Excitable Tissues and Neurons Overview

<p>–70 mV (C)</p> Signup and view all the answers

<p>Potassium leak channels (C)</p> Signup and view all the answers

<p>Myelinated fibers propagate action potentials only at nodes of Ranvier (B)</p> Signup and view all the answers

<p>It can display summation (D)</p> Signup and view all the answers

<p>The membrane potential rises towards 0 mV and beyond (C)</p> Signup and view all the answers

<p>Na+-K+ ATPase pump (A)</p> Signup and view all the answers

<p>Threshold stimulus (C)</p> Signup and view all the answers

<p>0.5-2 m/sec (C)</p> Signup and view all the answers

<p>The membrane potential decreases below –70 mV (A)</p> Signup and view all the answers

<p>Potassium ions (K+) (B)</p> Signup and view all the answers

<p>Volt-sensitive sodium channels (C)</p> Signup and view all the answers

<p>Threshold stimulus is applied (A)</p> Signup and view all the answers

<p>Resting phase (B)</p> Signup and view all the answers

<p>Sodium ions flowing into the muscle fiber (C)</p> Signup and view all the answers

<p>Hydrolysis of acetylcholine by acetylcholinesterase (A)</p> Signup and view all the answers

<p>Troponin-tropomyosin complex (B)</p> Signup and view all the answers

<p>It is unidirectional with a delay of about 0.5 milliseconds (D)</p> Signup and view all the answers

<p>It decreases the release of acetylcholine significantly (D)</p> Signup and view all the answers

<p>Binding of actin and myosin filaments (B)</p> Signup and view all the answers

<p>Botulinum toxin (B)</p> Signup and view all the answers

<p>Motor end plate potential (EPP) (B)</p> Signup and view all the answers

<p>Type I (C)</p> Signup and view all the answers

<p>Anaerobic glycolysis (A)</p> Signup and view all the answers

<p>They have zero mechanical efficiency. (C)</p> Signup and view all the answers

<p>They destroy the receptors. (A)</p> Signup and view all the answers

<p>Type IIb (D)</p> Signup and view all the answers

<p>Increases the level of ACh at the motor end plates. (A)</p> Signup and view all the answers

<p>Type IIb (A)</p> Signup and view all the answers

<p>Isometric contraction (B)</p> Signup and view all the answers

<p>To protect and insulate the nerve fibers (C)</p> Signup and view all the answers

<p>Dendrites (C)</p> Signup and view all the answers

<p>They can change shape to open or close (C)</p> Signup and view all the answers

<p>By allowing selective ion diffusion across the membrane (A)</p> Signup and view all the answers

<p>They open when specific neurotransmitters bind (B)</p> Signup and view all the answers

<p>Formed by a lipid bilayer with various proteins (A)</p> Signup and view all the answers

<p>Ion diffusion from high to low concentration (D)</p> Signup and view all the answers

<p>They require active transport to operate (C)</p> Signup and view all the answers

<p>It blocks the transmission by competitive inhibition at the cholinergic receptors. (D)</p> Signup and view all the answers

<p>Myosin binds to actin and pulls the actin filament. (C)</p> Signup and view all the answers

<p>Partial hydrolysis recocks the myosin head for another cycle. (B)</p> Signup and view all the answers

<p>The thin actin filaments slide over the thick myosin filaments. (A)</p> Signup and view all the answers

<p>Muscle relaxation occurs. (C)</p> Signup and view all the answers

<p>Succinylcholine. (A)</p> Signup and view all the answers

<p>It relates to the force generated when muscles are at optimal length. (A)</p> Signup and view all the answers

<p>Organic phosphorus compounds. (C)</p> Signup and view all the answers

Tissues (like nerves and muscles) that respond to stimuli by changing electrical properties and generating impulses.

The basic unit of the nervous system, responsible for transmitting signals.

A fatty layer that insulates nerve fibers, speeding up signal transmission.

The barrier between the inside and outside of a cell, controlling what enters and exits.

The difference in electrical charge across a cell membrane, crucial for nerve signals.

Protein channels in cell membranes that allow ions to pass through.

Ion channels that are always open, allowing continuous ion movement.

Ion channels that open and close in response to stimuli (e.g., chemicals, voltage).

The difference in electrical potential across the cell membrane of excitable tissues (nerve and muscle) at rest. A typical RMP is -70mV.

A reduction in the membrane potential, becoming less negative than the resting potential.

An increase in the membrane potential, becoming more negative than the resting potential.

Channels that allow potassium ions to passively leak out of the cell, contributing to the resting membrane potential.

Active transport that moves 3 sodium ions out and 2 potassium ions in, maintaining the concentration gradient and RMP.

A transient change in membrane potential of excitable cells (nerve or muscle) which is in response to a threshold stimulus.

The minimum level of stimulus required to trigger an action potential.

The initial period before an action potential occurs, characterized by the resting membrane potential.

A small, variable change in membrane potential that doesn't travel far.

Action potentials either happen completely or not at all.

Action potential conduction in unmyelinated axons. Continuous, slow process.

Action potential conduction in myelinated axons. Fast, leaping process.

Gaps in the myelin sheath where action potentials occur.

A brief period after an action potential where a neuron cannot fire another.

Calcium ions entering a nerve ending trigger the release of acetylcholine, a neurotransmitter, from vesicles.

Acetylcholine binds to nicotinic receptors on the motor end plate of a muscle fiber, initiating muscle contraction.

The depolarization of the muscle fiber membrane caused by the influx of sodium ions through acetylcholine-gated channels.

Calcium ions released from the sarcoplasmic reticulum bind to troponin, allowing actin and myosin to interact and initiate muscle contraction.

Calcium ions are pumped back into the sarcoplasmic reticulum, causing troponin-tropomyosin to block the binding sites on actin and halting muscle contraction.

Signals travel from the nerve to the muscle, but not vice versa, ensuring one-way control of muscle activity.

Repeated stimulation can deplete acetylcholine vesicles, leading to muscle fatigue.

Calcium ions enhance acetylcholine release, while magnesium ions decrease release.

A drug that blocks the transmission of nerve signals to muscles by competitively inhibiting acetylcholine receptors.

Causes persistent depolarization of muscle cells, leading to paralysis.

A drug that causes persistent depolarization of muscle cells, leading to paralysis.

Stimulates the nicotinic receptors, leading to muscle activation.

Drugs that increase acetylcholine levels in the synapse, leading to enhanced muscle activity.

Drugs that temporarily inhibit cholineesterase activity, allowing acetylcholine levels to increase.

Drugs that permanently inhibit cholineesterase activity, causing long-lasting increases in acetylcholine levels.

The series of events that occur during muscle contraction, involving the interaction between actin and myosin filaments.

Slow-twitch muscle fibers that are highly oxidative, meaning they rely on oxygen for energy. They are fatigue-resistant and important for endurance activities.

Fast-twitch muscle fibers that are both oxidative and glycolytic, meaning they can use both oxygen and glucose for energy. They are moderately fatigue-resistant and contribute to both endurance and strength activities.

Fast-twitch muscle fibers that are primarily glycolytic, meaning they rely on glucose for energy. They are easily fatigued and are crucial for explosive movements.

A muscle contraction where the muscle length changes, resulting in movement. It can be concentric (muscle shortens) or eccentric (muscle lengthens).

A muscle contraction where the muscle length stays the same, generating force without movement.

An autoimmune condition where the body attacks its own acetylcholine receptors at the neuromuscular junction, causing muscle weakness and fatigue.

Treatment for Myasthenia Gravis involves either increasing acetylcholine levels at the neuromuscular junction with drugs like neostigmine, or suppressing the immune system with immunosuppressants.