Kolinergisten

Kolinergisten (the cholinergic system) refers to the network of neurons, receptors, and signaling processes that use acetylcholine (ACh) as their neurotransmitter. It includes cholinergic neurons in the central and peripheral nervous systems and the two main classes of acetylcholine receptors: nicotinic and muscarinic. The system is essential for a wide range of physiological and cognitive functions.

Acetylcholine is synthesized in the presynaptic terminal from choline and acetyl-CoA by the enzyme choline acetyltransferase (ChAT). It is stored in synaptic vesicles and released in response to calcium influx after nerve stimulation. Once released, ACh is rapidly hydrolyzed by acetylcholinesterase (AChE) or butyrylcholinesterase into choline and acetate; choline is reclaimed by the presynaptic neuron via the high-affinity choline transporter for reuse.

Receptors in the kolinergisten include nicotinic acetylcholine receptors (nAChRs), which are ion channels located at the neuromuscular junction and in autonomic ganglia, and muscarinic acetylcholine receptors (mAChRs), which are G protein-coupled receptors distributed widely in tissues such as the heart, smooth muscle, glands, and various brain regions. The cholinergic system modulates attention, learning, memory, arousal, and autonomic functions.

Physiological roles: In the peripheral nervous system, muscarinic activation slows heart rate, increases gastrointestinal motility, and causes pupil constriction; nicotinic receptors mediate skeletal muscle contraction and transmit signals in autonomic ganglia. In the central nervous system, cholinergic pathways contribute to cognitive processes and behavioral regulation.

Clinical relevance: Disturbances in cholinergic signaling are linked to several disorders. Myasthenia gravis involves impaired nicotinic transmission at the neuromuscular junction; Alzheimer’s disease features loss of central cholinergic neurons. Cholinesterase inhibitors (e.g., donepezil, rivastigmine) enhance cholinergic signaling and are used in treatment, while organophosphate poisoning inhibits AChE, causing a cholinergic crisis. Therapies also target muscarinic or nicotinic receptors in various conditions.