An action potential (AP) is a rapid, transient change in the membrane potential of a neuron, enabling rapid communication. It involves a sequence of events driven by the opening and closing of voltage-gated ion channels:

Rising Phase (Depolarization):

• A stimulus causes a small depolarization of the neuronal membrane. If this depolarization reaches the threshold potential (typically -55mV), voltage-gated sodium (Na+) channels open.
• Na+ ions rush into the neuron down their electrochemical gradient, causing a rapid influx of positive charge. This further depolarizes the membrane, creating a positive feedback loop that drives the AP.
• The membrane potential rapidly rises towards +30mV.

Falling Phase (Repolarization):

• As the membrane potential reaches its peak, Na+ channels begin to inactivate, preventing further influx of Na+.
• Voltage-gated potassium (K+) channels open, allowing K+ ions to flow out of the neuron down their electrochemical gradient.
• The outflow of positive K+ ions repolarizes the membrane, bringing the potential back towards the RMP.

Refractory Period:

• The refractory period is a period after an action potential during which it is difficult or impossible to trigger another action potential. It exists because of the inactivation of Na+ channels and the continued opening of K+ channels.
• Absolute Refractory Period: During this period, no stimulus, no matter how strong, can trigger an action potential. This is due to the inactivation of Na+ channels.
• Relative Refractory Period: During this period, a stronger-than-normal stimulus is required to trigger an action potential. This is due to the continued efflux of K+ ions and the recovery of some Na+ channels.

The sarcoplasmic reticulum (SR) plays a vital role in muscle contraction by acting as the primary calcium store and regulating the availability of calcium ions (Ca²⁺) within the sarcoplasm. Here's a detailed explanation:

Calcium Stores: The SR is a specialized network of tubules within muscle cells that acts as a reservoir for Ca²⁺. It stores a significantly higher concentration of Ca²⁺ than the sarcoplasm. This high concentration is maintained by the activity of Ca²⁺ pumps (SERCA - Sarcoplasmic Reticulum Ca²⁺ ATPase) which actively transport Ca²⁺ from the sarcoplasm into the SR lumen.

Calcium Release: The release of Ca²⁺ from the SR into the sarcoplasm is tightly regulated. This process is primarily mediated by voltage-sensitive calcium channels called Ryanodine receptors (RyRs) located on the SR membrane. The opening of RyRs is triggered by the influx of Ca²⁺ into the T-tubules, which is itself initiated by the action potential. The influx of Ca²⁺ into the T-tubules activates DHPRs, leading to the opening of RyRs on the SR. This allows a rapid and large release of Ca²⁺ into the sarcoplasm.

Calcium Reuptake: Muscle relaxation requires the removal of Ca²⁺ from the sarcoplasm back into the SR. This is accomplished by the SERCA pumps, which actively transport Ca²⁺ from the sarcoplasm into the SR lumen. This process requires ATP. The activity of SERCA is regulated by phosphorylation, which can be influenced by various signaling pathways.

Importance for Muscle Relaxation: The reuptake of Ca²⁺ into the SR is essential for muscle relaxation. When Ca²⁺ concentration in the sarcoplasm decreases, it detaches from troponin, allowing tropomyosin to block the myosin-binding sites on actin. This prevents the formation of cross-bridges and allows the muscle fibre to relax. Without the SR's ability to efficiently reuptake Ca²⁺, muscle relaxation would be impaired, leading to sustained muscle contraction.

Non-myelinated neurons transmit impulses continuously down the entire length of the axon. The action potential is regenerated at every point along the axon membrane. This process requires a significant amount of energy to maintain the ion gradients and the depolarization/repolarization cycles. The speed of transmission is relatively slow, typically around 1 metre per second.

Myelinated neurons, as described previously, transmit impulses via saltatory conduction. The action potential 'jumps' between the nodes of Ranvier. Because the action potential is only regenerated at the nodes, the transmission is much faster, typically around 10-100 metres per second. This is a significant increase in speed.

Comparison Table:

The energy expenditure is lower in myelinated neurons because the action potential is regenerated less frequently. The myelin sheath also reduces the metabolic demands of the neuron by minimizing ion leakage and maintaining the resting membrane potential. Therefore, the increased speed of transmission in myelinated neurons is a significant evolutionary advantage.