Nervous Coordination Flashcards
Resting Potential
- polarised axon
- potential difference of -70mV
- axon more negatively charged relative to outside
Explain why concentrations of Na+ and K+ mean axon has a negative potential difference at rest even though Na+ and K+ both have the same charge
- concentration of Na+ outside axon is higher than concentration of K+ inside axon
- large anions are found inside axon
Explain how resting potential is maintained
- 3 Na+ actively transported out and 2 K+ into axon
via sodium potassium pump - membrane more permeable to K+ than Na+ so K+ leaks out
- Na+ channels mostly closed so Na+ cannot enter axon
- large anions are found inside axon
Action Potential
- travelling wave of depolarisation
- depolarised axon
- potential difference +40mV
- axon more positively charges relative to outside
Explain the process by which an action potential is produced in an axon and how the axon returns to resting potential
- stimulus which exceeds threshold voltage opens some voltage-gated Na+ channels
- Na+ diffuses into axon down electrochemical gradient
- pd becomes less negative which causes more voltage-gated Na+ channels to open
- pd reaches +40mV
- repolarisation of axon occurs so voltage-gated Na+ channels close so no more Na+ can enter axon
- voltage-gated K+ channels open so K+ diffuse out down electrochemical gradient
- outward diffusion of K+ causes temporary overshoot so hyperpolarisation of axon (reaches -80mV)
- K+ voltage-gated channels close
- sodium potassium pump causes axon to return to resting potential at -70mV
Suggest how action potentials determine the strength of a response given they have a constant amplitude
- frequency of impulses
- different neurones have different threshold values and brain interprets types of neurones stimulated
Describe the passage of an action potential along an unmyelinated axon
- stimulus exceeding threshold voltage causes influx of Na+
- depolarisation of axon induces voltage-gated Na+ channels to open further along axon
- localised currents established between adjacent regions along axon
- (more) depolarisation over length of axon
Describe the passage of an action potential along a myelinated axon
- fatty myelin sheath acts as electrical insulator
- depolarisation occurs at Nodes of Ranvier only
- localised currents form between adjacent nodes
- by saltatory conduction (action potential ‘jumps’)
Suggest factors which increase the speed of conductance of an action potential and explain why
- myelination due to saltatory conduction so action potential does not occur along whole length of axon
- larger diameter due to reduced ion leakage
- high temperature due to increased diffusion and enzyme action in respiration to produce ATP for Na+/K+ pump
All or None Principle
- action potential is exactly the same size regardless of the size of the stimulus
- providing it reaches the threshold value
Explain the importance of the all or none principle for action potentials
prevents minor stimuli causing nerve impulses and overloading the brain
Refractory Period
- period where membrane is hyperpolarised (K+ channels open)
- voltage-gated Na+ channels are closed preventing Na+ diffusing into axon
- greater stimulation required to reach threshold value
- no action potential generated
Explain the purpose of a refractory period in the passage of an action potential
- ensures unidirectional
- produces discrete impulses (new impulse cannot be generated immediately after)
- limits strength of impulse (only certain number of action potentials can pass in a given time)
Explain why a nerve impulse can only cross a synapse in one direction
- neurotransmitter only released by presynaptic neurone
- neurotransmitter diffuses down concentration gradient
- receptors only present on post synaptic neurone
Summation
- process which determines whether or not threshold voltage is reached
- to trigger action potential in postsynaptic neurone
- by combined effects of excitatory and inhibitory signals
Spatial Summation
- different presynaptic neurones together release enough neurotransmitter
- increases/decrease the probability that the potential will reach the threshold potential
- hence generate an action potential
Temporal Summation
- one presynaptic neurone releases neurotransmitter many times over a short period of time
- to reach threshold value of postsynaptic neurone
- hence generate an action potential
Suggest a benefit of postsynaptic neurone synapsing with two different presynaptic neurones
- modulation (control over) activity of postsynaptic neurone
- impulse transmission is not inevitable
Explain how an action potential is passed along an excitatory chemical synapse
- depolarisation of presynaptic neurone causes Ca2+ channels to open and Ca2+ diffuses in down concentration gradient
- vesicles containing acetyl choline fuse with presynaptic membrane
- acetyl choline released to synaptic cleft and diffuses down concentration gradient
- binds to receptors of post synaptic neurone
- ligand-gated Na+ channels open and Na+ enters neurone
- axon depolarised above threshold value
Explain how neurotransmitter acetyl choline is reused by presynaptic neurone
- reabsorbed by active transport
- degraded by acetyl cholinesterase to acetyl and choline
- reabsorbed by pre synaptic neurone and mitochondria produce ATP to synthesis acetyl choline
Explain briefly how an inhibitory chemical synapse functions
- neurotransmitter binds to ligand-gated Cl- channels
- Cl- moves into post-synaptic neurone by facilitated diffusion
- induces opening of nearby K+ channels so K+ moves out of postsynaptic neurone
- hyperpolarisation
- no passage of action potential since stimulation does not reach threshold level
Explain how an electrical synapse functions
- single protein channel acts as junction between pre and postsynaptic neurone bridging cytoplasms
- Na+ diffuses directly into postsynaptic neurone
Contrast chemical and electrical synapses
- single protein channel between neurones for electrical
- gap between synapses in smaller for electrical
- faster transmission with electrical since Na+ diffuses directly into postsynaptic neurone
- chemical synapses have synaptic plasticity
Synaptic Plasticity
- property of chemical synapses enabling them to alter synaptic strength (ability to pass on action potential)
- change in amount of neurotransmitter released per action potential
- change number of receptors available to bind
Cholinergic Synapse
- gap between neurones
- neurotransmitter is acetyl choline
- (found in peripheral nervous system)
Neuromuscular Junction
- chemical synapse
- between motor neurone and skeletal muscle fiber
State differences between motor and sensory neurone
- dendrites emerge from cell body in motor neurone but from dendron in sensory
- motor neurone has cell body on end but sensory has cell body on side
- motor neurone has many short dendrons but sensory has one long dendron
Explain function of myelin sheath
- myelin insulates
- action potential only produced at nodes
- travels by saltatory conduction
- faster transmission of nerve impulse
- insulated action potential to prevent leaking
Suggest ways in which drugs can affect synapses
- release neurotransmitter from vesicles without impulses
- prevent vesicles from releasing neurotransmitter
- block reuptake of neurotransmitter
- block receptors
- produce more or less neurotransmitter
Name inhibitory neurotransmitters
- GABA
- serotonin (in pain pathways)
- dopamine
Explain characteristic features of the Pacinian corpuscle
- respond only to specific stimuli (mechanical pressure and not light, heat or sound)
- produces a generator potential from mechanical energy of stimulus by acting as a transducer
Suggest places Pacinian corpuscle receptors are typically found
- fingers
- soles of feet
- joint (ligaments/tendons)
Explain how Pacinian corpuscle produces an action potential in sensory neurone
- pressure deforms Pacinian corpuscle and STRETCHES membrane so Na+ channels OPEN
- influx of Na+ results in depolarisation of axon producing a generator action potential
- action potential passes along sensory neurone to CNS
Describe how rod cells in the eye work
- only one type so cannot distinguish between different wavelengths of light (black and white vision)
- stimulated in low light intensity
- many rod cells connected to a single bipolar cell so summation occurs to reach threshold value for generator potential
- pigment called rhodopsin broken down
- brain cannot distinguish separate sources of light so low visual acuity (resolving power)
- relatively more and found at periphery of retina
Describe how cone cells in the eye work
- three different types which respond to different wavelengths of light (coloured vision)
- stimulated in high light intensity
- cone cells attached to separate bipolar cells
- types of pigments called iodopsin break down
- brain distinguishes between separate light sources so high visual acuity (resolving power)
- relatively fewer and found near fovea of retina
Explain how inhibitory neurotransmitters inhibit transmission of nerve impulses at postsynaptic neurone
- open chloride channels causing hyperpolarisation
- stimulation (from excitatory neurotransmitters) does not reach threshold value
- reducing effect of Na+ entering so no depolarisation
- no action potential produced
Myogenic
Contracts without nervous or hormonal stimulation
How would removing the nerve connections from the brain to the SAN affect the beating of the heart
Unable to change the heart rate so it would remain constant
Explain how the heart beats
- wave of electrical excitation spreads out from SAN across both atria
- atria contract
- wave of excitation enters AVN
- after a short delay spreads over ventricles down the bundle of His and along Purkyne tissues
Explain why contraction happens at the bottom of the ventricles
- non conductive tissue of AV septum prevents wave of excitation directly over ventricles
- forced to travel along the bundle of His
- so contraction starts at the apex of ventricles
Explain why contraction occurs when ventricles are full
- wave of excitation is delayed at AV
- non conductive tissue at AV septum prevents it travelling directly over ventricles
- allows time for ventricles to fill
Explain why damage to myelin sheath of neurones can lead to problems controlling muscle contraction
- no saltatory conduction so slower transmission of action potential results in delayed muscle contraction
or - action potential leaks into adjacent neurones so wrong motor neurone stimulated
Describe the gross structure of a skeletal muscle
- made of bundles of muscle fibres known as fascicles surrounded by connective tissue
- muscle fibres (cells) consist of many myofibrils which are specialised intracellular structures
- run parallel to each other to maximise strength
Describe the microscopic structure of a skeletal muscle
- myofibrils are made of protein filaments actin and myosin forming sections known as sarcomeres
- thinner actin consists of two twisted strands forming a helical structure with long threads of tropomyosin wound around it
- thicker myosin consists of a long, fibrous tail and two bulbous, globular heads projecting from one side
Describe the structure of muscle fibres and explain why muscle cells are not found as individual cells
- muscle cells are fused together to form muscle fibres to maximise strength
- nuclei are located along the edges of fibre
- shared cytoplasm known as sarcoplasm contains a high concentration of mitochondria and sarcoplasmic reticulum
- muscle cells are NOT individual since there would be weakness at junctions between cells
Suggest what is meant by a sarcomere and describe its structure
- sarcomere is distance between adjacent z lines
- consists of light I band and dark A bands
- A bands are where thick and thin filaments overlap
- I bands are regions between A bands where there is only thin filament (no overlap)
- H zone refers to centre of A band where there is only thick filament
- Z lines are boundaries between adjacent sarcomeres
Compare and contrast transmission across cholinergic synapse and neuromuscular junction
- both have neurotransmitters transported by diffusion
- both use enzymes to break down neurotransmitter
- both have receptors that cause influx of Na+ on binding of neurotransmitter
- both use Na-K pump to repolarise axon
- NMJ excitatory only where CS excitatory / inhibitory
- NMJ links neurones to muscles where CS links neurones to neurones or other effector organs
- NMJ is where action potential ends where CS is where new action potential is produced at post-synaptic neurone
Contrast slow and fast twitch muscle fibres
- FT contract more rapidly and produce powerful contractions over short period
- FT adapted for intense exercise in short bursts but ST for endurance work
- FT are thicker with more myosin filaments
- FT have higher concentration of glycogen and enzymes involved in anaerobic respiration
- FT has store of phosphocreatine (allows ADP to rapidly reform ATP in anaerobic conditions)
- ST have larger store of myoglobin (oxygen store to ensure aerobic respiration + avoid lactate build up)
- ST have richer blood supply for oxygen/glucose
- ST have more mitochondria to produce ATP
Describe how a muscle fibre contracts based on the sliding filament theory
- actin filaments slide past myosin filaments in opposite directions to each other
- distance between Z lines decreases
- sarcomere shortens
Give evidence for the sliding filament theory of muscle contraction and explain why this means filaments do not shorten
- I band/H zone becomes narrower
- Z lines more closer together
- sarcomere shortens
- A band remains same width since determined by length of myosin filament which does NOT change
Describe the process by which skeletal muscle contracts
- depolarisation of sarcolemma from arrival of action potential
- wave of depolarisation travels down T tubules and opens Ca2+ channels on sarcoplasmic reticulum
- Ca2+ diffuses into sarcoplasm from sarcoplasmic reticulum down concentration gradient
- Ca2+ causes tropomyosin blocking binding sites on actin to pull away
- myosin heads (attached to ADP) attach to actin at troponin binding sites forming cross bridges
- performs POWERSTROKE (change position to a lower energy state) and PULLS actin filaments along
- myosin head detaches so next myosin head can bind along actin filament
Describe the process by which skeletal muscle relaxes
- ATP binds to myosin head causing it to detach from actin filament
- ATPase hydrolyses ATP to ADP
- provides energy for myosin heads to return to original position
- Ca2+ actively transported back to sarcoplasmic reticulum
- tropomyosin blocks binding sites on actin once again
- myosin heads unable to bind to actin so muscle relaxes
Suggest uses for hydrolysis of ATP in muscle contraction
- energy for myosin heads to detach from actin filament
- hydrolysis of ATP provides energy for myosin heads to move back to original position
- ADP on myosin heads allows them to bind to actin and form cross bridges
- energy for active transport of Ca2+ back to sarcoplasmic reticulum
Phosphocreatine
- energy source for muscle contraction (naturally present in skeletal muscle)
- supplies phosphate to regenerate ATP
- ATP formed more rapidly compared to from aerobic and anaerobic (glycolysis) respiration
Suggest how phosphocreatine store in skeletal muscles is replenished
inorganic phosphate produced from hydrolysis of ATP
Describe the role of tropomyosin in myofibril contraction
- moves out of way when calcium binds
- allows myosin heads to bind and form cross bridges with actin filament
Describe role of myosin in myofibril contraction
- binds to actin filament and moves so it slides past
- detaches using ATP and reattaches further actin filament
Explain why fast twitch muscle fibres have a high glycogen content
- large supply of glucose available
- for MORE anaerobic respiration (compare to aerobic respiration for marking point)
- faster source of ATP but inefficient (yield of 2 ATP)
Explain why slow twitch muscle fibres have many capillaries is close contact
- short diffusion path for oxygen
- rich oxygen supply
- for MORE aerobic respiration (compare to anaerobic respiration for marking point)
Explain why mitochondrial disease results in muscle weakness
- reduction in ATP from aerobic respiration
- less force generated due to fewer myosin and actin interactions
- anaerobic respiration = lactate which causes muscle fatigue
