Topic 6B - Nervous Coordination Flashcards
Describe the structure of a typical neurone that explains how they are adapted to carry electrochemical signals (electrical impulses)
Myelinated neurone = myelin sheath, which is a fatty, insulating layer made up of Schwann cells (provide protection) to stop electrical impulses being carried to other nearby neurones along the axon.
Long dendrons into dendrites to cell body, connected to other neurones.
Presence of Nodes of Ranvier aid in saltarary Conduction
Many neurones have voltage - gated channels, meaning
they only open when surrounding membrane depolarises
resting potential
more relatively negative inside cell (due to more positive ions on the outside) - membrane POLARISED (-70mV); potential difference across membrane; when neurone the not stimulated
does maintaining the resting potential require ATP?
- side task to think why resting potential is so important
Yes, the sodium - potassium pump is a carrier protein that requires ATP from respiration to release energy
SOPI
3 sodium out, 2 potassium in
- results in more sodium ions outside than the amount inside (potassium only 2), overall bigger + charge outside
Where is acetylcholinesterase stored in a neuromuscular junction?
(clefts) in postsynaptic membrane
What are differences between a cholinergic synapse and a neuromuscular junction?
seneca…
role of Pacinian corpuscle
Pacinian corpuscle is a sensory receptor and its role is to convert pressure into an electrical impulse.
List the TWO features of sensory reception shown by the Pacinian corpuscle.
It is specific to one type of stimulus.
It establishes a generator potential.
Desc. how the membrane of the axon maintains resting potential / polarised
- hydrolysis of ATP (resp.) used for energy by sodium potassium pump to actively transport (3 sodium out, 2 potassium in). Results in more positive charge/ more sodium outside…
- so allows then little facilitated diff. of Na + into axon via voltage-gated sodium ion channels [link to how lots of these are closed anyway at resting] > Only open when big enough voltage.
- facilitated diff: membrane more permeable to k+ ions as many voltage-gated potassium ion channels are open & more leave axon down electrochemical gradient : less positive than outside
Desc. how action potentials work.
- an action potential occurs when a neurone sends an e. impulse down an axon, away from cell body.
- note generator potentials are caused by stimulus and become action potential when threshold men
it’s all about sodium ions first and then potassium
- think Sadie Pearson
- Voltage-gated sodium in channels open due to stimulus, permeability to sodium increases & Na + enters INTO axon (facilitated) down electrochemical gradient… inside starts to become more positive.
- Depolarising
If potential diff/ generator p. = threshold =MORE NA+ ION CHANNELS OPEN, more diffuse in via facilitated - Repolarising
(around 30mV) sodium ions calm down and start to close… voltage-gated POTASSIUM ions start to open - more permeable to K+ and leave (facilitated) neurone down electrochem. gradient - Hyperpolarisation
Voltage-gated potassium ion channels are slow to close!, too many K + ions diffuse out - Resting potential
Channels reset and Na/k pump returns polarised membrane
The refractory period occurs after action potential (around hyperpolarisation where ion channels need to be reset).
Why is it needed?
- time delay between the action potentials to limit frequency - organism might be overwhelmed
- so the a. potentials can pass along as discrete impulses (no overlap) to distinguish stimulus & where it came from
- so a. potentials can be unidirectional (if both directions, the threshold wouldn’t be reached)
Threshold may not be met due to…
weak Stimulus so not enough Na + moving into sensory neurone or due to inhibitory neurotransmitters
Desc. waves of depolarisation
- example of positive feedbade
where a wave of an action potential is carried away from the cell body, along the axon, leaving behind a refractory period > unidirectial (messages don’t clash)
1. sodium ions enter neurone at start and some diffuse sideways.
2. Voltage-gated Na + channels in next section open, causing more Na + facilitatedly diffuse in… = wave along neurone
Desc. all or nothing principle
When threshold is not reached = failed initiation, no action p. fired.
Also encompasses how bigger / stronger stimuli don’t fire bigger a. potentials, but instead more frequent
Speed of conduction of electrical impulses across axon depends on Which 3 factors?
- myelin sheath
- axon diameter
- temp
How myelination impacts conduction:
1. why does depolarisation only happen at Nodes of Ranvier (if myelinated axon)?
2. desc. saltatory conduction
- Sodium ions can’t diffuse through insulating lipid layer, sodium ion channels conc. around nodes of ranvier
- In myelinated neurone, depolarisation at nodes. The neurone cytoplasm contains enough electrical charge to depolarise the next node!
Impulse jumps to nodes and so is much faster than non- myelinated
Desc. how the axon diameter impacts speed of conduction
Large axon (more space for cytoplasm erc) = less resistance to flow of ions in cyto, compared to small one. Wave of depolarisation can occur quicker
(proportional relationship)
How temp impacts speed of conduction
* watch vid on
- how would above optimum impact speed
^ kinetic energy = ^ rate of conduction and nerve impulse AND ^ activity of resp. enzymes = ^ ATP for active transport of ions (e.g. to more quickly return membrane to polarised?)
Maybe ions have more energy too.
- denature (enzymes and ion channels), decrease speed
COLD BLOODED ANIMALS MOST AFFECTED in terms of rate of nervous system as suffer if environment too hot / cold
why do so many SER need to be in pre-synaptic neurone (cholinergic synapse)
to make proteins like enzyme acetylcholinesterase and to finish synthesis of acetylcholine!
Why are neurotransmitters unidirectional?
vesicles containing them only exist in pre synaptic neurone (so high conc. on one side), and complementary receptors for them only exist on the post synaptic neurone
synapse
junction between 2 nerve cells
neurotransmitters
Chemically transfer as potential across synaptic cleft
cholinergic synapse
A synapse using acetylcholine, and can be excitatory or inhibitory
Desc how a cholinergic synapse transmits an action potential
- all channels are voltage-gate
- Incoming action potential depolarises pre-synaptic membrane : voltage gated CALCIUM ION CHANNELS open & flood into knob by facilitated diff.
- influx of ca+ ions fuse w/ vesicles containing acetylcholine - causes them to move to & fuse w/ membrane (exocytosis): acetylcholine DIFFUSES across cleft
- ACh binds to complementary receptor site on Na + ion channels (opens channels) on post-synaptic membrane, sodium diffuse down gradient by facilitated > DEPOLARISES membrane
- If depolarisation (generator) reaches threshold value, a. potential sent along post-synaptic axon
- Acetylcholinesterase hydrolyses acetylcholine (acetyl, ethanoic acid, and choline), these parts diffuse back across cleft and back into pre-synaptic neurone via reuptake pump > TO NOT KEEP FIRING new A. POTENTIALS
- energy from mito released to condense acetyl and choline at SER to recycle & store again in vesicles.
- sodium in channels close when no ACh, synapse ready to be reused
Desc. how excitatory neurotransmitters work
They bind to receptors of sodium ion channels - depolarising post-synaptic membrane and a. potential if threshold met
Desc. how inhibitory neurotransmitters work
(example you can use probably) Bind to chloride ion channels on post synapse : Cl - ions entering decreases membrane potential below resting (hyperpolarisation), preventing a. potential
What is summation? Name the 2 types
Where the effect of the neurotransmitter is added together : temporal summation and spatial summation (E.g, rod cells)
Desc. spatial summation
- Where many pre-synaptic neurones are spaced out
Several connect to 1 post-synaptic neurone : small amount of neurotransmitters at same time add up and cause depolarisation - if most neurotransmitters are inhibitory ones, then no a. potential as majority rules (more + or - determines if depolarisation, on hyperp.,happens)
if a stimulus is weak…
only small amount of neurotransmitter released & binds to sodium ion channels (no a. potential)
temporal summation
(often excitatory and inhibitory neurotransmitters together can control frequency of a potentials in post synapse)
- temporal like over time…
one neurone synapses to another : a. potential arrive in quick successions, as neurotransmitters released repeatedly into cleft So depolarisation becomes more likely (eg. after 3 impulses from pre-synaptic neurone, then may be enough neurotransmitters binding to enough complementary receptors on Na + channels to let enough ions in to depolarise)
What’s a neuromuscular junction?
junction between motor newone ana muscle cell
nicotinic Cholinergic receptors
ones on muscle cell membrane (sarcolemma) that acetylcholine binds to
neuromuscular junction
(a type of cholinergic synapse)
A junction between motor neurone and muscle cell
Why isn’t therejust one neuromuscular junction per neurone?
the muscle is large, many junctions to muscle cells = rapid, powerful contractions of muscle (Several action potentials stimulate muscle at same time)
what are some useful terms in muscles to know
Sarcolemma (Membrane of myofibril and sarcomeres)
Sarcoplasm
Sarcoplasmic reticulum
acetylcholine
T tubule
3 types of cells that have neurotransmitter receptors
nerve cell, muscle cell and gland cell
Drugs have an effect on synapses :
Desc what agonist and antagonistic ones might do.
Agonists= same shape as neurotransmitter (e .g. ACh and nicotine) So agonists mimic their actions at complementary receptors - more receptors activated.
Antagonist drugs block receptors so less are activated by neurotransmitters (may not be fully complementary or non competitive even, not sure)
3 ways drugs affect synapses
- blocking or binding to post-synaptic receptors
- (agonist) drug acting as inhibitors to enzymes that break down neurotransmitters at cleft
- Stimulate (agonist) or inhibit (antagonist) the release of neurotransmitters, pre synaptic neurone
how do drugs either stimulate or inhibit the release of neurotransmitters
Stim: drug forces neurotransmitter out of vesicle (fuses) - SO increases effect of neurotransmitters and stronger response.
Inhibit: can block calcium ions in pre synapse, less Ca + ions entering synaptic knob less vesicles fuse - less neurotransmitters released SO no response from effector.
note muscles good essay topic
.
3 types of body muscles & desc.
- Smooth muscle : contracts w/o conscious control (blood vessels, intestine)
- Cardiac muscles : exclusively in heart, contract without conscious control
- Skeletal muscle! (Striated / striped / voluntary muscle), ATTACHED TO BONE, conscious control to move (biceps)…
What are ligaments and joints?
- antagonistic?
Joint: where 2 bones meet
Lig: Attach bones to other bones
Antagonistic muscles work together to move a bone (needed as muscles can only pull/ contract, NOT push)
Tendons
Joins SKELETAL MUSCLE and bones
In terms of muscles, which is the agonist and antagonist?
Eg. straightening your arm
Agonist: (starts the action) contracts the muscle
- the tricep
Antagonist: the muscle that has to relax
- bicep
see drown notes for muscle and its structures
Sarcoplasm
cytoplasm of muscle fibre cell
sarcomere
repeating unit within myofibril (section within cell)- Contracts
Myofibril
arrangement of thick/thin protein filaments (actin and myosin)
- actin is thin
I band and H- zone
Both are where isolated molecules are (and so are lighter regions, apart from M-line)
Isotropic band: actin filament only (skinny I region)
H-zone: myosin only in middle (within A band)
A band
Where the 2 filaments overlap is the darkest.
Anisotropic band encompasses where all the myosin in
Z line
Sarcomere ends, made of actin, joins to neighbouring actin
How is muscle contraction explained
Sliding filament theory
What happens to components of myofibrils when contracting
H zone and I band shorten
A band stays the same
Sarcomere length shortens
How would you explain that you know a muscle is antagonistic to another
say its relaxing
role of sarcoplasmic reticulum in muscle contraction
stores and releases calcium ions needed for contraction
desc the arrival of an action potential at neuromuscular junction, before myofibrils contract
- A. potential arrives
- ACh via exocytosis released into cleft, diffusion across Junction, binding to post -synaptic receptors
- Voltage gated sodium ion channels open, membrane more permeable as influx of Na + & depolarising sarcolemma
- Depolarisation / a, potential spreads like wave of excitation across sarcolemma and down Transverse (T) tubule to then sarcoplasmic reticulum.
- causes ca + to be released from there, where it’s stored into sarcoplasm and myofibril
myosin structure
- 2 globular heads are hinged to move backwards & forwards
- each head has binding site for ATP & actin
actin structure
- actin myosin binding sites
- troponin that holds tropomyosin in active site
desc. the sliding filament theory
on samsung note
ATP is hydrolysed a few times during contraction of the sarcomeres/ sliding filament theory, what’s the energy used for?
- bend myosin head in ratchet motion to move actin f. toward M line.
- Detaching /breaking or hydrolysing actin myosin cross bridge
- Active transport Ca + ions into sarcoplasmic reticulum again when muscle relaxes
What happens when, in terms of the sarcomeres, stimulation stops from nervous pathway/ neuromuscular junction?
Calcium ions are actively transported back into sarcoplasmic reticulum. Troponin and tropomyosin return to original shape or place to block the actin - myosin binding site.
- actin filament slide back
- muscle fibre relax
conductance
( link to factors affecting speed of conductance)
how easily charged ions can move across a membrane
discrete impulses
unidirectional impulses and cannot happen immediately after each other - So all e. impulses as all have gaps between a. potentials
electrochemical gradient
grad. of charges particles
depolarisation
Where membrane becomes more positively charged
synaptic knob
end of synapse that pertrudes
resp. recap and state how the phosphocreatine system works (PCr)
Aerobic:
Most ATP from oxidative phosphorylation in mitochondria - requires oxygen, suitable for long periods of low intensity exercise (long walk)
Anaerobic:
ATP made V. quickly by glycolysis to make pyruvate - converted into lactate by lactate fermentation.
Lactic acid builds up in muscles and can cause fatigue (short, hard exercise)
Many muscle fibres stare phosphocreatine. It phosphorylated ADP to ATP, which is mde v. quickly this way but PCr runs out after few seconds (good for tennis serve); best for short bursts of exercise.
- no oxygen needed, no lactare formed.
how is phosphocreatine made
a phosphate is added to creatine, it’s phosphorylated by it using an ayme kinases.
ATP is made using it and can be recycled.
note
different muscles (and different people) have different proportions of slow and fast twitch muscle fibres in skeletal muscle
desc. general structure and properties of slow twitch muscle fibres
- what type of exercise is it for (under properties category)?
- long and fairly low intensity (more aerobic work)
Endurance activity, slow to fatigue.
Generation of ATP is slow making contractions weaker.
Have lots of mitochondria, great blood supply and so high concentration of myoglobin in muscles = red colour.
desc. general structure and properties of slow twitch muscle fibres
- what type of exercise is it for (under properties category)?
- Fast bursts of activity
Anaerobic resp, stores large amounts of phosphocreatine (in cytoplasm)- quick source of ATP.
Lactate produced & fatigues quickly.
Few mito as anaerobic, few blood vessels and muscle is paler as less myoglobin (Which stores oxygen)
