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1. Resting Potential The neuron is in a resting state with a voltage of approximately
-70 mV, maintained by the sodium-potassium pump.
2. Threshold A certain threshold (usually around -55 mV) is reached when a
stimulus causes slight depolarization, triggering an action poten-
tial.
3. Depolarization Voltage-gated sodium channels open rapidly, allowing Na⁺ ions
to rush into the cell, causing the membrane potential to reach up
to +30 mV.
4. Peak Phase At the peak of the action potential, the inactivation gates of
sodium channels close, stopping Na⁺ influx, while voltage-gated
potassium channels open.
5. Repolarization K⁺ ions flow out of the cell through opened potassium channels,
making the inside of the cell more negative and returning to-
wards resting potential.
6. Hyperpolarization The potassium channels are slow to close, causing an overshoot
where the membrane potential becomes more negative than the
resting potential.
7. Return to Resting Potential The sodium-potassium pump restores the resting potential by
transporting Na⁺ ions out and K⁺ ions back into the neuron.
8. Calcium Imbalance Calcium imbalances can significantly affect the action potential of
neurons.
9. Hypercalcemia High extracellular calcium levels can increase the threshold re-
quired to initiate an action potential and enhance synaptic re-
lease.
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10. Hypocalcemia Low extracellular calcium reduces the threshold for action poten-
tial initiation, increasing excitability and leading to symptoms like
muscle spasms.
11. Potassium Imbalance Potassium imbalances can also significantly affect the action po-
tential of neurons.
12. Hyperkalemia High potassium levels decrease the resting membrane potential,
bringing it closer to the threshold but can impair action potential
firing over time.
13. Hypokalemia Low potassium levels make the membrane potential more nega-
tive, reducing excitability and making it harder for neurons to fire
action potentials.
14. Muscle Weakness Chronic depolarization from hyperkalemia can lead to long-term
paralysis or weakness due to inactivation of sodium channels.
15. Neuromuscular Effects of Hypocalcemia can lead to increased neuromuscular excitability,
Hypocalcemia muscle cramps, and tingling sensations.
16. Muscle Weakness and Hypokalemia can lead to muscle weakness, cramps, and in severe
Cramps from Hypokalemia cases, paralysis due to reduced neuronal and muscular activity.
17. Refractory Period The period during hyperpolarization where the neuron is less
likely to fire another action potential.
18. Sodium-Potassium Pump A mechanism that actively transports Na⁺ ions out of the cell and
K⁺ ions into the cell to maintain resting potential.
19. Neurotransmitter Release Calcium is critical in neurotransmitter release at synaptic termi-
nals.
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20. Spontaneous Action Poten- Low extracellular calcium can lead to spontaneous action poten-
tials tials due to increased excitability.
21. Calcium Stabilization Calcium stabilizes the membrane, making neurons less excitable
and requiring stronger stimuli to trigger action potentials.
22. Chronic Depolarization A condition where persistent depolarization can inactivate sodi-
um channels, impairing action potentials.
23. Atrophy Decrease in size and function
24. Hypertrophy Increase in size
25. Hyperplasia Increase in the number of cells; Size of organ increases
26. Metaplasia One cell type replaced by another
27. Dysplasia Disorganized cellular growth
28. Physiologic Atrophy Example: Shrinkage of the thymus during early development and
aging.
29. Pathophysiologic Atrophy Example: Muscle atrophy due to prolonged immobilization, such
as when a limb is in a cast.
30. Physiologic Hypertrophy Example: Enlargement of skeletal muscle fibers due to consistent
exercise and resistance training.
31. Pathophysiologic Hypertro- Example: Cardiac hypertrophy due to chronic hypertension.
phy
32. Physiologic Hyperplasia Example: Breast glandular tissue proliferation during pregnancy
and lactation.