nervous system Flashcards
muscle contraction
- action potential depolarises sarcolemma, spreads down t-tubules to sarcoplasmic reticulum
- causes Ca2+ to be released into sarcoplasm
- Ca2+ binds to troponin causing tropomyosin to change shape
- means tropomyosin pulled out of binding site
- exposes myosin binding site and allows myosin to bind to actin
- creates an actin-myosin cross bridge
- myosin pulls actin (requires energy, ADP and Pi released)
- actin pulled towards centre of sarcomere
- ATP attaches to myosin head, causes actin-myosin bridge to break (shape change)
- ATP is hydrolysed by ATP hydrolase, energy released to re-cock myosin head, binds to different BS further along actin
- actin pulled closer to centre of sarcomere
- process repeats (if Ca+ present)
what is a receptor?
detect specific stimuli
(each detect one specific stimulus eg light or pressure)
resting potetial - difference in charge across membrane
stimulus excites membrane - more permeable to ions, more in and out
results in change of potential difference = generator potential
what is a pacinian corpuscle?
mechanoreceptor
only detect mechanical stimuli - eg pressure or vibrations
found in skin
sensory nerve ending wrapped in lamellae
activation of a pacinian corpuscle
- pressure deforms membrane
- causes stretch mediated sodium ion channels to open
- sodium ions flow in
- depolarisation
- leads to generator potential
control of heartbeat
- SAN (wall of right atrium) sends wave of electrical activity over the atria
- this causes both atria to contract at the same time
- non-conducting tissue stops the impulse reaching the ventricles
- waves transferred from SAN to AVN
- AVN passes waves of electrical activity to bundle of His
this carries waves from ventricles to apex of heart - bubble splits into pukinje fibres which carry waves up the muscular walls
- causes ventricles to contract at same time from the bottom up
(slight delay before AVN reacts to allow atria to empty)
control of heart rate
- stimuli detected by chemoreceptors (chemicals) and baroreceptors (pressure)
- in aorta and carotid arteries
- impulse sent along sensory neurone in autonomic NS to medulla
increasing heart rate
due to increased rate of respiration in muscles
- chemoreceptors detect rise in CO2
or baroreceptor detect low blood pressure
- in aortic arch or carotid arteries - sends impulses to cardiac centre in medulla
- increased frequency of impulses to SAN along sympathetic NS
- noradrenaline released (bind to SAN) increases frequency of impulses from SAN
decreasing heart rate
due to increased blood pressure or decreased respiration
- chemoreceptors detect high O2, pH or low CO2
baroreceptors detect high blood pressure
- in carotid arteries or aortic arch - sends impulses to cardiac centre in medulla
- increased frequency of impulses to SAN along parasympathetic NS
- acetylcholine released (binds to SAN) decreases frequency of impulses from SAN
what is a resting potential?
- when the neurone isn’t being stimulated
- outside of membrane more + than inside
(more positive ions outside) - membrane is polarised (there’s a difference in charge across membrane)
how is a resting potential made?
- sodium potassium pump moves Na+ out of axon and K+ into axon
- by active transport - creates an Na+ electrochemical gradient, more Na+ out than in
- K+ diffuse out of axon
- through K+ channels, by FD
sodium ion channels closed (can’t get back in)
creates more + charge on outside than inside axon
- membrane is polarised
action potenial
- stimulus triggers Na+ channels to open
- Na+ diffuse down gradient into axon - if potential difference reaches threshold, more Na+ channel open, more diffuse in
- inside of axon becomes less -
(depolarisation)
creates wave of depolarisation
- some Na+ diffuse sideways
- causes channels further down neurone to open
- repolarisation
repolarisation
getting neurone back to resting potential for next impulse
- Na+ channels close, stops more Na+ moving in
- K+ channels open
- so diffuse out down gradient
start to get membrane back to resting potential
- outside becomes more + again
- hyperpolarisation
what is hyperpolarisation?
K+ channels slow to close
- too many K+ diffuse out axon
- potential difference becomes more - than resting potential
what is the all or nothing principle?
once threshold is reaches, action potential will fire
- all same size
bigger stimulus doesn’t mean bigger action potential
- instead increases frequency
what is the refractory period + its purpose?
period of time after action potential when neurone cannot fire as membrane is not sufficiently polarised
creates time delay
means action potentials are:
- unidirectional
- can’t overlap (discrete)
- limited frequency
what is saltatory conduction?
action potential jumps between nodes of ranvier
on myelinated neurones
- increases speed of condition
3 factors that affect speed of conductance
- myelination
- axon diameter
- temperature
how does myelination affect speed of conductance?
myelin sheath acts as an electrical insulator
- made of Schwann cells with nodes of ranvier between (bare membrane)
- Na+ channels concentrated there
SPEEDS UP rate of conductance
depolarisation only happens at nodes of ranvier and jumps between them
in non mylenated neurones, depolarisation must happen along whole axon, slower
how does axon diameter affect speed of conductance?
larger diameter = faster
less RESISTANCE to flow of ions
means depolarisation can reach other parts of membrane faster
= faster wave of depolarisation
how does temperature affect speed of conductance?
increased temperature = faster
ions have more kinetic energy so can diffuse faster
but only increased to certain temperature
- proteins begin to denature (in carriers)
- speed decreases
2 types of summation
temporal
- 2 or more impulses arrive in quick succession from SAME presynaptic neurone
- action potential more likely as more NTs released into synapse
spatial
- many presynaptic neurones can join to one post synaptic neurone
- small amounts of NTs released from each can be added to reach threshold
- therefore more likely to trigger AP
what is summation?
NTs released from one neurone may not be enough to reach threshold
NTs released from multiple impulses/ neurones added tighter to reach threshold
and fire an action potential
Excitatory neurotransmitters
Depolarise lost synaptic membrane
Fires action potential if threshold met
Inhibitory neurotransmitters
Hyperpolarise post synaptic membrane
(Potential difference more negative)
Prevents it firing action poteinal
difference between inhibitory and excitatory neurotransmitters
inhibitory
- hyperpolarise postsynaptic membrane more
- prevents an action potential
excitatory
- depolarise postsynaptic membrane
- action potiential more likely to be fired, if threshold met
transmission across a synapse
- action potential reaches synaptic knob
- causes calcium ion channels to open - calcium ions diffuse into presynaptic neurone
- influx causes vesicles (containing NTs) to move to presynaptic membrane and fuse - vesicles release acetylcholine into synaptic cleft
- diffuses across and binds to specific receptors on post synaptic membrane
- causes Na+ channels to open in postsynaptic
- influx causes depolarisation
- if threshold met, action potential fired - acetylcholine broken down (acetyl and choline) by acetylcholinesterase - products reabsorbed into presynaptic knob
why is transmission across a synapse unidirectional?
specific receptors only on postsynaptic - can only bind to one side
neurotransmtter only released from one side
acetylcholine broken down and removed from synapse - stops reaction happening
transmission across a neuromuscular junction
synapse between neurone and muscle cell (sarcomere)
works the same as a normal synapse
but:
- spreads dwon t tubules
- postsynaptic membrane has more receptors than other synapses
- has folds called clefs which store acetylcholinesterase
- acetylcholine always excitatory - more likely to trigger action potential and therefore response in muscle
leads to depolarisation of sarcomere and musce contraction
sarcomere has t tubules
how can drugs affect synapse transmission?
drugs can:
block receptors
- can’t be activated
- reduces transmission
mimic neurotransmitters
- same shape
- more receptors activated
- increase transmission
stimulate/ inhibit release of NTs
- more/ less receptor activated
- increase/ decrease transmission
inhibit enzyme that breaks down NTs
- more left in synapse to bind to receptors
- increase transmission
structure of skeletal muscles
made of muscle fibres
- large bundles of long cells
- membrane called sarcolemma
contain myofibrils - organelles
made of actin and myosin
parts of sarcolemma fold inwards into sarcoplasm - t tubules
sarcoplasmic reticulum in sarcoplasm
- sots and releases Ca+
- many mitochondria to provide ATP
structure of myofibrils
contain myosin - thick myofilaments
actin - thin myofilaments
A bands - dark
- thick myosin and overlapping actin
I bands - light
- thin actin filaments
myofibril made of short units - sarcomeres
z line - end of each sarcomere
m line - middle of each sarcomere (and middle of myosin)
h zone - only myosin filaments (around m line)
outline sliding filament theory
muscle contract as myosin and actin slide over each other
- myofilaments themselves don’t contract
- sarcomeres do
sarcomeres shorten
- H zone and I bands
how is ATP made for muscle contraction
aerobic respiration
- most generated by oxidative phosphorylation in mitochondria
- only works with oxygen, long periods of low intensity exercise
anaerobic repiration
- ATP made by glycolysis
- glycolysis makes pyruvate with is made into lactate
- builds up in muscle causing fatigue, good for short periods of intense exercise
phosphocreatine
(see next)
how is phosphocreatine used to make ATP?
ATP made from phosphorylating ADP
- adding a phosphate from phosphocreatine
- stored inside cells, generates ATP fast
- used up very fast - used for short vigorous bursts
doesn’t require oxygen
doesn’t create lactate
slow twitch muscle fibres
- contract slowly
- work for long period of time - without tiring
- good for endurance activities eg maintaining posture
- energy released slowly by aerobic respiration (many mitochondria and blood vessels for O2)
- higher amounts of myoglobin - red
fast twitch muscle fibres
- contract quickly
- get tired very fast
- good for fast, short movements eg sprinting
- energy released fast by anaerobic respiration using glycogen (few mitochondria and blood vessels)
- less myoglobin = paler
2 respiratory substrates
amino acids
fatty acids and glycerol from lipids
how are amino acids used as a substrate?
deaminated =
3c molecule used to make pyruvate
4/5c compounds used in Krebs cycle
how are lipids used a substrates?
glycerol phosphorylated
= triose phosphate
fatty acids converted to acetyl
How do photoreceptors work?
Covert light to electrical impulses
Light absorbed by light sensitive optical pigments
breaksdown
= generator potential
- if reaches threshold, impulse along bipolar neurone
Cone cells
Concentrated in fovea
Colour vision
less sensitive to light (best in bright)
- one cone joins one neurone
- takes more light to reach threshold to trigger action potential (not added)
high visual acuity
- close together and one cone joins one neurone
- light from 2 points generates 2 action potentials (one from each cone) so point can be distinguished
Rod cells
Peripheral parts on retina
Black and white
sensitive to light (work well in dim)
- many rods join to one neurone
- many weak generator potentials combine to reach threshold for action potential
low visual acuity
- many rods join same neurone
- light from two close points can’t be told apart, only generate one action potential
activation of rod cells
- rhodopsin breaks down when light shines on it
- into retinal and opsin
- results in generator potential produced
ATP needed to resynthesise rhodopsin
How is colour seen?
Rod and cones have differential optical pigments -> sensitive to different wavelengths of light
3 types of cone cells, with different optical pigments
Red, green and blue SENSITIVE
Stimulated in different proportions to see different colours
On a graph… why does potential/charge increase?
Sodium ion channels open
Influx of sodium ions
Have positive charge (so increase charge)
On a graph… why does potential/charge decrease?
Sodium ions channels close
Potassium ion channels open, diffuse out
Potential difference of membrane (on graph)
Resting potential (flat section)
- potential difference across membrane
- polarised
- outside more positively charge (more + ions)
Action potential (going up)
- depolarises membrane
- Na+ channels open, diffuse in
- makes inside of neurone less negative
- increased PD across membrane
Repolarisation (going down)
- Na+ channels close and K+ open
- membrane back to resting
- more + on outside
Hyperpolarisation (dip after peak)
- K+ channels slow to close
- too many K+ diffuse out
- potential difference more negative then resting
what is a generator potential?
change in potential difference (across a membrane) due to a stimulus
bigger stimulus excites membrane more (potential difference changes more) so bigger generator produced
if generator potential big enough (threshold met) - triggers action potential
reflex arc
stimulus
receptor
sensory
relay
motor
effector
response
fast and automatic
doesn’t involve brain decisions
role of Ca+ in contraction
causes tropomyosin to move out of binding site on actin
- allows myosin to bind
