LS 7C flash cards

Keeping internal conditions, such as body temperature and blood glucose, within a narrow range despite changes outside.

It counteracts a change, pushing the variable back toward its set point.

When body temperature rises, sweating and widened skin blood vessels shed heat until it falls again.

Contractions stretch the cervix, which signals the brain to release more oxytocin, bringing stronger contractions until birth ends the loop.

It halves. Surface area grows 2² = 4 times while volume grows 2³ = 8 times.

This is why cells stay small, and why large animals need lungs, guts and blood vessels to exchange materials.

At rest the membrane is most permeable to K⁺, which leaks out down its gradient and leaves the inside negative, about −70 mV.

The sodium-potassium pump builds the K⁺ and Na⁺ gradients that make this possible.

About −89 mV. log(5/140) ≈ −1.45, and 61.5 × (−1.45) ≈ −89 mV.

The resting potential is less negative than this because the membrane also lets some Na⁺ leak in.

Voltage-gated Na⁺ channels open at threshold, Na⁺ rushes in, and the inside becomes positive.

Na⁺ channels inactivate and voltage-gated K⁺ channels open, so K⁺ flows out and the inside turns negative again.

The slow K⁺ channels stay open a little too long, causing a brief undershoot below rest.

The Na⁺ channels it just passed are inactivated, so that patch of membrane is refractory and cannot fire again right away.

It insulates the axon, so the signal jumps from one node of Ranvier to the next instead of regenerating along every patch.

This is saltatory conduction. The nodes are gaps in the myelin packed with voltage-gated Na⁺ channels.

By firing action potentials more often. Their frequency carries the strength, not their size.

The action potential opens voltage-gated Ca²⁺ channels in the axon terminal, and the entering Ca²⁺ makes vesicles release their contents.

An EPSP depolarizes the postsynaptic cell, toward threshold. An IPSP hyperpolarizes it, away from threshold.

It raises heart rate and slows digestion, preparing the body for fight or flight.

The parasympathetic division does the opposite, for rest and digest.

Myosin heads pull the actin filaments toward the sarcomere's center. The sarcomere shortens, but the filaments keep their length.

Ca²⁺ binds troponin, which shifts tropomyosin away from the myosin-binding sites on actin, so cross-bridges can form.

The Ca²⁺ comes from the sarcoplasmic reticulum, released when an action potential spreads into the fiber.

ATP binding releases the myosin head from actin, and splitting the ATP re-cocks the head for its next stroke.

Acetylcholine is not broken down, so it lingers in the synapse and keeps stimulating the muscle fiber.

By recruiting more motor units, so more muscle fibers contract at once.

Firing each motor unit faster also helps, because twitches summate before the fiber relaxes.

Steroids change gene transcription, which takes time to make new proteins. Peptides set off fast second-messenger cascades on proteins already there.