Topics:
GABAA-Rs and Cys-loop superfamily of ligand-gated ion channels
Glutamate receptors and anesthethics
Controversis on potassium channels (They ca be modulated by halothane, but they are insensitive to clinically relevant concentrations of intravenous anesthetics, like propofol)
Hyperpolarization-activated cyclic nucleotide-gated (HCN): a family of channels that increases pacemaker currents with rhythmic or oscillatory activity, regulating the dendritic excitability and the neuronal response to synaptic input.
Voltage-gated Na+ and Ca2+ channels, critical to excitability and synaptic transmission.
G-protein-coupled receptor (GPCR) signaling: there is evidence that Metabotropic glutamate receptors carry transmembrane segments similar to other G-protein coupled receptors. These ligand-receptors are possible targets for anesthetics, because some anesthetics inhibit the functions of Gq-coupled receptors, including muscarinic acetylcholine M1, metabotropic type 5 glutamate, 5-hydroxytryptamine 2A, and substance P receptors.
Interference of external (i.e., BZDs) and endogenous factors. For example, GABAA-R subunits are subject to the action of different ligands, like kinases, structural proteins, and neurosteroids which are the principal endogenous modulators of GABAA-Rs.
Different anesthetics induce different patterns of brain activity: for instance ketamine and Xenon
The possible activation of different neuronal circuits by different anesthetics during different phases of narcosis.
In summary, I wrote about 70%.
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