Histamine Receptors
The histamine receptors are classified into H1, H2, H3, and H4 type G protein receptors, or GPCR.
Type H1 receptor(αq) activates PLA2 and causes inflammatory responses. The receptor activates PLA2 which activates cyclooxygenases, 12-lipoxygenase, and 5-lipoxygenase. NE, 5HT, NMDA, FMRFamide(Ca2+ mediated) hydrolyzes IP and release FA including arachidonic acid. The eicosanoids mediate a form of presynaptic inhibition by the peptide FMRFamide in Aplysia through direct activation of a K+ channel. The arachidonic acid is converted to prostaglandins(PG) by cyclooxygenases, and to 12-HPETE(OH-peroxy-eicosa-tetra-enoic acids) and 5-HPETE by 12-lipoxygenase, 5-lipoxygenase, and cytchrome P450 heme containing complex. The 5-HPETE is converted to leukotriens. The eicosanoids are amphiphilic and diffusable, and act as second messengers as retrograde messengers as NO. Antagonist: ramitidine.
The type H2 receptors (αs) activate adenylate cyclase (AC) and stimulates gastric acid secretion. Antagonist: diphenhydramine.
Type H3 receptors (αi) produce the inhibitory presynaptic IPSP's by inhibiting AC. The H3 receptors are synthesized at locus ceruleus, tuberomammiliary nuclei, and are especially abundant in the thalamus and caudate nucleus. Antagonist: thioperamide, clobenpropit. Agonist: R-α-methyl-histamine.
