Nervous coordination Flashcards
Structure of a myelinated motor neurones
Dendrites
Nodes of Ranvier
Nucleus
Cell body
Myelin sheath made of Schwann cells
Axon
The establishment of a resting potential
The sodium-potassium ion pump actively transports 3 sodium ions out of axon and 2 potassium ions into axon
An electrochemical (concentration) gradient is created e.g. higher concentration of potassium ions inside axon than outside or higher concentration of sodium ions outside axon than inside
Membrane more permeable to potassium ions (open K+ channels) than sodium ions (closed Na+ channels)
Potassium ions move out of axon by facilitated diffusion
The inside of axon negatively charged relative to outside; axon is polarised = resting potential
Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.
(Stimulus)
Excites the neurone cell membrane
Membrane more permeable to sodium ions as sodium ion channels open
Sodium ions diffuse into neurone down the sodium ion electrochemical gradient
Makes the inside of the neurone less negative
Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.
(Depolarisation)
If potential difference reaches threshold, action potential generated because more voltage-gated sodium ion channels open
More sodium ions diffuse rapidly into neurones
Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.
(Repolarisation)
Sodium ion channels close (membrane less permeable to sodium ions) whilst (voltage-gated) potassium ion channels open so potassium ions diffuse out of neurone down the potassium-ion concentration gradient
This starts to get the membrane back to its resting potential
Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.
(Hyperpolarisation)
Potassium ion channels are too slow to close so there’s a slight overshoot – too many potassium ions diffuse out of neurone
The potential difference becomes more negative than the resting potential
Changes in membrane permeability lead to depolarisation and the generation of an action potential. The all-or-nothing principle.
(Resting potential restored)
Resting potential is restored by the sodium-potassium pump
Ion channels reset
Maintained until the membrane is excited by another stimulus
The nature and importance of the refractory period
Refractory period is the time to restore axon to resting potential/no further action potential can be generated (time delay)
Produces discrete and discontinuous impulses (action potentials don’t overlap)
Limits frequency of impulse transmission at a certain intensity (limits strength of stimulus that can be detected); higher intensity stimulus causes higher frequency of action potentials but only up to certain intensity
Unidirectional action potential – can’t be propagated in a region that is refractory (only travel in one direction)
All or nothing nature of action potentials
Once threshold is reached, an action potential will always fire with the same change in voltage, no matter how big the stimulus is
If the threshold isn’t reached, an action potential wont fire (all or nothing)
A bigger stimulus won’t cause a bigger action potential but will cause them to fire more frequently
Factors affecting the speed of conductance
(Myelination)
The myelin sheath is an electrical insulator present on some neurones
Depolarisation only occurs at Nodes of Ranvier in myelinated neurone
Saltatory conduction (which is faster) can occur (impulse jumps from node to node)
Impulse doesn’t travel whole axon/no need to depolarise along whole length of axon unlike non-myelinated neurone, where depolarisation happens along the whole length of the membrane
Factors affecting the speed of conductance
(Axon diameter)
Bigger diameter means less leakage of ions/less resistance to flow of ions
So depolarisation reaches other parts of the neurone cell membrane quicker
Factors affecting the speed of conductance
(Temperature)
Increases rate of movement of ions Na+ and K+ as more kinetic energy (active transport/diffusion)
Higher rate of respiration (enzyme activity faster) so ATP produced faster and energy released faster, so active transport also occurs faster
But proteins could denature past a certain temperature and speed will decrease
The passage of an action potential along a non-myelinated axon, resulting in nerve impulses
Action potential moves along the neurone as a wave of depolarisation
Influx of sodium ions in one region increases permeability of adjoining region to sodium ions by causing voltage-gated sodium ion channels to open so adjoining region depolarises
The passage of an action potential along a myelinated axon, resulting in nerve impulses
Depolarisation of axon at nodes of Ranvier only
Resulting in saltatory conduction
So there is no need for depolarisation along whole length of axon
What is synapse
Structure
Synapse is the junction between a neurone and another neurone or between a neurone and an effector cell e.g. a muscle or gland cell
The gap between the cells at a synapse is called the synaptic cleft
Presynaptic neurone has a swelling called a synaptic knob which contains synaptic vesicles filled with chemicals called neurotransmitters
When action potential reaches end of a neurone, neurotransmitters are released into the synaptic cleft and diffuse across to the postsynaptic membrane, binding to specific receptors (which might trigger an action potential, causing muscle contraction or hormone secretion)
Transmission across a cholinergic synapse
- Action potential arrives at the synaptic knob of a pre-synaptic neurone causing calcium ion channels to open and calcium ions diffuse into pre-synaptic neurone
- This causes the synaptic vesicles containing neurotransmitter/ acetylcholine (which is made only in the presynaptic neurone) to fuse with pre-synaptic membrane, releasing acetylcholine into synaptic cleft (exocytosis)
- Neurotransmitters diffuse across synaptic cleft and bind to specific cholinergic receptors found only on post-synaptic membrane
- This causes sodium ion channels in the post-synaptic neurone to open and sodium ions diffuse into post-synaptic knob, causing depolarisation which initiates action potential (excitatory synapse)
- Neurotransmitter removed from synaptic cleft so response doesn’t keep happening. It is broken down by an enzyme called acetylcholinesterase (AChE) and the products are reabsorbed by the presynaptic neurone and used to make more acetylcholine
Neuromuscular junctions
A neuromuscular junction is a synapse between a motor neurone and a muscle cell
Neuromuscular junctions use the neurotransmitter acetylcholine (ACh), which binds to cholinergic receptors called nicotinic cholinergic receptors
Comparison of transmission across cholinergic synapses and neuromuscular junctions
Cholinergic synapses go from neurone to neurone WHEREAS neuromuscular go from neurone to muscle
Neuromuscular junction: ACh is always excitatory and never inhibitory, so always triggers generator/action potential in a muscle cell
Neuromuscular junction: Post-synaptic membrane has more receptors than other synapses
Neuromuscular junction: Lots of folds on post-synaptic membrane which form clefts to store the enzyme (Acetylcholinerase/AChE) to break down neurotransmitter (Acetylcholine/Ach)
Why synapses result in unidirectional nerve impulses
Neurotransmitter only made in/released from pre-synaptic neurone
Receptors only on post-synaptic membrane so impulses can only travel in one direction
What is summation
Addition of a number of impulses converging on a single post-synaptic neurone
i.e. where the effect of neurotransmitter released from many neurones (or from one neurone that is stimulated a lot in a short period of time) is added together
Spatial summation
Many pre-synaptic neurones share the same synaptic cleft/post-synaptic neurone i.e. many neurones connect to one neurone
Collectively release a sufficient amount of neurotransmitter to reach threshold in the postsynaptic neurone to trigger an action potential
If some neurones release an inhibitory neurotransmitter then the total effect of all the neurotransmitters might be no action potential
Temporal summation
One pre-synaptic neurone releases neurotransmitter many times over a short period/in rapid succession
It is likely that there will be sufficient neurotransmitter released into the synaptic cleft to reach the threshold to trigger an action potential
Excitatory neurotransmitters
Depolarise postsynaptic membrane, making it fire an action potential if threshold reached
e.g. acetylcholine is an excitatory neurotransmitter at cholinergic synapses in the CNS
It binds to cholinergic receptors to cause an action potential in the postsynaptic membrane and at neuromuscular junctions
Inhibitory neurotransmitters
Hyperpolarise the postsynaptic membrane (make the potential difference more negative), preventing it from firing an action potential/inhibits transmission of nerve impulses by postsynaptic membranes
Can’t be depolarised and reduces the effect of sodium ions entering so much less likely to reach threshold
e.g. acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart, when it binds to receptors here, it can cause potassium ion channels to open on the postsynaptic membrane, hyperpolarising it
By having both excitatory and inhibitory neurones forming synapses with the same postsynaptic membrane, this gives control of whether post-synaptic membranes ‘fire’ or not, therefore ‘firing’ is not inevitable and stimulation can be overridden
Effects of specific drugs on a synapse
(shape)
Some drugs are the same shape as neurotransmitters so they mimic their action at receptors (agonists)
This means more receptors are activated
e.g. nicotine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain
Effects of specific drugs on a synapse
(block receptors)
Some drugs block receptors so they cant be activated by neurotransmitters (antagonists)
This means fewer receptors can be activated
e.g. curare blocks the effects of acetylcholine by blocking nicotinic cholinergic receptors at neuromuscular joints, so muscle cells cant be stimulated, leading to paralysis
Effects of specific drugs on a synapse
(inhibit enzyme)
Some drugs inhibit the enzyme that breaks down neurotransmitters
More neurotransmitters in the synaptic cleft to bind to receptors and they are there for longer
e.g. nerve gases stop acetylcholine from being broken down in the synaptic cleft, leading to loss of muscle control
Effects of specific drugs on a synapse
(stimulate)
Some drugs stimulate the release of neurotransmitter from the presynaptic neurone so more receptors are activated e.g. amphetamines
Effects of specific drugs on a synapse
(inhibit neurotransmitter)
Some drugs inhibit the release of neurotransmitters from the presynaptic neurone so fewer receptors activated e.g. alcohol
