take place all the way along an axon and this takes more time
difference between action potentials in myelinated and unmyelinated axons
NON-MYELINATED
-action potential passes a wave of depolarisation
-influx of Na+ in one region increases permeability of adjoining region of Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises
MYELINATED
-provides electrical insulation
-depolarisation of axons at NOR only -resulting in saltatory conduction ( local current circuits)
-so there’s no need for depolarisation along whole length of axon
damage to myelin sheath causes what
-less/no saltatory conduction > so nerve impulse takes longer to reach neuromuscular junction /delay muscle contraction
-ions/depolarisation may pass > causing wrong muscle fibres to contract
factors affecting speed at which neurones travel - myelin sheath
-acts as electrical insulator . prevent a.p. forming in the part of the axon covered in myelin
-it does jump from one node of ranvier to another (saltatory conduction) > increases speed of conductance from 30 ms-1 in unmyelinated neurone to 90ms-1 in similar myelinated one
factors affecting speed at which neurones travel - diameter of axon
- greater diameter the axon , faster the speed of conductance > due to less leakage of ions from a large axon (leakages make membrane potentials harder to maintain)
factors affecting speed at which neurones travel - temp
-affects rate of diffusion of ions and so the higher the temp, the faster the nerve impulse
-energy for active transport comes from respiration for Na/K pump that is controlled by enzymes which function more rapidly at higher temps up to a point> after certain point they and plasma membrane proteins are denatured and impulses fail to be conducted at all
why is temperature an important factor in cold blooded animals
their body temps vary in accordance with their environment
Describe and explain the all or nothing principle
-There is a certain level of stimulus - threshold value - that triggers an action potential. -Below threshold no action potential or impulse (nothing), -above threshold action potential occurs but they are all the same size (all)
why can’t the strength of a stimulus be detected by the size of the action potential
all action potentials are more or less the same size
how can an organism perceive the size of a stimulus
-no. of impulses passing in a given time > larger the stimulus, the more impulses that are generated in a given time
-having different neurones with different threshold values > brain interprets the no. + type of neurone that pass impulses as a result of given stimulus thereby determines the size
refractory period
Period of time time after an action potential when no further action potential can occur because the voltage gated sodium ion channels are closed.
3 purposes of refractory period
-ensures that action potentials are propagated in one direction only > as action potentials cannot be propagated in a region that is refractory
-produced discrete impulses > due to refractory period a new action potential cannot be formed immediately behind first one > ensures a.p is separated
-limits the no, of a.p > this is due to them being separated > so this limits strength of stimulus that can be detected
Define synapse
Junction between neurons, they don’t touch and have a small gap (synaptic clef) through which n.t are passed
structure of a synapse
-n.t transmitted from one neurone to another
-neurones separated by small gap (synaptic cleft)
-presynaptic neurone releases n.t
-axon of presynaptic neurone ends in a swollen portion known as synaptic knob
-this processes many mitochondria and large amounts of endoplasmic reticulum
-these are required in manufacture of n.t which takes place in axon
-nt stored in synaptic vesicle
features of synapse - unidirectionality
-can pass info in one direction > from presynaptic neurone to postsynaptic neurone
summation
entails a rapid build up of nt in synapse by either spatial or temporal summation
spatial summation
no of different presynaptic neurones together release enough n.t to exceed threshold value of posy synaptic neurone
-so together they trigger a.p
temporal summation
-single presynaptic neurone releases n.t many times over a short period
-if conc of n.t exceeds threshold value of postsynaptic neurone, a new a.p is triggered
how is it possible for impulses to travel 1 direction
- neurotransmitter is only stored in the presynaptic neurone
- neurotransmitter receptors are only found on the postsynaptic neurone
· Explain how a synapse is involved in inhibition
-Inhibitory synapses make it less likely that an action potential is triggered in the postsynaptic neurone:
- The neurotransmitter released binds to chloride ion channels on post synaptic neurone
-Chloride ion channels open and chloride ions enter the postsynaptic neurone by facilitated diffusion
-Binding of neurotransmitter opens potassium ion channels and potassium ions move out of the postsynaptic neurone
-Movement of negative chloride ions in and positive potassium ions out makes the inside of postsynaptic membrane more negative and outside more positive > the membrane potential increase to -80mV (hyperpolarisation). This makes an action potential less like as more sodium ions need to enter to reach threshold.”
Describe the functions of a synapse
-Transmit information from neurone to another allowing:
- single impulse along 1 neurone to initiate new impulses in a no of diff neurones at a synapse > allows single stimulus to create a no. of simultaneous responses
- no of impulses to be combined at a synapse > allows nerve impulses from receptors reacting to diff stimuli to contribute to a single response
Explain how a cholinergic synapse functions
-depolarisation of presynaptic neurone
-Ca2+ channels open and Ca2+ diffuse (facilitated) into presynaptic neurone
-causes vesicles to move downwards towards presynaptic membrane and fuse to release acetylcholine into synaptic cleft
-acetylcholine diffuses across synaptic cleft
-acetylcholine binds to receptors on postsynaptic neurone
-acetylcholine binds to Na+ gate channels in membrane causing them to open
-Na+ enter postsynaptic neurone leading to depolarisation
-when it reaches a certain threshold there’s an influx of Na+
Explain how acetylcholine is recycled
-Acetylcholine is hydrolysed by acetylcholinesterase into choline and ethanoic acid (acetyl)
-this prevents a continuous action potential in the postsynaptic neurone
-Choline and ethanoic acid (acetyl) diffuse back into the presynaptic neurone to be recombined into acetylcholine using ATP
what are muscles
effector organs that respond to nervous stimulation by contracting and so bring about movement
the 3 types of muscles
-cardiac
-smooth
-skeletal
where is cardiac muscle found
heart
where is smooth muscle found
wall of blood vessels and gut
which muscles are not under conscious control
cardiac and smooth muscles
skeletal muscle
-makes up the bulk of body muscle in vertebrates
-attached to bone and acts under voluntary control
what are individual muscles made out of
-millions of tiny myofibrils
-in themselves they produce almost no force while collectively they can be extremely powerful
in order to maximise strength how are myofibrils arranged
lined up parallel to each other in order to maximise its strength
what are muscles composed of
smaller units bundled into progressively larger ones
what would have happened if muscles were made up of individual cells joined end to end
-wont able to perform its function of contraction very efficiently
-due to junction between adjacent cells wont be a point of weakness that would reduce the overall strength of the muscle
how do muscles overcome reduceness of the overall strength due to not being on a point of weakness
-separate cells have become fused together into muscle fibres
-these muscles fibres share nuclei and cytoplasm ( sarcoplasm) that’s mostly found around circumference of the fibre
-within sarcoplasm = large conc of mitochondria and endoplasmic reticulum
what 2 protein filaments are myofibrils made of
-actin = thinner, consists of 2 strands twisted around one another
-myosin = thicker, consists of long rod-shaped tails with bulbous heads that project to the side
how are myosin molecules joined together
tail to tail in the thick filament Z-line
why do myofibrils appear stripped
due to their alternating light coloured and dark coloured bands
name of light bands
I bands ( isotropic bands)
why do I bands appear lighter
because the thick and thin filaments do not overlap in this region
name of dark bands
A bands ( anisotropic bands)
why do A bands appear darker
thick and thin filaments overlap in this region
what is at the centre of the A band
-lighter coloured region called H-zone
what is at the centre of each I band
line called Z-line
what is the distance called between adjacent Z-lines
sarcomere
what happens to the sarcomere when muscles contract
sarcomeres shorten and pattern of light and dark band changes
another protein found in muscles
tropomyosin
function of tropomyosin
forms fibrous strand around actin filament
2 types of muscle fibre
-slow-twitch fibre
-fast-twitch fibre
what do slow-twitch fibres do
-contract more slowly and provide less powerful contractions but over a longer period
-adapted to endurance work
-common in calf muscles which must contract constantly to maintain the body in an upright position
how are slow-twitch fibres suited to their role
-adapted to aerobic respiration > to avoid build up of lactic acid that would cause them to function less effectively and prevent long-duration contraction
how are slow-twitch fibres adapted for aerobic respiration
-large store of myoglobin > (bright red molecule that stores o2 which accounts for red colour of slow-twitch fibres)
-rich supply of blood vessels > deliver o2 and glucose for aerobic respiration
-numerous mitochondria for ATP production
what to fast-twitch fibres do
-contract more rapidly and produce powerful contractions but for a short period of time
-adapted to intense exercise eg weight-lifting
-more common in muscles which need to do short bursts of intense activity eg bicep
how are fast-twitch fibres adapted to their role
-thicker and more numerous myosin filaments
-high conc of glycogen
-high conc of enzymes involved in anaerobic respiration which provides ATP rapidly
-store of phosphocreatine > molecule that can rapidly generate ATP from ADP in anaerobic conditions and so provide energy for muscle contraction
what are neuromuscular junctions
point where a motor neurone meets a skeletal muscle fibre
there are many such junctions along muscle, what would have happened if there was only 1 junction
-take time for a wave of contraction to travel across the muscle
-not all fibres would contract simultaneously and movement would be slow
why are rapid and coordinated muscle contraction frequently essential for survival
-there are more neuromuscular junctions spread throughout the muscle
-ensure contraction of a muscle is rapid and powerful when it is stimulated by action potentials
whats a motor unit
all muscle fibres supplied by a single motor neurone act together as a single functional unit
what does the arrangement of motor unit give
-control over the force that muscles exerts
-if only slight force needed, only few units are stimulated
-if greater force is required, a large no. of units are stimulated
comparison of neuromuscular junction and synapse
-have n.t that are transported by diffusion
-have receptors that on binding with the n.t, cause an influx of Na+
-use a Na/K pump to repolarise the axon
-use enzymes to breakdown the n.t
differences between neuromuscular junction and cholinergic synapse
neuromuscular junction
-only excitatory
-only links neurones to muscles
-only motor neurones are involved
-action potential ends here (end of neural pathway)
-acetylcholine binds to receptors on membrane of muscle fibre
cholinergic synapse
-may be excitatory/inhibitory
-links neurones to neurones or neurones to other effector organs
-motor, sensory and intermediate neruones may be invovled
-a new action potential may be produced along another neurone (postsynaptic neurone)
-acetylcholine binds to receptors on membrane of post-synaptic neurone
Describe the gross structure of skeletal muscle
Sarcomere - myofibril - muscle fibre (cells fused end to end sharing nuclei, mitochondria and other organelles) - bundle of muscle fibres - muscle
Describe the microscopic structure of skeletal muscle
-Protein filaments actin and myosin form sarcomeres.
-These overlap each other and appear striped on a micrograph.
I band - light - actin and myosin do not overlap
A band - dark - actin and myosin overlap
H zone - light - at the centre of the A band
Z line - dark - marks the ends of the sarcomere”
· Explain how actin and myosin are arranged in a myofibril
-Actin - two thin strands twisted together, has binding sites for myosin heads.
-Tropomyosin wrapped around actin filament covering the myosin head binding sites
-Myosin - thick, rod shaped tails with bulbous heads to the sides
-Myosin filaments are joined tail to tail with heads protruding outwards, actin filaments are arranged in between the myosin, partially overlapping”
Describe and explain the difference between slow-twitch and fast-twitch fibres
-Slow twitch - contract slowly with less power over longer periods of time. Adapted for aerobic respiration: large quantity of myoglobin (stores oxygen), rich blood supply, many mitochondria
-Fast twitch - contract rapidly, with power for a shorter period of time. Adapted by: thicker and more numerous myosin, high concentration glycogen, high concentration of enzymes for anaerobic respiration, store phosphocreatine (makes ATP from ADP in anaerobic conditions)”
Describe the structure of a neuromuscular junction
-Presynaptic neurone (before synapse) and myofibril separated by a gap.
-The end of the presynaptic neurone has a synaptic knob that contains vesicles of neurontransmitter and many mitochondria.
-Myofibril has membrane folded into T tubles that are at right angles to the surface membrane and receptors for neurotransmitter.
Explain what is meant by antagonistic muscles and how they operate
-Muscles can contract but they cannot extend, for this reason they are found in pairs.
-One muscle contracts and in order to return it to its original position the paired muscle contracts.
Describe and explain how the sliding filament theory causes muscles to contract and relax
-Ca ions bind and move tropomyosin uncovering myosin head binding site on actin;
-This allows myosin heads to attach to actin filaments forming cross bridges;
-Myosin heads change angle causing actin to slide relative to myosin shortening the sarcomere;
-Binding of ATP causes myosin head to detach from actin;
-Hydrolysis of ATP releases energy which causes recocking of the myosin head;
· Summarise the evidence that supports the sliding filament mechanism of muscle contraction
-Myofibrils appear darker where the actin and myosin filaments overlap.
-When muscle contraction occurs sliding filament theory suggests that there will be less light areas.
-This is evident from: I band narrower, H zone narrower, Z lines closer together.
-A band remains constant evidence the length of the myosin filament does not change.
Describe the energy supply during muscle contraction
-Energy required for recocking myosin heads and actively transporting Ca ions into endoplasmic (sarcoplasmic) reticulum.
-Provided by hydrolysis of ATP to ADP and Pi.
-ATP provided by aerobic and anaerobic respiration.
-Phosphocreatine regenerates ATP during anaerobic respiration. It is stored in muscle and supplies phosphate to ADP
