acetylcholineinduced

Acetylcholine-induced refers to any physiological or pharmacological effect that results from the action of acetylcholine (ACh), the principal neurotransmitter of cholinergic neurons in both the central and peripheral nervous systems. The phrase describes receptor-mediated responses following ACh release at synapses or neuromuscular junctions, as well as endogenous or experimental administration of acetylcholine.

Mechanisms involve two major receptor families: nicotinic acetylcholine receptors (nAChRs), ligand-gated ion channels, and muscarinic acetylcholine receptors (mAChRs), which are G protein-coupled receptors with five subtypes (M1–M5). Activation of nAChRs typically produces rapid depolarization; at the neuromuscular junction this leads to muscle fiber contraction. Activation of neuronal nAChRs in the CNS modulates neurotransmitter release and neuronal excitability. Activation of mAChRs regulates many autonomic and CNS functions, with M2 in the heart reducing heart rate, M3 governing smooth muscle contraction and glandular secretion, and other subtypes influencing cognition and memory.

Physiological relevance: In the periphery, ACh-induced effects include skeletal muscle contraction, bronchoconstriction, salivation, and pupillary constriction. In the heart, ACh-induced bradycardia. In the brain, ACh-induced modulation of attention, learning, and synaptic plasticity.

Synthesis and termination: In cholinergic neurons, choline acetyltransferase catalyzes synthesis of ACh from choline and acetyl-CoA. ACh is stored in synaptic vesicles, released in response to action potentials, and rapidly broken down by acetylcholinesterase into choline and acetate. Choline is reuptaken for reuse.

Clinical and experimental context: Ach-induced responses are exploited in pharmacology to study receptor subtypes and signal transduction; cholinergic agonists mimic ACh, while anticholinergic drugs block ACh effects. Acetylcholinesterase inhibitors elevate ACh levels and can produce acetylcholine-induced overstimulation, with therapeutic uses and toxic risks depending on exposure.