Pharmacodynamics

Ligand-Gated Ion Channel

TRLigand Kapılı İyon Kanalı
Also known as:Ionotropic receptor · Ligand-gated channel · Transmitter-gated ion channel

A transmembrane ion channel that opens (or, less often, closes) directly when a specific ligand, usually a neurotransmitter, binds to it, producing rapid changes in membrane potential within milliseconds.

In depth

Also called ionotropic receptors, these are multimeric proteins whose subunits surround a central pore. The main families are the pentameric Cys-loop receptors (nicotinic acetylcholine, GABA-A, glycine and 5-HT3 receptors), the tetrameric ionotropic glutamate receptors (AMPA, kainate, NMDA) and the trimeric P2X receptors. Cation-selective channels (nicotinic, 5-HT3, glutamate) are excitatory; chloride-selective channels (GABA-A, glycine) are usually inhibitory.

Drugs act on them as agonists, competitive antagonists, channel blockers or allosteric modulators: neuromuscular blockers at muscle nicotinic receptors, benzodiazepines and barbiturates at GABA-A receptors, ondansetron at 5-HT3 receptors, and ketamine and memantine at NMDA receptors.

Clinical pearl

Drugs acting on GABA-A receptors (benzodiazepines, barbiturates, propofol, alcohol) have additive or synergistic CNS and respiratory depressant effects, and the risk rises further when opioids are added.

Example drugs

Diazepam Ondansetron Rocuronium Ketamine Varenicline
TRIn Turkish

Ligand Kapılı İyon Kanalı

Belirli bir ligandın, genellikle bir nörotransmiterin, doğrudan kendisine bağlanmasıyla açılan (daha seyrek olarak kapanan) ve milisaniyeler içinde membran potansiyelinde hızlı değişiklikler oluşturan transmembran iyon kanalıdır.

İyonotropik reseptörler olarak da adlandırılan bu yapılar, alt birimleri merkezi bir poru çevreleyen multimerik proteinlerdir. Başlıca aileler pentamerik Cys-loop (sistein ilmekli) reseptörler (nikotinik asetilkolin, GABA-A, glisin ve 5-HT3 reseptörleri), tetramerik iyonotropik glutamat reseptörleri (AMPA, kainat, NMDA) ve trimerik P2X reseptörleridir. Katyon seçici kanallar (nikotinik, 5-HT3, glutamat) eksitatör, klorür seçici kanallar (GABA-A, glisin) ise genellikle inhibitördür.

İlaçlar bu kanallarda agonist, yarışmalı antagonist, kanal blokeri veya allosterik modülatör olarak etki eder: kas tipi nikotinik reseptörlerde nöromüsküler blokerler, GABA-A reseptörlerinde benzodiazepinler ve barbitüratlar, 5-HT3 reseptörlerinde ondansetron, NMDA reseptörlerinde ise ketamin ve memantin buna örnektir.

GABA-A reseptörleri üzerinden etki eden ilaçların (benzodiazepinler, barbitüratlar, propofol, alkol) SSS ve solunum depresyonu etkileri aditif veya sinerjiktir; opioid eklendiğinde risk daha da artar.

Diğer adları:İyonotropik reseptör · Ligand kapılı kanal
Updated 24.09.2026 0 views Educational reference — verify against current sources before clinical use.

Read next

ReceptorReseptör

A macromolecule, usually a protein, to which a drug or endogenous ligand binds specifically and thereby initiates a change in cell function that produces a biological response.

 G Protein-Coupled ReceptorG Proteinine Kenetli Reseptör

A member of the largest family of cell-surface receptors, a single polypeptide with seven transmembrane α-helices that transduces ligand binding into intracellular signals by activating heterotrimeric G proteins.

 Allosteric ModulatorAllosterik Modülatör

A ligand that binds to a site on a receptor distinct from the orthosteric (endogenous agonist) site and changes the receptor's affinity for, or response to, the orthosteric agonist.

 Non-Competitive AntagonismYarışmasız Antagonizma

Antagonism that cannot be overcome by increasing the agonist concentration, because the antagonist binds irreversibly or acts at a site or step distinct from agonist binding; the maximal agonist response is reduced.

 LigandLigand

Any molecule, such as a drug, hormone or neurotransmitter, that binds to a specific site on a receptor or other macromolecule; binding alone does not imply activation or blockade.

 SynergismSinerji

An interaction in which two drugs that each produce a given effect on their own cause a combined effect greater than that predicted from their individual effects under additivity.