Achinduced

AChinduced is a term used to describe physiological, electrophysiological, or pharmacological responses that are elicited by acetylcholine (ACh) binding to cholinergic receptors. The label is often applied to describe effects such as ACh-induced currents, potentials, or changes in excitability observed in neurons, muscle, or other tissues following ACh exposure.

The primary receptor families mediating ACh-induced responses are nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels, and muscarinic acetylcholine receptors (mAChRs), which are G protein–coupled receptors. ACh-induced effects vary with receptor subtype and cellular context. At the neuromuscular junction, ACh-induced end-plate potentials result from Na+/K+ influx through nAChRs, leading to muscle contraction. In the heart, ACh-induced responses via mAChRs typically slow heart rate and decrease conduction. In the central nervous system, ACh-induced signaling modulates arousal, attention, and learning through cholinergic pathways.

Mechanistically, ACh binding to nAChRs opens ion channels and causes rapid depolarization, while binding to mAChRs triggers diverse intracellular cascades that can influence ion channels, enzyme activity, and second messenger systems. The duration and magnitude of ACh-induced effects are regulated by acetylcholinesterase, which rapidly hydrolyzes ACh in synaptic spaces.

Pharmacologically, ACh-induced responses can be augmented by acetylcholinesterase inhibitors and blocked by receptor antagonists such as atropine (M receptor antagonist) or curare (nAChR antagonist at skeletal muscle). Clinically, dysregulation of cholinergic signaling underlies conditions like myasthenia gravis and certain dementias, making ACh-induced processes a central focus of research and therapy.