Dopamine stability

Atypical antipsychotic (benzamide possibly a dopamine stabilizer and dopamine partial agonist)... 

Mediates its atypical antipsychotic properties via novel actions on dopamine receptors, perhaps dopamine stabilizing partial agonist actions on dopamine 2 receptors... 

Dopamine partial agonist (dopamine stabilizer, atypical antipsychotic, third generation antipsychotic sometimes included as a second generation antipsychotic also a mood stabilizer)... 

Important products derived from amino acids include heme, purines, pyrimidines, hormones, neurotransmitters, and biologically active peptides. In addition, many proteins contain amino acids that have been modified for a specific function such as binding calcium or as intermediates that serve to stabilize proteins—generally structural proteins—by subsequent covalent cross-hnk-ing. The amino acid residues in those proteins serve as precursors for these modified residues. Small peptides or peptide-like molecules not synthesized on ribosomes fulfill specific functions in cells. Histamine plays a central role in many allergic reactions. Neurotransmitters derived from amino acids include y-aminobutyrate, 5-hydroxytryptamine (serotonin), dopamine, norepinephrine, and epinephrine. Many drugs used to treat neurologic and psychiatric conditions affect the metabolism of these neurotransmitters. 

Excellent biological arguments exist for a direct impact of fever specifically on neurological outcome. On a local level, fever produces increased levels of excitatory amino acids (e.g., glutamate and dopamine), free radicals, lactic acid, and pyr-uvate. There is an increase in cell depolarizations and BBB breakdown. Enzymatic function is impaired and cytoskeletal stability reduced. These events lead to increased cerebral edema, with a possible reduction in CPP as well as larger volumes of ischemic injury. " ... 

The oxidation of N ADH has been mediated with chemically modified electrodes whose surface contains synthetic electron transfer mediators. The reduced form of the mediator is detected as it is recycled electrochemically. Systems based on quinones 173-175) dopamine chloranil 3-P-napthoyl-Nile Blue phenazine metho-sulphatemeldola blue and similar phenoxazineshave been described. Conducting salt electrodes consisting of the radical salt of 7,7,8,8-trtra-cyanoquinodimethane and the N-methylphenazium ion have been reported to show catalytic effects The main drawback to this approach is the limited stability... 

Tamminga, C. A. and Carlsson, A. Partial dopamine agonists and dopaminergic stabilizers, in the treatment of psychosis. Curr. Drug Targets CNS Neurol. Disord. 2 141-147, 2002. 

There is evidence for the contribution of serotonin dysfunction to mania, and in the mechanism of action of mood stabilizers [19], however, specific data on the serotonergic system and mania are fewer and variable. Moreover, altered functioning of other neurotransmitters in mania such as norepinephrine, dopamine, acetylcholine, and GABA, and their interaction with serotonin, are also likely to be involved in the pathogenesis of mood disorders. Differences in these neurotransmitter systems possibly underlie differences in the pathogenesis of depressive and manic episodes. 

If we dehne a mood stabilizer as a medication that is both an effective anti-manic and antidepressant, then lithium arguably remains to this day the prototypical mood stabilizer. Lithium not only reduces the symptoms of acute BPAD, it also prevents the recurrence of additional mood episodes. Despite the fact that lithium has revolutionized the treatment of BPAD and remains nearly 50 years after its introduction as the single best treatment for many patients with BPAD, there is still no consensus as to how it works. Lithium exerts effects on several neurotransmitter systems (e.g., serotonin, dopamine, norepinephrine, acetylcholine), on second messenger systems inside the nerve cell, and on nerve cell gene expression. Yet, precisely how these varied effects produce lithium s therapeutic benefit remains unclear. 

The oxidation of dopamine by ceruloplasmin yielded a free radical with a very short lifetime, characterized by an EPR signal at g = 2.006 Dimethyl-p-phenylenediamine was oxidized faster by the enzyme to the free radical Wurster s red, which was further oxidized by the enzyme in another one-electron step. The free radical seemed, moreover, to be stabilized by ceruloplasmin... 

The autoxidation of ascorbate, a cosubstrate of dopamine P-monooxygenase, induces the degradation of most proteins including catalase and dopamine p-monooxygenase, but with the exception of (Cu,Zn)-SOD. Catalase protects dopamine P-monooxy-genase and is therefore generally added in the assay systems . The apparent activation or rather the stabilization of the enzyme (6.5 pg) by small amounts of catalase (3.1 pg) was enhanced by native but not by boiled SOD (100 pg) and also by similar amounts of serumalbumin (100 pg) or of boiled catalase (65 pg)... 

Although the hydrolytic stability of some phosphazene polymer makes them attractive as structural materials, it is possible to create hydrolytically sensitive phosphazenes that may be useful medically as slow-rdease drugs. Steroids, antibiotics. and catecholamines (e.g., dopamine and epinephrine) have been linked to a polyphosphazene skeleton (Fig. 16.27) with the intention that slow hydrolysis would provide these drugs in a therapeutic steady state. 

Electrochemical binding assays have also been applied for testing computational predictions which render the highest stabilization energy for the pre-polymerization mixture of several formulations traditionally used in non-covalent MIPs [119]. The batch binding assays and voltammetric detection confirm the theoretically best monomer-porogen solvent mixture for preparation of a recognition material for the dopamine metabolite homovanillic acid. 

Thickness of the barrier layer, optimized at 220 nm [133], played a crucial role with respect to the chemosensor sensitivity, selectivity and LOD. So, eventually, the chemosensor architecture comprised a gold-film electrode, sputtered onto a 10-MHz resonator, coated with the poly(bithiophene) barrier layer, which was then overlaid with the MIP film. This architecture enabled selective determination of the amine at the nanomole concentration level. LOD for histamine was 5 nM and the determined stability constant of the MIP-histamine complex, XMn> = 57.0 M 1 [131], compared well with the values obtained with other methods [53, 136, 137]. Moreover, due to the adopted architecture, the dopamine chemosensor could determine this amine with the stability constant for the MIP-dopamine complex, XMip = (44.6 4.0) x 106 M-1 and LOD of 5 nM [133], which is as low as that reached by electroanalytical techniques [138]. The MIP-QCM chemosensor for adenine [132] also featured low, namely 5 nM, LOD and the stability constant determined for the MIP-adenine complex, XMIP = (18 2.4) x 104 M, was as high as that of the MIP-adenine complex prepared by thermo-induced co-polymer-ization [139]. The linear concentration range for determination of these amines extended to at least 100 mM. 

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