At autonomic ganglia and after post ganlionic parasympathetic fibres. With few exceptions
ACh (acetylcholine) binds to receptors at the NMJ (neuromuscular junction) to induce contraction of muscle.
Acetylcholine (ACh) receptors are primarily found in the neuromuscular junctions of skeletal muscles, where they play a crucial role in muscle contraction by responding to the neurotransmitter acetylcholine. Additionally, ACh receptors are present in the central and peripheral nervous systems, where they mediate various functions including cognition, memory, and autonomic nervous system responses. There are two main types of ACh receptors: nicotinic receptors, which are ionotropic and found at neuromuscular junctions and autonomic ganglia, and muscarinic receptors, which are metabotropic and found in various tissues including the heart and glands.
A deficiency of ACh receptors in a motor end plate would cause muscle weakness or paralysis. This condition is called myasthenia gravis.
Acetylcholine (ACh) is released from the presynaptic neuron into the synaptic cleft. It then binds to ACh receptors on the postsynaptic neuron, causing ion channels to open and allowing for the transmission of the nerve impulse. Any remaining ACh is broken down by the enzyme acetylcholinesterase, ensuring that the signal is quickly terminated.
When acetylcholine (ACh) receptors open, sodium ions (Na+) primarily flow into the postsynaptic membrane. This influx of positively charged sodium ions leads to depolarization, making the inside of the cell more positive. If the depolarization reaches a certain threshold, it can trigger an action potential in the postsynaptic neuron.
Nicotinic ACh receptors are ionotropic receptors that mediate fast neurotransmission, while muscarinic ACh receptors are metabotropic receptors that modulate cell signaling through G-proteins. Nicotinic receptors are typically found at neuromuscular junctions and in the central nervous system, whereas muscarinic receptors are more widely distributed in peripheral tissues and the brain.
ACh (acetylcholine) binds to receptors at the NMJ (neuromuscular junction) to induce contraction of muscle.
Acetylcholine (ACh) receptors are primarily found in the neuromuscular junctions of skeletal muscles, where they play a crucial role in muscle contraction by responding to the neurotransmitter acetylcholine. Additionally, ACh receptors are present in the central and peripheral nervous systems, where they mediate various functions including cognition, memory, and autonomic nervous system responses. There are two main types of ACh receptors: nicotinic receptors, which are ionotropic and found at neuromuscular junctions and autonomic ganglia, and muscarinic receptors, which are metabotropic and found in various tissues including the heart and glands.
AChE destroys the ACh and they are removed from the membrane receptors.
ACh esterase, which breaks ACh down into an acetyl group and a choline group. This is then taken up by the neurone and some is reformed into ACh.
Neostigmine is a competitive irreversible inhibitor of Acetylcholinesterase (AChE), an enzyme responsible for breaking down acetylcholine (ACh). Myasthenia gravis is caused by the body producing too little ACh receptors. As stimulating the ACh receptors is needed for nervous transmission, the nerve signals cannot be transmitted causing muscle weakness and fatigue. Neostigmine is hence used to inhibit AChE so that less ACh gets broken down. This leads to more ACh binding to the ACh receptors causing muscular contraction.
ACH receptors can be defined as an integral membrane protein that responds to the binding of acetylcholine, a neuoyansmitter. Two example are nicotinic acetyl line receptors and muscarinic acetylcholine receptors. .
they stimulate the action of ACh at post ganglionic muscarinic receptors.
A deficiency of ACh receptors in a motor end plate would cause muscle weakness or paralysis. This condition is called myasthenia gravis.
Competes with ACh at the nerve receptors and results in under stimulatin of the receptors.
It doesn't atropine only acts on muscarinic receptors (it's a competitive antagonist here for ACh), but histamine acts on different receptors (histamine receptors). There is no direct interaction between atropine and histamine receptors
Preganglionic fibers for the SNS release ACh; so a drug that stimulates ACh receptors would stimulate the postganglionic fibers of sypathetic nerves, resulting in increased sympathetic activity