Co-ordination + muscles Flashcards
How is a resting potential maintained?
- membrane less permeable to Na than to K, fewer Na+ channels open
- Na+ actively transported out by pump, K+ pumped in
- high conc. of Na+ outside so inside more negatively charged
- K+ diffuse out of axon through channel proteins until repelled -> electro-chemical gradient balanced
What happens in a neuron during an action potential?
- Na+ diffuse down gradient into cell
- membrane depolarises and reaches -50mV
- voltage gated Na+ channels open so Na+ flood in
- membrane potential reaches +40mV
- sodium channels close, potassium channels open
- K+ diffuse out of cell (repolarisation)
- potential difference overshoots slightly (hyperpolarisation) but is then restored to -70mV
Explain the importance of hyperpolarisation
Creates refractory period when no action potentials can be produced - ensures movement of impulse is unidirectional, that separate impulses can be distinguished, and that the number of impulses is limited
How does an action potential move along a neurone?
- Na+ channel opens allowing Na+ to diffuse in
- localised increase in Na+ conc inside neurone
- Na+ ions diffuse along axon away from region of higher conc
- Sodium voltage gated channel opens due to Na+ movement so action potential can move along neurone as Na+ ions enter
How does myelination of a neurone increase the speed of an impulse?
myelin sheath (schwann cells) acts as insulator, gaps in insulation are called nodes of Ranvier
Action potential can jump from node to node (saltatory conduction) and so travels down axon faster -> as it does not have to generate action potential along entire length of the axon
What factors affect the speed at which an action potential travels?
myelination - saltatory conduction
diameter of axon - greater diameter means less leakage of ions
temperature - higher rates of diffusion + enzyme r.o.r
How is a nerve impulse transmitted across a synapse?
- depolarisation of pre-synaptic mem.
- Ca2+ channels open and calcium ions enter
- causes vesicles containing NT to fuse w/ pre-synaptic mem. releasing NT into cleft
- NT diffuses across synaptic cleft and binds to receptors on ost-synaptic mem.
- Na+ channels open, sodium ions diffuse down gradient into post-synaptic membrane causing depolarisation
What is cholinesterase?
Enzyme that hydrolyses acetylcholine in the synapse, inactivating it
How do inhibitory synapses work?
- NT binds to chloride ion channel receptors on post synaptic mem. so Cl- moves in
- K+ channels open nearby, K+ moves out
- post synaptic neurone is hyperpolarised
so any stimulus less likely generate impulse that reaches threshold level as more Na+ needed to move in and depolarise
What are the two types of summation?
Temporal - frequency of APs releases enough NT to reach threshold in post synaptic mem.
Spatial - more than 1 pre-synaptic neurone needed to release NT to reach threshold in post-synaptic mem.
In what ways can drugs stimulate more APs?
mimic - similar shape to NT + so complimentary to receptor on post-synaptic mem.
cause release of more NT
stop breakdown + release of NT from receptor on post-synaptic mem.
In what ways can drugs inhibit APs?
stop the release of NT
block post-synaptic receptors -> competes w/ NT to bind to receptor
What are the features of actin and myosin?
actin thinner + consist of 2 strands twisted around each other
myosin thicker + consists of long rod-shaped tails w/ bulbous heads that project to sides
form myofibrils
What do t-tubules do?
In sarcolemma + carry action potentials from neuromuscular junction to sarcoplasmic reticulum
Sliding filament theory (muscle contraction)
Depolarisation
- Ca2+ released from sarcoplasmic reticulum
- (binds to troponin) cause tropomyosin to move + uncover myosin binding sites on actin
- myosin head attaches to binding site on actin, forming cross bridge
- myosin head changes angle moving actin filament along, ADP released
- ATP binds to myosin head, cross bridges detach
- ATP hydrolysed by ATPase so myosin heads re-energised + reorientated
