Words similar to ligand-gated
Example sentences for: ligand-gated
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The nicotinic acetylcholine receptor (nAChR) is a ligand-gated ion channel that mediates neurotransmission at the neuromuscular junction, autonomic ganglia and at some sites in the central nervous system.
ATP functions as a neurotransmitter in the central nervous system [ 1 2 3 ] . Synaptically released ATP acts on a class of ligand-gated ion channels called P2X [ 4 5 6 7 ] . While the dynamics of these channels have been studied [ 8 9 ] , a common assumption is that the channels are independent.
Distinct nAChR subtypes exist that can be stimulated by the neurotransmitter acetylcholine, the natural product nicotine, or by synthetic compounds [ 1 ] . nAChR is the prototype for a protein superfamily that includes the receptors for the excitatory amino acids glutamate and aspartate, the inhibitory amino-acids gamma-aminobutyric acid (GABA) and glycine, as well as the serotonin 5-HT 3 receptor [ 1 ] . Like most ligand-gated ion channels, nAChRs are homo- or hetero-pentameric, each monomer belonging to a pull of 8 alpha- or 3 beta-subunits (alpha 2-9 , beta 2-4 ). While each subunit has four transmembrane domains, the agonist binding sites are located at the subunit interfaces [ 2 ] . Both natural and synthetic ligands can display varied affinity for different receptor subtypes.
In some ligand-gated ion channels, such as ACh receptors, the agonist not only activates the receptors, but also blocks the pore as well [ 25 26 ] . In order to test if ATP blocks the P2X 2 receptors and affects open channel noise, we recorded single channel currents activated by different concentrations of ATP.
Several of these changes are maladaptive in the sense that they contribute to the generation of the abnormal sensations that constitute neuropathic pain, by producing ectopic spontaneous activity into the CNS, altering synaptic drive, increasing excitability and diminishing inhibitory action in the dorsal horn of the spinal cord, and by making novel synaptic contacts with inappropriate neurons [ 1 4 ] . A number of the injury-regulated genes we describe here may contribute directly to this altered sensory processing; CB1 receptor, VGF, the phospholemman ion channel, SNAP25 A, endothelin-1 and the ligand-gated 5-HT3 receptor (Table 4, see additional file 3).
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