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