Muscle Contraction and Walk Along Theory Quiz

Troponin binds to calcium ions, leading to a change in tropomyosin's shape, revealing the active sites on actin where myosin can bind.

Myosin is attached to actin in a 'rigor state'. ATP binds to myosin, weakening its affinity for actin, causing it to detach.

Myosin detaches from actin and undergoes a conformational change, known as the recovery stroke. This involves the myosin head moving to a position ready to bind again.

Myosin is in a relaxed state, primed and ready to reattach to actin, but it needs calcium to bind. This state is known as the 'recharged' state.

Calcium binds to troponin, causing a change in shape that allows myosin to reattach to actin, forming a weak binding.

The specialized synapse between a motor neuron and a muscle fiber where nerve impulses trigger muscle contraction.

A localized depolarization of the muscle fiber membrane caused by the binding of acetylcholine (ACh) to its receptors.

An enzyme that breaks down acetylcholine (ACh) in the neuromuscular junction, terminating the signal and allowing the muscle to relax.

Calcium ions (Ca2+) are released from the sarcoplasmic reticulum (SR) and bind to troponin, triggering a conformational change in the troponin-tropomyosin complex, which exposes binding sites on actin for myosin to attach.

A voltage-sensitive receptor on the T-tubule membrane that senses the action potential and triggers the release of calcium from the sarcoplasmic reticulum (SR).

The ability of a receptor to respond selectively to a specific type of stimulus, determining how the sensation is perceived.

A type of stimulus that involves physical stretching or bending of the receptor membrane, opening ion channels and creating a receptor potential.

A type of stimulus that involves the binding of chemicals to receptors, altering membrane permeability and generating a receptor potential.

The change in membrane potential of a receptor in response to a stimulus. The stronger the stimulus, the larger the receptor potential and the higher the frequency of action potentials generated.

The gradual decrease in the response of a receptor to a continuous stimulus. Receptors are more sensitive to changes in stimuli, allowing them to detect new events.

Cardiac muscle cells are connected by low-resistance intercalated disks, allowing for coordinated contractions. These fibers are intertwined, forming sheets for efficient pumping.

Cardiac muscle is organized into sheets, unlike skeletal muscle which is aligned in linear bundles. The sheets allow for coordinated contraction and efficient blood pumping.

Atria are the upper chambers of the heart that receive blood, while ventricles are the lower chambers that pump blood out of the heart.

Deoxygenated blood enters the right atrium, then right ventricle, then to the lungs for reoxygenation. Oxygenated bood returns to the left atrium, left ventricle, and finally pumped through the aorta to the body.

A cardiac action potential involves rapid depolarization caused by sodium influx, followed by a plateau phase due to calcium influx, and finally repolarization through potassium efflux.

The absolute refractory period is a short period after an action potential where the cardiac muscle cannot be re-excited. It ensures coordinated contractions and prevents tetany.

An action potential travels down T tubules and triggers calcium release from the sarcoplasmic reticulum (SR). This calcium further stimulates more calcium release from SR, amplifying the signal.

The sliding filament mechanism describes how actin and myosin filaments interact, resulting in muscle contraction. Calcium ions bind to troponin, allowing myosin to bind to actin and pull, shortening the sarcomere.

Chemical messengers that transmit signals across synapses between neurons, exciting or inhibiting the postsynaptic neuron.

A neurotransmitter associated with the parasympathetic nervous system, involved in muscle contraction and memory.

A neurotransmitter associated with the sympathetic nervous system, involved in fight-or-flight responses.

A neurotransmitter that acts both in the nervous system and as a hormone, also involved in fight-or-flight responses.

A neurotransmitter associated with mood, sleep, and appetite regulation.

A major excitatory neurotransmitter in the brain, involved in learning and memory.

A major inhibitory neurotransmitter in the brain, involved in reducing anxiety and promoting sleep.

The junction between two neurons, where neurotransmitters are released to transmit signals.

Small sacs within the presynaptic neuron that contain neurotransmitters.

The small gap between the presynaptic and postsynaptic neurons, where neurotransmitters are released.

The process by which neurotransmitters are released from the presynaptic neuron, triggered by calcium influx.

Proteins on the postsynaptic neuron that bind to neurotransmitters, initiating a response.

A component of some receptors that either opens an ion channel or activates a second messenger system.

Prolonged changes in neuronal activity that can last for seconds to months, often involving G-protein coupled receptors.

A depolarizing potential caused by the influx of sodium ions into the postsynaptic neuron, making it more likely to fire an action potential.

The opiate system plays a critical role in pain suppression, especially during stressful situations. It helps reduce pain sensitivity, enhancing an organism's ability to react to emergencies like defense, predation, dominance, and adaptation to challenging environments.

Visceral pain, originating from internal organs, is often perceived as coming from a different, distant area of the skin. This happens because sensory nerves from the skin and viscera share pathways in the spinal cord.

The brain itself is not sensitive to pain. However, the membranes covering the brain, including the dura mater, blood vessels, and venous sinuses are pain-sensitive structures.

Meningitis, an inflammation of the meninges, causes severe headaches due to irritation of the pain-sensitive brain membranes.

Migraines are characterized by abnormal blood vessel activity, starting with a spasm followed by prolonged dilation. This dilation stretches the membranes covering the vessels, causing pain.

Hangover headaches are caused by the irritation of the meninges by alcohol breakdown products and additives.

Tension headaches are triggered by emotional tension, leading to muscle spasms in the neck and scalp. These spasms irritate the scalp coverings, causing pain.

Sinus headaches are caused by irritation of the nasal structures.

Eye strain headaches result from excessive contraction of the ciliary muscle in the eye, trying to focus, and contraction of facial muscles.

There are more cold receptors than warm receptors throughout the body. The density of cold receptors varies, being highest on the lips and lowest on the trunk.

Freezing cold and burning hot temperatures stimulate pain receptors, causing the same sensation.

Cold receptors respond best at 25°C, while warm receptors respond best at 44°C. The relative degree of stimulation of these receptors determines the temperature sensation.

Thermal receptors adapt to stimuli, but not completely. This means that while they become less sensitive over time, they never fully stop responding to the temperature.

The vasomotor center regulates blood vessel diameter, while the respiratory center controls breathing. They are separate, though both are located in the brainstem.