Kolinergiske

Kolinergiske refers to nerve pathways, receptors, and signals that use acetylkolin (ACh) as the neurotransmitter. The kolinergic system includes both peripheral and central components and plays a key role in motor control, autonomic function, and cognition.

Key components and actions

Acetylkolin is synthesized in presynaptic nerve terminals by the enzyme choline acetyltransferase from choline and acetyl-CoA, stored in synaptic vesicles, and released into the synaptic cleft upon nerve stimulation. It is rapidly inactivated by acetylcholinesterase, which splits it into choline and acetate; choline is recycled for new ACh synthesis. Kolinergic signaling operates through two main receptor families: nicotinic receptors (Nm at the neuromuscular junction, Nn in autonomic ganglia and CNS) and muscarinic receptors (M1–M5) found throughout the CNS and various organs.

Physiological roles

In the peripheral nervous system, kolinergic transmission enables skeletal muscle contraction at the neuromuscular junction and mediates parasympathetic activity in organs such as the heart, gut, and glands. In the brain, cholinergic neurons, especially those originating from the basal forebrain, influence learning, memory, attention, and arousal.

Clinical relevance

Disorders and treatments linked to the kolinergic system include myasthenia gravis (autoantibodies against nicotinic receptors, treated with acetylcholinesterase inhibitors), and Alzheimer’s disease (degeneration of cholinergic neurons; symptomatic treatment with acetylcholinesterase inhibitors such as donepezil, rivastigmine, galantamine). Organophosphate poisoning inhibits acetylcholinesterase, causing widespread excess ACh and requiring atropine and antidotes. Anticholinergic drugs (e.g., atropine, scopolamine) block muscarinic receptors, while nicotinic agents like nicotine have limited therapeutic use. Pilocarpine and bethanechol are muscarinic agonists used in specific clinical contexts.