Nervous coordination and muscles

Question 1

why is the heart myogenic

Answer 1

it relies on muscular contraction

Question 2

Pathway of heart contraction and relaxation

Answer 2

The SAN in the atria releases a wave of depolarisation across the atria, causing contraction

once the wave of depolarisation from the SAN reaches the AVN, there is a delay, then it releases another wave of depolarisation

there is a non conductive layer between the atria and ventricles to prevent waves of depolarisation from reaching the ventricles prematurely

The bundle of His transmits the wave down the septum to the purkinje fibres in the ventricle walls, apex contracts then ventricle walls contract

Cardiac muscles will relax as are repolarised

the delay between the first and second wave of depolarisation allows time for the atria to pump all blood into the ventricles before the ventricles contract

Question 3

What controls heart rate

Answer 3

The medulla oblongata controls heart rate via the autonomic nervous system

Question 4

The two main centres of the medulla oblongata and how they affect heart rate

Answer 4

Heart rate is increased via the sympathetic nervous system that is linked to the SAN

Heart rate is decreased via the parasympathetic nervous system that is linked to the SAN

Question 5

How does increased pressure affect heart rate

Answer 5

the pressure increase is detected by pressure receptors in the wall of the aorta and carotid artery

impulses are sent to the medulla oblongata then back to the SAN via the parasympathetic nervous system

Decrease in frequency of electrical signals, so heart rate will decrease

Question 6

How does decreased pressure affect heart rate

Answer 6

detected by pressure receptors in the aorta and carotid artery

impulses sent to the medulla oblongata and back to the SAN via the sympathetic nervous system

increase in frequency of electrical signals so heart rate increases

Question 7

How do decreased pH levels affect heart rate

Answer 7

this happens due to increased respiration rate

This pH drop is detected by chemoreceptors in the aorta and carotid artery

impulses sent to the medulla oblongata and back to the SAN via the sympathetic nervous system

increase in frequency of electrical signals in the heart, so heart rate increases

therefore a higher volume of blood is delivered to the lungs to remove CO2

Question 8

What is cardiac output

Answer 8

heart rate x stroke volume

Question 9

8 parts of the structure of a myelinated neuron

Answer 9

Dendrites
cell body
nucleus
axon
Schwann cells
nodes of Ranvier
myelin sheath
axon terminals

Question 10

What is the job of a cell body of a neuron

Answer 10

to produce proteins and neurotransmitters

Question 11

What is the job of the dendrites on a neuron

Answer 11

to carry action potentials to surrounding cells

Question 12

What is the job of the axon in a neuron

Answer 12

to carry nervous impulses along a neuron

Question 13

What is the job of the myelin sheath and what is it made of

Answer 13

made of Schwann cells, it is a protective layer, as it is a lipid it doesnt allow charged ions or an impulse to pass through

acts as an insulation

Question 14

What is resting potential and what is the usual value and why

Answer 14

it is the difference in electrical charge inside and outside of the neuron when an impulse is not being conducted

-70mV as there are more Na+ and K+ outside of the neuron

Question 15

How is resting potential maintained

Answer 15

by a sodium potassium pump, which requires ATP as is active transport

2 potassium ions are pumped in while 3 sodium ions are transported out

as there is a concentration gradient of K+ across the neurone membrane, K+ can diffuse back out maintaining the resting potential

The membrane isnt permeable to Na+ so Na+ cannot move back into the neuron

Question 16

How is an action potential created

Answer 16

When an impulse is received by receptors, sodium ion channels open, so Na+ will enter the neuron, causing depolarisation, so the electrical charge will become positive

if depolarisation reaches the threshold potential (around -50mV) , voltage gated sodium ion channels will be opened, causing an increased influx, which can lead to an action potential if the potential reaches around +40mV

Question 17

What happens after the potential of a neuron reaches +40mV, thus an action potential is created

Answer 17

Voltage gated Na+ channels close, and voltage gated K+ channels open, repolarising the neuron as K+ will move out

this eventually causes hyperpolarisation as the potential drops below resting potential, so voltage gated K+ channels close

then the sodium potassium pump will return the neuron back to resting potential

Question 18

What is the all or nothing response

Answer 18

once threshold potential is reached, each action potential will depolarise the axon to the same voltage each time by voltage gated sodium ion channels

Question 19

What is the refractory period and why is this important

Answer 19

the period in which the axon cannot be depolarised again to initiate another action potential

is important because
- it limits the frequency of action potentials
- ensures action potentials only travel in one direction and are discrete

Question 20

How does an action potential travel down a non myelinated neuron

Answer 20

like a Mexican wave

when depolarisation occurs, voltage gated sodium ion channels will open further down the axon, so parts of the axon will be repolarised before the depolarisation has spread the whole length across

Question 21

How does an action potential travel down a myelinated neuron

Answer 21

as action potentials will only occur at the nodes of Ranvier because the myelin sheath is non conduction, so they will jump between nodes of Ranvier

this is much quicker than in a non-myelinated neuron, it is called saltatory conduction

Question 22

Factors that affect speed of action potentials

Answer 22

Myelination increases speed due to saltatory conduction

increased axon diameter will increase the speed

increased temperature increases speed as Na+ and K+ ions can diffuse quicker (unless it is past optimum as enzymes will denature)

Question 23

Structure of a synapse

Answer 23

axon terminal(pre synaptic knob)

voltage gated Ca2+ channels on axon terminal

neurotransmitters contained in synaptic vesicle

synaptic cleft

sodium ion channels with neurotransmitter receptors ( on post synaptic membrane )

post synaptic membrane ( dendritic spine)

(muscle rather than post synaptic membrane in neuromuscular junction)

Question 24

Transmission of a cholinergic synapse and repolarisation

7 steps

Answer 24

1. When an action potential arrives at the pre synaptic knob, it becomes depolarised so voltage gated Ca2+ channels open allowing Ca2+ to diffuse into the synaptic knob
2. the influx of Ca2+ causes vesicles containing acetylcholine to fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft by exocytosis
3. acetylcholine diffuses across the synaptic cleft and binds to complementary cholinergic receptors on the post synaptic membrane
4. this causes Na+ channels on the post synaptic membrane to open and Na+ diffuses into the post synaptic neuron causing depolarisation
5. if the threshold potential is reached, an action potential is formed
6. acetylcholine removed from the synaptic cleft and are degraded by acetylcholine esterase to PREVENT A CONTINUOUS IMPULSE
7. products of this degradation are transferred back into pre synaptic neuron and Na+ channels close, allowing post synaptic neuron to reach resting potential

Question 25

How can cholinergic synapses be inhibitory

Answer 25

Chloride ions move into the post synaptic neuron and potassium ions move out

this causes hyperpolarisation, preventing an action potential

Question 26

describe the 2 types of summation

Answer 26

temporal summation is when 1 neuron releases neurotransmitters repeatedly over a short period of time so that the threshold value is exceeded

special summation is when many neurons collectively stimulate an action potential by combining the neurotransmitters they release to exceed threshold value

Question 27

compare neuromuscular junctions to cholinergic synapses

Answer 27

they are both unidirectional as neurotransmitter receptors are only in the post synaptic membrane

neuromuscular junctions cannot be inhibitory, they are only excitatory

neuromuscular junctions connect neurons to muscles rather than neurone to neurone, so are the end point of the action potential

Question 28

How can drugs mimic and inhibit neurotransmitters

Answer 28

They can mimic the shape of neurotransmitters, so will bind to receptors on post synaptic membrane and cause action potentials

they can inhibit as they may bind to the receptor, blocking it, so action potentials are prevented

they can bind to acetylcholine esterase, meaning less enzyme substrate complexes will be formed, causing a continuous impulse

can cause the rapid release or block the release of neurotransmitters

Question 29

How do a skeletal muscles act

Answer 29

in antagonistic pairs against an incompressible skeleton to create movement

Question 30

What are muscle fibres made up of and what are these made up of

Answer 30

made up of myofibrils and these are made of repeating units called sarcomeres

individual muscle fibre cells are called the sarcoplasm

Question 31

Structure of a sarcomere

and what are the two types of filament

Answer 31

M line - attachment of myosin
H zone - region of only myosin
I bands - region of only actin
A band - region of both actin and myosin
Z discs - attachment of actin

thick myosin
thin actin

Question 32

describe the sliding filament theory in detail

Answer 32

1. action potential travels to muscle fibres, causing depolarisation of the sarcolemma via t tubules, this causes a release of calcium ions from the sarcoplasmic reticulum
2. Ca2+ binds to tropomyosin, causing it to move, revealing myosin binding sites along the actin filament
3. myosin head will bind, forming an actin-myosin cross bridge, ATP is hydrolysed into ADP and Pi so a power stroke occurs as myosin head will pull actin towards centre of sarcomere , this causes the sarcomere to shorten and essentially causes a muscular contraction
4. ATP binds to the myosin head causing it to detach, allowing reattachment at a site further along the actin to repeat step 3
5. when the impulse stops, calcium ions are actively transported back into the sarcoplasmic reticulum
6. tropomyosin will move back to its original position, prevent formation of an actin-myosin cross bridge

Question 33

what is the role of phosphocreatine and why is this important

Answer 33

it regenerates ATP by adding Pi to ADP which is released upon muscle contraction

it is important as muscles require lots of ATP to contract, and aerobic respiration may not be able to produce enough ATP to meet this demand

Question 34

Properties of slow twitch muscle fibres

Answer 34

Slow twitch are adapted for endurance activities
- high concentration of myoglobin
- lots of mitochondria
- have a rich blood supply
- contract slowly

Fast twitch are adapted for intense exercises
- thicker
- more myosin
- high storage of phosphocreatine and glycogen
- contract faster