By Tahira Farooqui, Akhlaq A. Farooqui
Biogenic amines are evidently taking place amines which are derived via enzymic decarboxylation of the average amino acids. They belong to a category of neurotransmitters together with catecholamines (dopamine, norepinephrine, and epinephrine), indolamine (serotonin), and imidazoleamine (histamine). Biogenic amines have nice pharmacological and physiological value. the most target of this publication is to give readers with finished details on pharmacology, neurochemistry and molecular neurobiology of biogenic amine within the CNS of vertebrate and invertebrates in one quantity textual content. The e-book has been organised into chapters and sections to supply a greater stream of data. additionally, this precise quantity presents its readers with innovative info on biogenic amines. it may be utilized by graduate scholars, postdoctoral fellows, researchers, and scientists who paintings on the pharmaceutical as a instruction manual, which describes all elements of biogenic amine metabolism.
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Extra resources for Biogenic Amines: Pharmacological, Neurochemical and Molecular Aspects in the CNS
ABSTRACT Aromatic L-amino acid decarboxylase (AAAD) is a required enzyme for the formation of catecholamines, indolamines and trace amines. AAAD gene and protein analyses have provided evidence for enzyme activity regulation at the transcriptional and post-translational levels. Extensive studies in neuronal tissues have demonstrated that AAAD activity is regulated by activation and induction, protein phosphorylation and gene transcription. A number of neurotransmitter receptors including dopamine (D1-4), glutamate (NMDA), serotonin (5-HT1A, 5-HT2A) and nicotinic acetylcholine receptors regulate AAAD activity in the rodent brain.
The surprise result was that the double mutant did display the cholinergic phenotype in spite of not having produced norepinephrine earlier. Thus in spite of having developed the cholinergic phenotype, no sweating occurred. That was contrary to the prediction . The pigmented TH-nulls showed another result. Unlike their albino counterparts, they did sweat and they did also acquire the cholinergic phenotype. Thus the fraction of the normal quantity of norepinephrine (that was about 20% of wild-type levels) made by the mutant‘s sympathetic innervation of the sweat gland functioned to permit sweating in the mouse in response to pilocarpine .
In striatum, kinetic activation of AAAD is rapid, short-lasting and characterized by changes in the apparent Vmax for both the substrate and the cofactor pyridoxal-5‘-phosphate, suggesting partial phosphorylation of the enzyme . Indeed, phosphorylation appears to play a role in the activation of the enzyme in vivo. Injection of either forskolin  or phorbol-12,13-myristic acid (PMA)  icv increases the activity of AAAD in striatum, a response that can be blocked by selective inhibitors of PKA or PKC.