6.2 Nervous Coordination + Synapses Flashcards
Neurone vs nerve
A nerve is a bundle of neurones
Where do motor neurones go from/to?
From CNS to effector
Function of dendrites
Carrying action potentials/nerve impulses towards the body
Connecting to many other neurones and receiving impulses from them, forming a network for communication
Structure & function of cell body
Lots of RER
Production of proteins & neurotransmitters
Contains typical organelles in animal cell
Function of axon
Carries impulses away from cell body along the motor neurone
What is the myelin sheath made of?
Lipid/Schwann cells
Function of myelin sheath
Doesn’t allow charged ions to pass through (insulation!)
Speeds up impulse transmission
Where are the nodes of Ranvier?
Small uninsulated sections of the axon (sections without the myelin sheath)
What do nodes of Ranvier enable?
Saltatory conduction: the impulse jumps from one node to the next, which speeds up conduction of the impulse
Function of Schwann cells
Protect the axon & provide electrical insulation
Phagocytosis (removal of cell debris)
Nerve regeneration
How exactly do Schwann cells form the myelin sheath?
They wrap around the axon along its length
What type of transport is associated with Na+ & K+?
Facilitated diffusion!
Are the sodium-potassium pumps in the axon considered as co-transport? Why/why not?
NONONONO
Na+ & K+ are moving in DIFFERENT DIRECTIONS
What is resting potential?
When there is no stimulus, so no impulse. There is a p.d. between the outside and inside of the axon.
The inside is more negative than the outside. ~-65 mV
What two factors are responsible for establishing and maintaining the resting potential?
- Active transport of Na+ & K+
- Differential membrane permeability
Factors responsible for establishing & maintaining resting potential: active transport
Sodium-potassium pumps (carrier proteins) use ATP to actively transport 3 Na+ OUT for every 2 K+ actively transported IN.
There is a larger [+ve ions] outside the axon than inside.
Movement of ions via Na-K pumps establishes an ELECTROCHEMICAL GRADIENT
Factors responsible for establishing & maintaining resting potential: differential membrane permeability
Proteins channels MORE PERMEABLE TO K+ than Na+ (more K+ channels, some channels remain permanently open).
This means K+ can diffuse back down their conc gradient, out of the axon, at a FASTER RATE than Na+
What is an action potential/what is it caused by?
When an impulse is passed along a neurone, p.d. across membrane briefly reversed (i.e. inside more +ve than outside).
This is due to the rapid movement of Na+ & K+ across the membrane of the axon.
How is an action potential formed? (4)
- Stimulus causes voltage-gated Na+ channels in the axon membrane to open
- DEPOLARISATION: Na+ diffuse into the cell DOWN THE ELECTROCHEMICAL GRADIENT
- Depolarisation triggers more channels to open: more Na+ enters, causes more depolarisation (positive feedback)
- If the threshold potential is reached, an action potential of around +40 mV is generated
How does hyperpolarisation happen?
- Voltage-gated Na channels close, voltage-gated K channels open
- K+ diffuses out of axon, so axon becomes more negative
- Potential differences more negative than -70mV: hyperpolarised
- Voltage-gated K channels close
How does axon return to resting potential after hyperpolarisation?
Voltage-gated K channels close
Na+ and K+ restored back to original positions by Na-K pump
Why does the membrane enter a refractory period?
Can’t be stimulated: Na channels are recovering & can’t be opened
Why is the refractory period important (3 reasons)?
- DISCRETE IMPULSES produced - action potential CAN’T be generated immediately after another, so each is separate
- action potentials TRAVEL IN ONE DIRECTION: stops it spreading out in two directions, which would prevent a response
- LIMITS # OF IMPULSES TRANSMITTED: prevents overreacting
How does temperature affect speed of conductance/transmission along an axon?
Ions diffuse faster
Enzymes involved in respiration work faster: more ATP for active transport in Na/K pump
How does axon diameter affect speed of conductance/transmission along an axon?
Wider diameter = higher speed
Less leakage of ions so action potential travels faster
How does having a myelin sheath affect speed of conductance/transmission along an axon?
Myelin sheath is insulating, so ions can’t diffuse in/out, so they jump to regions without insulation (SALTATORY CONDUCTION)
Action potential jumps from node to node, so faster b/c doesn’t have to generate it along the entire length
What is the all or nothing principle?
If depolarisation doesn’t exceed the threshold potential (-55 mV), no action potential is produced.
Any stimulus that triggers depolarisation to -55 mV ALWAYS PEAKS AT THE SAME MAXIMUM VOLTAGE
Effect of bigger stimuli on action potentials
Bigger stimuli increase the FREQUENCY of action potentials!!
ALL ACTION POTENTIALS ARE THE SAME SIZE!!!!
What organelles are inside the pre-synaptic neurone?
Mitochondria
Smooth endoplasmic reticulum
Vesicles containing neurotransmitters
Describe synapse transmission (7)
- Action potential arrives at SYNAPTIC KNOB
- Depolarisation of synaptic knob leads to VOLTAGE-GATED Ca channels to open, so Ca2+ diffuses into synaptic knob via FACILITATED DIFFUSION
- Vesicles with neurotransmitters move towards & FUSE with presynaptic membrane
- Vesicles release neurotransmitters into SYNAPTIC CLEFT
- Neurotransmitters diffuse & bind to receptors on Na+ channels in post-synaptic membrane
- Na+ channels open, Na+ diffuses in
- If enough Na+ moves into post-synaptic neurone to exceed threshold potential, depolarisation occurs
How does the neurotransmitter go back into the presynaptic neurone?
Enzymes hydrolyse the neurotransmitter, which diffuse back across the synaptic cleft into the presynaptic neurone.
This prevents neurotransmitters from continuously generating new action potentials, so THE TRANSFER OF INFORMATION IS DISCRETE.
ATP combines hydrolysed components of neurotransmitters back together & into vesicles
Named example of a neurotransmitter and how it is restored back to the neurotransmitter?
Acetylcholine
Acetylcholinesterase hydrolyses it into acetyl & choline
How do synapses ensure that action potentials are unidirectional?
- Neurotransmitters are only released from the presynaptic neurone
- Only receptors for neurotransmitters in postsynaptic neurone, only voltage-gated Ca channels in presynaptic neurone
What is summation, and what are the two types?
The rapid buildup of neurotransmitters to help generate an action potential by two methods: spatial or temporal summation
Why is summation needed?
Some action potentials are too low frequency, so they don’t release neurotransmitters of a sufficient concentration to generate an action potential
Describe neurone arrangement of spatial summation
2 presynaptic, 1 postsynaptic
How does spatial summation work?
An action potential is only triggered (i.e. threshold potential is only exceeded at the postsynaptic neurone) if neurotransmitters are released from two presynaptic neurones instead of one
Describe neurone arrangement of temporal summation
1 presynaptic, 1 postsynaptic
How does temporal summation work?
One neurone release neurotransmitters at a high frequency (several action potentials in quick succession) in order to exceed threshold value
How do inhibitory synapses work?
- Neurotransmitters diffuse across synaptic cleft: bind to receptors on post-synaptic membrane
- This causes CHLORIDE ION CHANNELS to open, so Cl- moves into postsynaptic neurone
- K+ channels also open, so K+ moves OUT of the postsynaptic neurone
- Inside of postsynaptic neurone more negative relative to outside: HYPERPOLARISATION
This means an action potential is less likely to be triggered in the postsynaptic neurone
How do some drugs stimulate the nervous system
Creating more action potentials in the post-synaptic neurone
1. Mimicking neurotransmitter
2. Stimulating release for more neurotransmitter
3. Inhibiting breakdown of neurotransmitter
How do some drugs inhibit the nervous system?
Creating fewer action potentials in postsynaptic neurone
1. Inhibiting release of neurotransmitter
2. Blocking receptors on post-synaptic membrane
