Ligand-Gated Ion Channels Library
ChemDiv’s Ligand-Gated Ion Channels Library contains 4,000 compounds.
Ligand-gated ion channels (LGICs) mediate intercellular communication by converting the binding of a neurotransmitter that is released from the presynaptic terminal into an ion flux in the postsynaptic membrane. They are integral membrane proteins that carry an orthosteric-binding site for the neurotransmitter and an ion channel that spans the membrane. Under resting conditions, the channel is closed, and binding of the agonist triggers a conformational change that opens the gate. Once the channel is opened, cations or anions diffuse through the pore at rates approaching tens to hundreds of millions of ions per second. In addition to their well-established role in neurotransmission, it is now recognized that some LGICs are critical in nonexcitable cells, such as endothelial cells, suggestive of a wider functional role of these receptors outside the peripheral and central nervous system. LGICs thus represent attractive targets for new therapeutic agents.
LGICs have been shown to be involved in several diseases including neurodegenerative disorders. Among those are Alzheimer’s Disease and Parkinson’s Disease, as well as with epilepsy, hyperekplexia, and neuropathic pain because they are characterized by major LGIC dysfunctions. [1]
[1] D. Lemoine, R. Jiang, A. Taly, T. Chataigneau, A. Specht, and T. Grutter, “Ligand-gated ion channels: New insights into neurological disorders and ligand recognition,” Chem. Rev., vol. 112, no. 12, pp. 6285–6318, 2012, doi: 10.1021/cr3000829.
Ligand-gated ion channels (LGICs) mediate intercellular communication by converting the binding of a neurotransmitter that is released from the presynaptic terminal into an ion flux in the postsynaptic membrane. They are integral membrane proteins that carry an orthosteric-binding site for the neurotransmitter and an ion channel that spans the membrane. Under resting conditions, the channel is closed, and binding of the agonist triggers a conformational change that opens the gate. Once the channel is opened, cations or anions diffuse through the pore at rates approaching tens to hundreds of millions of ions per second. In addition to their well-established role in neurotransmission, it is now recognized that some LGICs are critical in nonexcitable cells, such as endothelial cells, suggestive of a wider functional role of these receptors outside the peripheral and central nervous system. LGICs thus represent attractive targets for new therapeutic agents.
LGICs have been shown to be involved in several diseases including neurodegenerative disorders. Among those are Alzheimer’s Disease and Parkinson’s Disease, as well as with epilepsy, hyperekplexia, and neuropathic pain because they are characterized by major LGIC dysfunctions. [1]
[1] D. Lemoine, R. Jiang, A. Taly, T. Chataigneau, A. Specht, and T. Grutter, “Ligand-gated ion channels: New insights into neurological disorders and ligand recognition,” Chem. Rev., vol. 112, no. 12, pp. 6285–6318, 2012, doi: 10.1021/cr3000829.