Nervous Coordination Flashcards
(10 cards)
Stage 1 of action potential
- Resting Potential
• The neurone is polarised at around –70 mV.
• Maintained by the sodium-potassium pump, which actively transports
• 3 Na⁺ out of the neurone
• 2 K⁺ in,
creating a net negative charge inside.
• Membrane is more permeable to K⁺ than Na⁺ at rest.
Stage 2 of AP
⸻
- Depolarisation
• A stimulus causes Na⁺ voltage-gated channels to open.
• Na⁺ diffuses into the axon down its electrochemical gradient.
• This causes the inside to become less negative.
• If the threshold (~–55 mV) is reached, more Na⁺ channels open, causing a positive feedback loop.
• Membrane potential reaches up to +40 mV.
Stage 3 of AP
⸻
- Repolarisation
• At +40 mV, Na⁺ channels close.
• Voltage-gated K⁺ channels open.
• K⁺ diffuses out of the axon down its electrochemical gradient.
• This causes the inside of the membrane to become negative again.
⸻
Stage 4 of AP
- Hyperpolarisation
• K⁺ channels are slow to close, so too many K⁺ ions leave.
• The membrane becomes more negative than resting potential (e.g. –80 mV).
• Na⁺/K⁺ pump restores the original ion balance, returning the membrane to the resting potential.
Synaptic transmission
- Action potential arrives at the presynaptic neurone.
- This causes voltage-gated calcium ion (Ca²⁺) channels to open in the presynaptic membrane.
- Calcium ions diffuse into the presynaptic neurone by facilitated diffusion.
- Influx of Ca²⁺ causes synaptic vesicles to move towards and fuse with the presynaptic membrane.
- Neurotransmitter (e.g. acetylcholine) is released into the synaptic cleft by exocytosis.
- Neurotransmitter diffuses across the synaptic cleft.
- Neurotransmitter binds to specific complementary receptors on the postsynaptic membrane.
- This causes sodium ion (Na⁺) channels to open, leading to:
- Sodium ions diffuse into the postsynaptic neurone, causing depolarisation.
- If threshold is reached, an action potential is generated in the postsynaptic neurone.
- Neurotransmitter is broken down by an enzyme (e.g. acetylcholinesterase), and
- The products are reabsorbed into the presynaptic neurone or diffuse away to stop the response.
Neuromuscular junction transmission
- Action potential arrives at the presynaptic motor neurone.
- This causes voltage-gated calcium ion (Ca²⁺) channels to open in the presynaptic membrane.
- Calcium ions diffuse into the presynaptic neurone.
- Vesicles containing acetylcholine move to and fuse with the presynaptic membrane.
- Acetylcholine is released into the synaptic cleft by exocytosis.
- Acetylcholine diffuses across the synaptic cleft.
- Acetylcholine binds to receptors on the sarcolemma (postsynaptic membrane of the muscle fibre).
- This causes sodium ion (Na⁺) channels to open.
- Sodium ions diffuse into the muscle fibre, causing depolarisation of the sarcolemma.
- If threshold is reached, an action potential is generated in the muscle fibre.
- This action potential travels along the T-tubules and stimulates the release of calcium ions from the sarcoplasmic reticulum.
- Calcium ions initiate muscle contraction by interacting with troponin and tropomyosin, allowing actin and myosin to form cross-bridges.
- Acetylcholine is broken down by acetylcholinesterase in the cleft, and choline is reabsorbed into the neurone to stop further stimulation.
Differences of neuromuscular vs. a typical synapse
• Postsynaptic membrane is the muscle fibre membrane (sarcolemma), not another neurone.
• Always excitatory, never inhibitory.
• Leads to muscle contraction, not just another nerve impulse.
• Neurotransmitter is always acetylcholine.
• Has T-tubules and sarcoplasmic reticulum, unique to muscle fibres.
Sliding filament theory of muscle contraction
- Action potential travels along the sarcolemma and down T-tubules into the muscle fibre.
- This causes calcium ions (Ca²⁺) to be released from the sarcoplasmic reticulum into the sarcoplasm.
- Calcium ions bind to troponin, causing troponin to change shape.
- This moves tropomyosin away, exposing the myosin-binding sites on actin filaments.
- Myosin heads bind to actin, forming actin–myosin cross-bridges.
- Myosin heads perform a power stroke: they pivot, pulling the actin filament along, and ADP + Pi are released.
- ATP binds to the myosin head, causing the cross-bridge to break.
- ATP is hydrolysed by ATPase, which re-energises the myosin head (returns it to original position).
- Myosin head reattaches to a new binding site on actin and the cycle repeats.
- When stimulation stops, Ca²⁺ is actively transported back into the sarcoplasmic reticulum, tropomyosin re-covers the binding sites, and the muscle relaxes.
Control of heart rate by the autonomic nervous system for baroreceptors
When blood pressure is too high:
1. Baroreceptors in aorta and carotid arteries detect high pressure.
2. They send more impulses to the cardioinhibitory centre in the medulla.
3. This increases impulses along parasympathetic neurones (vagus nerve).
4. These neurones release acetylcholine at the SAN.
5. This decreases heart rate, reducing blood pressure.
When blood pressure is too low:
1. Baroreceptors send more impulses to the cardioacceleratory centre.
2. Increases impulses via sympathetic neurones.
3. These release noradrenaline at the SAN.
4. This increases heart rate, raising blood pressure.
Control of heart rate by the autonomic nervous system for chemoreceptors
When CO₂ is high (e.g. during exercise):
1. CO₂ dissolves in blood, forming carbonic acid → lowers pH.
2. Chemoreceptors in aorta and carotid bodies detect low pH/high CO₂.
3. Send impulses to cardioacceleratory centre.
4. Sympathetic neurones release noradrenaline at SAN.
5. Heart rate increases → blood is pumped to lungs faster → more CO₂ removed.
When CO₂ is low (resting):
1. Higher pH is detected by chemoreceptors.
2. Impulses sent to cardioinhibitory centre.
3. Parasympathetic stimulation of SAN → acetylcholine released.
4. Heart rate decreases.
