Nervous Conditions Flashcards
During an action potential the permeability of the axon membrane to sodium ions increases slowly and then increases rapidly. Explain these changes.
(Ion) channel proteins open;
Sodium ions enter in;
Changes membrane potential/makes inside of axon less negative/positive/depolarisation/reaches threshold;
More channels open/positive feedback;
During an action potential, the membrane potential rises to +40 mV and then falls. Explain the fall in membrane potential
Potassium ion channels open;
Potassium ions move out;
Sodium ion channels close;
After exercise, some ATP is used to re-establish the resting potential in axons. Explain how the resting potential is re-established
Pump/active transport/transport against concentration gradient;
Of 3 sodium ions out of the axon for every 2 potassium ions into the axon;
Describe how the resting potential is established in an axon by the movement of ions across the membrane.
active transport / pump of Na+ out of axon;
Active transport of K+ into the axon;
The axon membrane is more permeable to K+ than Na+ so there is diffusion of K+ out of axon but very little Na+ diffusion into the axon;
Explain how an action potential passes along a motor neurone
Depolarisation of axon membrane/influx of Na+ establishes local
currents;
Change permeability to Na+ /open Na+ gates of adjoining region;
Adjoining region depolarises / influx of Na+ ;
This process repeated along axon / self propagation;
Correct reference to/description of saltatory conduction;
Fewer action potentials occur along a myelinated axon than along an unmyelinated axon of the same length. Explain why.
Myelin insulates axon / ions can only pass through (plasma membrane
of axon) at gaps in myelin sheath;
(Gaps in sheath are called) nodes of Ranvier;
Above a certain strength stimulus, the refractory period makes it impossible for information about the differences in the stimulus strength to reach the brain. Explain why.
- (Refractory period) leads to discrete / separate nerve impulses / time when another nerve impulse can’t happen;
OR
(Refractory period) limits number of impulses per second / frequency of nerve impulses; - When maximum frequency reached / exceeded, no further increase in information / all (higher) strength stimuli seem the same;
Explain how the release of acetylcholine at an excitatory synapse reduces the membrane potential of the postsynaptic membrane.
Binds to receptor/proteins;
and opens Na+ channels;
Na+ enter and make membrane potential less negative/depolarised
Describe the sequence of events which allows information to pass from one neurone to the next neurone across a cholinergic synapse.
- (impulse causes) calcium ions/Ca2+ channels to open
- Ca2+ diffuse into axon;
- vesicles move towards and then fuse with (presynaptic) membrane;
- acetylcholine (released);
- (acetylcholine) diffuses across synaptic cleft/synapse;
- binds with receptors on (postsynaptic) membrane;
- sodium ions/Na+ enter (postsynaptic) neurone;
- depolarisation of (postsynaptic) membrane;
- if above threshold nerve impulse/action potential produced
Serotonin diffuses across the synaptic gap and binds to a receptor on the post-synaptic membrane. Describe how this causes depolarisation of the post-synaptic membrane
- Causes sodium ion channels to open;
2. Sodium ions enter (cell and cause depolarisation);
Explain what causes transmission at a synapse to occur in only one direction
(Vesicles containing) neurotransmitter only in presynaptic membrane/
neurone;
receptor/proteins only in postsynaptic membrane/neurone;
so neurotransmitter diffuses down concentration gradient;
GABA is a neurotransmitter which can inhibit the production of action potentials by interacting with K+ and Cl- channels. an action potential is less likely if GABA is released at the same time. Explain why
GABA opens K+ and Cl– channels;
K+ passes out and Cl– passes in;
Membrane potential more negative/hyperpolarised;
Requires increased stimulation/must open more Na+ channels / allow more Na+ to enter;
To reach threshold;
Give five differences between a cholinergic synapse and a neuromuscular junction
neurone to neurone and neurone to muscle;
action potential in neurone and no action potential in muscle/
sarcolemma;
no summation in muscle;
muscle response always excitatory (never inhibitory);
some neuromuscular junctions have different neurotransmitters;
How can inhibition of acetylcholinesterase result in muscles being permanently contracted?
- Acetylcholine not broken down / stays bound to receptor;
- Na+ ions (continue to) enter / (continued) depolarisation / Na+ channels (kept) open / action potentials / impulses fired (continuously);
- muscles stay contracted / cannot relax;