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
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?
once an action potential has been generated the sodium voltage gated channels close preventing further action potential from being generated
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
difference in membrane permeability in resting potential
-MORE permeable to K+ (somove out by facilitated diffusion
-LESS permeable to Na+ (closed channels)
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
At what point can sodium and potassium ions exchange in a myelinated axon
Nodes of Ranvier
Why can sodium and potassium only exchange at Nodes of Ranvier in a myelinated axon
because the remainder of the axon is covered by a myelin sheath that prevents ions being exchanged
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
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
define synapse
junction between neurones, they do not touch and have a small gap through which neurotransmitters pass
define the structure of a synapse
Presynaptic and postsynaptic neurone separated by synaptic cleft. the end of the presynaptic neurone has a synaptic knob that contains vesicles of neurotransmitters and many mitochondria
how is a synapse unidirectional
-neurotransmitter is only stored in the presynaptic
-neurotransmitter receptors are only found on the postsynaptic neurone
Spatial summation
several presynaptic neurones converge on one postsynaptic neurone and together release enough neurotransmitter to reach threshold and trigger an action potential
Temporal summation
A single presynaptic neurone releases neurotransmitter many times over a short period releasing enough neurotransmitter to reach threshold and trigger an action potential
describe the function of a synapse
Transmit information from neurone to another allowing
-a single presynaptic neurone to stimulate several postsynaptic neurones
-Several presynaptic neurones to stimulate only one postsynaptic neurone
Explain how a cholinergic synapse functions
-depolarisation of presynaptic neurone
-calcium ion protein channels open allowing calcium ions to diffuse into membrane
-synaptic vesicle fuses with presynaptic membrane releasing acetylcholine into synaptic cleft and diffuse across
-Acetylcholine bind with sodium ion channel in the postsynaptic membrane
-Sodium ions enter leading to depolarisation
explain how acetylcholine is recyled
acetylcholine is hydrolysed by acetylcholinesterase into choline and ethanoic acid this prevents continuous action potential in the postsynaptic neurone
-choline and ethanoic acid diffuse back into the presynaptic neurone to be recombined into acetylcholine using ATP
Explain how a synapse is involved in inhibition
-neurotransmitter released binds to chloride ion channels on postsynaptic neurone
-chloride ions enter the postsynaptic neurone
-Binding of neurotransmitter opens potassium ion channels and potassium ions move out
-leads to hyperpolarisation
-action potential less likely as more sodium ions needed to reach threshold
What are the three types of muscle
-cardiac
-skeletal
-smooth
What is an individual muscle fibre made up of
Myofibrils
What is the organisation of structures in muscle
-whole muscle is made up of bundles of muscle fibres
-bundles of muscle fibres contain lots of single muscle fibres which are made of myofibrils
-Myofibrils are made of sarcomere
What is sarcomere made from
Proteins actin and myosin
What happens to sarcomeres when the muscle contracts
-I band gets smaller/ shortens
-H zone gets smaller and disappears
-A band stays the same
-Z lines stay the same
What are myofibrils made from
sarcomere
What do bundles of muscle fibres contain
Blood capillaries and nerves
What do single muscle fibres contain
A nucleus, mitochondria, sarcoplasmic reticulum
What is the structure of actin
thinner filament consisting of two strands twisted around one another
What is the structure of myosin
thicker filament and consists of long rod shaped tails with bulbous heads that project to the side
Why do myofibrils appear striped
due to their alternating light and dark coloured bands
light bands= I bands (filaments don’t overlap)
dark bands= A bands
(filaments overlap)
what are the two types of muscle fibres
-slow-twitch
-fast-twitch
slow- twitch muscle fibres
contract more slowly and provide less powerful contractions but over a long period
What are the adaptations of slow-twitch muscle fibres
-large store of myoglobin
-rich supply of blood vessels
-numerous mitochondria to produce ATP
fast-twitch muscle fibres
contract more rapidly and produce more powerful contractions but only for a short period of time
What are the adaptations of fast-twitch muscle fibres
-thicker and more numerous myosin filaments
-a higher concentration of glycogen
-a higher concentration of enzymes involved in anaerobic respiration
-a store of phosphocreatine
neuromuscular junction
the point where a motor neurone meets a skeletal muscle fibre
Why are there many neuromuscular junctions along the muscle
to ensure the contraction of a muscle is rapid and powerful when it’s simultaneously stimulated by an action potential
muscle stimulation
-impulses in the motor neurone cause acetylcholine to be released at the neuromuscular junction
-this causes opening of sodium channels and depolarisation of the sarcolemma
-depolarisation of the muscle fibre cause the release of calcium ions into the sarcoplasm which causes the events of contraction into the sarcomere
how do muscles contract
-tropomyosin normally covers the myosin binding sites on the actin filament, so the myosin heads cannot bind
-stimulated muscle cells release calcium from sarcoplasmic reticulum
-calcium bind to troponin causing the tropomyosin to move exposing the myosin binding site
-myosin heads can then attach to the actin filament resulting in contraction
how ATP is used in muscle contraction
-myosin heads with ADP attach to the myosin binding sites on actin filaments
-ADP dissociates causing the myosin head to change shape moving the actin filament
-ATP then binds to myosin head, causing it to detach and reset
-myosin head hydrolyses ATP to ADP allowing it to bind further along
Relaxation of muscles
-when the impulses in the neuron stop, calcium ions are pumped back into the sarcoplasmic reticulum, lengthening the sarcomere
-The tropomyosin moves back to cover the myosin binding sites so the myosin heads cannot bind and pull the actin filaments
-So the actin filaments begin sliding back, causing the sarcomere to lengthen
