Neuromodulators: Difference between revisions
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*[[GABAA receptor]] | *[[GABAA receptor]] | ||
==[[GABA(A) receptor-associated protein]]== | ==[[GABA(A) receptor-associated protein]]== | ||
=Histamine= | |||
<scene name='82/829381/Cv/5'>Histamine</scene>. | |||
==Histamine receptors== | |||
Allergy symptoms are mostly caused by the release of histamine in response to allergens. The binding of histamine to the extracellular portion of the H1 receptor triggers a structural change of the transmembrane portion, leading to a change in the C terminal area. This c terminal region interacts with G proteins, leading to the activation of the Gq signalling pathway, which triggers allergy symptoms like itchy eyes and runny noses. Many allergy drugs are anti-histamines, in that they bind to the histamine receptor but do not cause the conformational change that leads to a response. The H1 receptor is a histamine receptor belonging to the family of rhodopsin-like G-protein-coupled receptors. The H1 receptor is linked to an intracellular G-protein (G<sub>q</sub>) that activates [[phospholipase C]] (see [[PLC beta 3 Gq|Unique bidirectional interactions of Phospholipase C beta 3 with G alpha Q]] and the inositol triphosphate (IP3) signalling pathway. When a ligand binds to a G protein-coupled receptor that is coupled to a G<sub>q</sub> heterotrimeric G protein, the α-subunit of G<sub>q</sub> can bind to and induce activity in the PLC isozyme PLC-β, which results in the cleavage of PIP2 into IP3 and DAG. | |||
*[[Histamine H1 receptor]] | |||
* [[3rze]] - human histamine H1 receptor with an antagonist doxepin. | |||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
