Neuro 2 Electrical Signaling & CICR Model and Skeletal Muscle

What two conditions are required for a membrane potential to exist?

Unequal ion concentrations across the membrane and selective membrane permeability.

What is the main role of the Na+/K+-ATPase in electrical signaling?

It uses ATP to maintain the Na+ and K+ concentration gradients over time. It contributes only a small direct voltage and does not repolarize the membrane after each action potential.

When a channel for one ion opens, toward what value does the membrane potential move?

Toward that ion's equilibrium potential. The direction and strength of movement depend on the difference between membrane potential and the ion's equilibrium potential.

• How do graded potentials differ from action potentials in amplitude and spread?

• Graded-potential amplitude varies with stimulus strength and decreases as the signal spreads.

• Action potentials are all-or-none and regenerate along the axon without decreasing in amplitude.

What is the functional difference between an EPSP and an IPSP?

An EPSP increases the likelihood of reaching threshold at the axon hillock. An IPSP decreases that likelihood or stabilizes the membrane away from threshold. The receptor and resulting ion conductance determine the effect.

How do temporal and spatial summation differ?

Temporal summation combines graded potentials that arrive close together in time. Spatial summation combines graded potentials arriving from different locations

Where are graded potentials integrated, and what happens if threshold is reached?

They are integrated at the axon hillock. Reaching threshold opens voltage-gated Na+ channels and initiates an action potential

What produces depolarization, repolarization, and after-hyperpolarization during a neuronal action
potential

Na+ entry through voltage-gated Na+ channels produces rapid depolarization. Na+ channel inactivation and K+ exit through voltage-gated K+ channels produce repolarization. Slow closure of K+ channels produces after-hyperpolarization.

Why can no second action potential begin during the absolute refractory period?

Most voltage-gated Na+ channels are open or inactivated. Inactivated channels cannot reopen until repolarization resets them

Why is a stronger stimulus required during the relative refractory period?

K+ conductance remains elevated and the membrane is hyperpolarized, so more depolarization is needed to reach threshold.

How does a neuron encode a stronger stimulus after threshold has been reached?

It increases action-potential frequency, not action-potential amplitude.

Why does an action potential normally propagate forward along an axon?

Local current depolarizes membrane ahead of the action potential, while Na+ channels behind it are refractory.

What two axon properties increase conduction velocity?

Myelination and larger axon diameter. Myelin reduces current loss and allows action potentials to regenerate mainly at nodes of Ranvier.

What directly causes neurotransmitter release from an axon terminal?

The arriving action potential depolarizes the terminal, opening voltage-gated Ca2+ channels. Ca2+ entry triggers synaptic-vesicle fusion.

How do ionotropic and metabotropic receptors differ?

Ionotropic receptors are ligand-gated ion channels that produce rapid responses. Metabotropic receptors activate G proteins and intracellular signaling, usually producing slower and longer-lasting responses

How can neurotransmitter signaling at a chemical synapse end?

Reuptake, enzymatic degradation, and diffusion away from the synapse can terminate signaling

What sequence connects a somatic motor-neuron action potential to a skeletal-muscle action potential?

The motor-neuron action potential opens terminal Ca2+ channels, causing ACh release. ACh opens nicotinic receptors at the motor end plate. The end-plate potential brings adjacent sarcolemma to threshold and opens voltage-gated Na+ channels.

What is the function of a skeletal-muscle T-tubule?

It carries the muscle action potential from the surface into the interior of the muscle fiber.

What structures form a skeletal-muscle triad?

One T-tubule and the two adjacent terminal cisternae of the sarcoplasmic reticulum.

Arrange these structures from largest to smallest: sarcomere, muscle fiber, myofibril, whole muscle, fascicle

Whole muscle, fascicle, muscle fiber, myofibril, sarcomere.

What are the boundaries of one sarcomere?

Two Z disks.

What happens to the A band, I band, H zone, and filament lengths when a sarcomere shortens?

The A band remains constant. The I band and H zone narrow. Thick and thin filaments keep their lengths while overlap increases.

What must happen before myosin can bind strongly to actin?

Ca2+ binds troponin C. Troponin changes shape and shifts tropomyosin away from the myosin-binding sites on actin

What is the sequence of the crossbridge cycle?

ATP binds and myosin releases actin. ATP hydrolysis cocs the myosin head. Myosin binds actin weakly. Pi release initiates the power stroke. ADP release returns myosin to the rigor state.

What are the major roles of ATP in skeletal-muscle contraction and relaxation?

ATP binding detaches myosin from actin. ATP hydrolysis re-cocks the myosin head. SERCA uses ATP to pump Ca2+ back into the SR. ATP also supports the pumps that maintain ion gradients.

Why does ATP depletion produce rigor rather than relaxation?

Without ATP, myosin cannot detach from actin and SERCA cannot efficiently remove cytosolic Ca2+. Strong binding persists.

What event ends thin-filament activation during relaxation?

SERCA lowers cytosolic Ca2+ by pumping it into the SR. Ca2+ leaves troponin, and tropomyosin again limits strong actin-myosin binding

Why can repeated stimuli produce more skeletal-muscle force than one stimulus?

• The muscle action potential ends before the twitch ends.

• Repeated stimuli can arrive before Ca2+ returns to baseline, so cytosolic Ca2+ and force summate

What distinguishes summation from tetanus?

Summation is increased force from overlapping twitches. During tetanus, stimulation is frequent enough that cytosolic Ca2+ remains elevated and individual twitches fuse

What is a motor unit?

One somatic motor neuron and all skeletal-muscle fibers it innervates.

How does motor-unit recruitment grade whole-muscle force?

The nervous system activates additional motor units as force demand rises. Small, fatigue- resistant units are recruited before larger, faster units

Why is active force lower when a sarcomere is extremely short or extremely stretched?

At very short lengths, filament interference limits productive crossbridges. At very long lengths, reduced thick-thin overlap limits crossbridge formation.

How do isometric, concentric, and eccentric actions differ?

During isometric action, force develops with little change in muscle length. During concentric action, the active muscle shortens. During eccentric action, the active muscle lengthens under load.

How do the major ATP sources change with exercise duration and intensity?

• Stored ATP provides only immediate energy.

• Phosphocreatine rapidly buffers ATP

• Glycolysis supports fast output with limited yield.

• Oxidative phosphorylation supports sustained output.

  • The pathways overlap rather than switching on one at a time.

Why is lactic acid alone an inadequate explanation for muscle fatigue?

Fatigue can reflect reduced motor drive, altered recruitment, Pi accumulation, impaired Ca2+ handling, or substrate depletion. The important cause depends on the activity.

What is the key excitation-contraction coupling difference between skeletal and cardiac muscle?

In skeletal muscle, the voltage sensor mechanically activates RyR1, so extracellular Ca2+ entry is not required for every twitch. In cardiac muscle, Ca2+ entry through L-type channels activates RyR2 and triggers Ca2+-induced Ca2+ release.

What Ca2+ movements are represented in the CICR model?

Ca2+ enters through an L-type channel, activates RyR to release more Ca2+ from the SR, and is then removed from the cytosol by SERCA, the Na+/Ca2+ exchanger, and a plasma-membrane Ca2+- ATPase