3.6.1 & 3.6.2 (neuroscience) Flashcards
Resting potential
-When the axon is not transmitting an electrical impulse
-The axon is polarised (-70Mv)
How resting potential is maintained
-The SODIUM POTTASIUM PUMP actively transports 3 Na+ ions out, and 2 K+ ions in
-ATP hydrolysed to create this energy
-This generates a elecrochemical gradient
-More K+ ion voltage-gated channel proteins are open, than Na+ ions channel proteins (more permeable to potassium ions)
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Action potential
- RP at -70mV (polarised)
- Stimulus causes Na+ voltage gated channel to open
- Enough Na+ enter to exceed the threshold value
- More Na+ entre (depolarised)
- Na+ voltage gated channels close
- Membrance repolarises
- K+ voltage gated channel remain open
- Tempory overshoot of K+ ions (hyperpolarisation)
- RP restored membrane is repolarised
Action potential in a myelinated neuron
-Schwann cells act as electrical insulators, preventing AP from forming
-AP jumps from one node of Ranvier to the next-SALTATORY CONDUCTION
Ways of speeding up an action potential
> Myelination-saltatory conduction
> Wider axon diameter-positive ions don’t leak as much, so membrane potentials are more easily maintained
> Higher temperatures-ions move quicker, so it increases the rate of diffusion of ions
Refactory period
The small time it takes for sodium ion influx to be possible again
Importance of the refractory period
- Ensures that action potentials are only propagated in one direction
-Can only stimulate the area next to it as the Na+ VGC can’t open until RP is restored - Ensures that action potentials are discrete-as a new AP cant be immediately after
- Means there is a maximum number of nerve impulses-this limits the strength of a stimulus that can be detected
How an action potential travels across a synapse
- Calcium ion channels open
- Neurotransmitter release-Neurotransmitter fuses with the presynaptic membrane, releasing neurotransmitters into the cleft
- The neurotransmitter diffuses across the cleft, to the postsynaptic membrane
- The neurotransmitter binds to the receptor on the ligand gated sodium ion channels. When they bind they change the shape of the Na+ channel, making it open
- If the threshold is exceeded, AP is triggered. Ap travels down the neuron until it reaches the synapses at the other end
- Acetylcholinesterase hydrolyses acetylcholine into acetate and choline
-Acetate and choline are actively transported back into ye synaptic knob, Na+ channels close again, and Ca+ are actively transported back out into the synaptic cleft
Spatial summation
Many different neurones collectively trigger a new action potential by combining the neurotransmitter they release to exceed the threshold
-So the effect of a stimulus can be magnified e.g retinal convergence
Temporal summation
One neurone releases neurotransmitter repeatedly over a short period of time to add up to enough to exceed the threshold value.
Inhibition at synapses
-Some neurotransmitters are inhibitory so prevent AP from being generated
-This enables specific pathways to be stimulated, while preventing random impulses
Methods of inhibition at synapses
-Neurotransmitters can cause both chloride(-) and potassium(+) ion channels to open
-Causing neg chloride ions to enter, and K+ to diffuse out
-Both of these cause the neuron to become hyperpolarised, making it harder to reach the threshold value,
Comparing neuromuscular and cholinergic synapses
Both are unidirectional due to neurotransmitter receptors being on the post-synaptic membrane
-Neuromuscular only excitatory. Cholinergic is excitatory or inhibitory
-MNJ connects neurons to muscles. Cholinergic connects two neurons
-Endpoint for AR at NMJ. New AP is generated in the next neuron at the cholinergic synapse
Cardiac muscle
Is myogenic, so it doesn’t need a stimulus to contract
Location of nodes in heart
SAN- located in the right atrium
AVN- located on the border of the right and left ventricle, in the atria still
Bundle of HIS- runs through septum
Purkyne fibres- in the walls of the ventricle
Control of heart rate biology
- SAN initiates the wave of contraction across the atrium
- The tissue between the atria and ventricles doesn’t conduct the excitatory wave
- AVN releases a wave of contraction across the ventricles
- The bundle of HIS conducts impulses down the septum and purkyne fibres, so the ventricle walls contract all the way around.
Where heart rate is controlled
-In the medulla oblingata
-Sympathetic NS speeds up heart rate
-Parasympathetic NS speeds up heart rate
Chemical changes in the blood
-Chemoreceptors detect changes in Co2 concentration
-Baroreceptors detect changes in pressure
-Found in the aorta walls and the carotid artery
How chemical changes in blood effect heart rate
- Increase in Co2 or decrease in blood pressure
- Stimulates receptors, accelerates centre in the medulla, sends impulses via sympathetic nerves
- SAN stimulated by noradrenaline, released at the synapse
