Nervous coordination and muscles Flashcards
why is the heart myogenic
it relies on muscular contraction
Pathway of heart contraction and relaxation
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
What controls heart rate
The medulla oblongata controls heart rate via the autonomic nervous system
The two main centres of the medulla oblongata and how they affect heart rate
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
How does increased pressure affect heart rate
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
How does decreased pressure affect heart rate
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
How do decreased pH levels affect heart rate
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
What is cardiac output
heart rate x stroke volume
8 parts of the structure of a myelinated neuron
Dendrites
cell body
nucleus
axon
Schwann cells
nodes of Ranvier
myelin sheath
axon terminals
What is the job of a cell body of a neuron
to produce proteins and neurotransmitters
What is the job of the dendrites on a neuron
to carry action potentials to surrounding cells
What is the job of the axon in a neuron
to carry nervous impulses along a neuron
What is the job of the myelin sheath and what is it made of
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
What is resting potential and what is the usual value and why
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
How is resting potential maintained
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
How is an action potential created
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
What happens after the potential of a neuron reaches +40mV, thus an action potential is created
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
What is the all or nothing response
once threshold potential is reached, each action potential will depolarise the axon to the same voltage each time by voltage gated sodium ion channels
What is the refractory period and why is this important
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
How does an action potential travel down a non myelinated neuron
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
How does an action potential travel down a myelinated neuron
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
Factors that affect speed of action potentials
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)
Structure of a synapse
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)
Transmission of a cholinergic synapse and repolarisation
7 steps
- 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
- the influx of Ca2+ causes vesicles containing acetylcholine to fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft by exocytosis
- acetylcholine diffuses across the synaptic cleft and binds to complementary cholinergic receptors on the post synaptic membrane
- this causes Na+ channels on the post synaptic membrane to open and Na+ diffuses into the post synaptic neuron causing depolarisation
- if the threshold potential is reached, an action potential is formed
- acetylcholine removed from the synaptic cleft and are degraded by acetylcholine esterase to PREVENT A CONTINUOUS IMPULSE
- products of this degradation are transferred back into pre synaptic neuron and Na+ channels close, allowing post synaptic neuron to reach resting potential
How can cholinergic synapses be inhibitory
Chloride ions move into the post synaptic neuron and potassium ions move out
this causes hyperpolarisation, preventing an action potential
describe the 2 types of summation
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
compare neuromuscular junctions to cholinergic synapses
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
How can drugs mimic and inhibit neurotransmitters
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
How do a skeletal muscles act
in antagonistic pairs against an incompressible skeleton to create movement
What are muscle fibres made up of and what are these made up of
made up of myofibrils and these are made of repeating units called sarcomeres
individual muscle fibre cells are called the sarcoplasm
Structure of a sarcomere
and what are the two types of filament
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
describe the sliding filament theory in detail
- 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
- Ca2+ binds to tropomyosin, causing it to move, revealing myosin binding sites along the actin filament
- 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
- ATP binds to the myosin head causing it to detach, allowing reattachment at a site further along the actin to repeat step 3
- when the impulse stops, calcium ions are actively transported back into the sarcoplasmic reticulum
- tropomyosin will move back to its original position, prevent formation of an actin-myosin cross bridge
what is the role of phosphocreatine and why is this important
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
Properties of slow twitch muscle fibres
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
