What happens when acetylcholine is released into the neuromuscular junction?
When an action potential reaches a neuromuscular junction, it causes acetylcholine to be released into this synapse. If enough of these sodium ions enter the muscle fibre to raise it from its resting potential of -95 mV to about -50 mV, they trigger a muscular action potential that spreads throughout the fibre.
What is the function of acetylcholinesterase?
Acetylcholinesterase (AChE) is a cholinergic enzyme primarily found at postsynaptic neuromuscular junctions, especially in muscles and nerves. It immediately breaks down or hydrolyzes acetylcholine (ACh), a naturally occurring neurotransmitter, into acetic acid and choline.
Is curare an agonist?
Receptor agonists and antagonists ACh, the native compound, binds to both nicotinic and muscarinic receptors. Carbechol is a muscarinic receptor agonist. Curare is a nicotinic receptor antagonist.
Where does curare act at the neuromuscular junction?
In modern medicine, curare is classified as a neuromuscular blocking agent—it produces flaccidity in skeletal muscle by competing with the neurotransmitter acetylcholine at the neuromuscular junction (the site of chemical communication between a nerve fibre and a muscle cell).
How does a muscle contraction occur?
Muscle contraction occurs when the thin actin and thick myosin filaments slide past each other. It is generally assumed that this process is driven by cross-bridges which extend from the myosin filaments and cyclically interact with the actin filaments as ATP is hydrolysed.
What is the correct order of events in the sliding filament theory of muscle contraction?
The correct order is: 6) Sarcoplasmic reticulum releases calcium ions, 2) Calcium ions bind to troponin, 5) Tropomyosin moves to expose active sites of actin, 4) ATP is split into ADP and P, 1) Myosin head binds to actin, 7) ADP and P released from myosin, 3) Myosin cross-bridges bend, pulling actin toward center of …
What are two regulatory proteins found in a Myofibril?
Tropomyosin and troponin are two main proteins that regulate muscle contraction and relaxation (Choi and Kim, 2009; Zot and Potter, 1987). They prevent the activation of actomyosin ATPase in the absence of calcium ions by interacting with actin filaments to block the myosin binding site.