Serotonin, complex

Riboflavin was discovered by Isenberg and Szent-Gyorgyi [210] to form a complex with serotonin, colored at low temperature in solution and the solid state. Unprotonated nicotinamide adenine dinucleotide (NAD+) forms a charge-transfer complex with serotonin creatinine sulfate [211]. Douzou [212] noted that decreasing temperature caused a partially reversible increase in optical density of the NAD-serotonin complex. He claims that aggregation of the complex constituents is followed by oxidation. Serotonin complexes of pteridines are also known [1]. 

Heparin-serotonin complexation to form an entity with anticoagulant activity and lytic activity different from that of plasmin with respect to the fact that it lysed unstabilized fibrin clots in the presence of EACA has been reported.93 Evidence of a protective action of vitamin C in deep vein thrombosis has also been reported.94... 

The pharmacology of amphetamine is considerably more complex. It does not only block monoamine reuptake, but also directly inhibits the vesicular monoamine transporter, causing an increase in cytosolic but not vesicular dopamine concentration. This may lead to reverse transport of the amines via the membrane-bound transporters. Further mechanisms of amphetamine action are direct MAO inhibition and indirect release of both dopamine and serotonin in the striatum. 

The TCAs, such as amitriptyline (Elavil) and dox-epin (Sinequan), inhibit reuptake of norepinephrine or serotonin at the presynaptic neuron. Drug classified as MAOIs inhibit the activity of monoamine oxidase a complex enzyme system that is responsible for breaking down amines. This results in an increase in endogenous epinephrine, norepinephrine and serotonin in the nervous system. An increase in these neurohormones results in stimulation of the CNS. The action of the SSRIs is linked to their inhibition of CNS neuronal uptake of serotonin (a CNS neurotransmitter). The increase in serotonin levels is thought to act as a stimulant to reverse depression. 

As with the other monoamines, 5-HT is found primarily in storage vesicles (30-35 nm diameter) where serotonin-binding proteins (SBPs) have also been identified. These seem to form a macromolecular complex with 5-HT. In fact, three such proteins have now been characterised, but only one of them, 45kDa SBP, appears to be secreted into the synapse along with 5-HT. Whether they serve any role other than forming an osmotically inert storage matrix for 5-HT is unknown. 

The triptans are considered specific therapies in that they target the pathophysiology underlying migraine.33 They abort headache through beneficial effects on neuronal imbalances.11 Triptans inhibit neurotransmission in the trigeminal complex and activate serotonin lb/Id pathways that modulate nociception in the brain stem. They also decrease the release of vasoactive peptides leading to vascular reactivity and pain.34 Triptans are a welcome addition to the therapeutic armamentarium in that they are available in intranasal, subcutaneous, and oral... 

Complicated processes govern wakefulness, sleep, and the transitions leading to sleep initiation and maintenance. Although the neurophysiology of sleep is complex, certain neurotransmitters promote sleep and wakefulness in different areas of the central nervous system (CNS). Serotonin is thought to control non-REM sleep, whereas cholinergic and adrenergic transmitters mediate REM sleep. Dopamine, norepinephrine, hypocretin, substance P, and histamine all play a role in wakefulness. Perturbations of various neurotransmitters are responsible for some sleep disorders and explain why various treatment modalities are beneficial. 

The second cell-specific regulatory element within the distal enhancer is named SER. Loss of this element, which is at the extreme distal edge of the enhancer, leads to a selective loss of DDC expression in the ventral lateral serotonin cells (Johnson et al., 1989 Lundell and Hirsh, 1992) (Fig. 6C). This element has been delimited to about 40 bp and shows unexpected complexity, consisting of two functionally redundant elements. These two subelements, SERl and SERr, are each sufficient to allow normal DDC expression in the ventral lateral serotonin neurons if the other is deleted. In spite of this functional similarity, no sequence similarity is apparent between the two regions. The region of conservation between D. melanogaster and D. virilis is limited to SERl. 

Schizophrenia is a chronic, complex psychiatric disorder affecting approximately 1% of the population worldwide. The chronic nature of the illness, in addition to the early age of onset, results in direct and indirect health care expenditures in the U.S., which amount to approximately 30 to 64 billion dollars per year [4]. It is perhaps the most devastating of psychiatric disorders, with approximately 10% of patients committing suicide. The dopamine hypothesis of schizophrenia postulates that overactivity at dopaminergic synapses in the central nervous system (CNS), particularly the mesolimbic system, causes the psychotic symptoms (hallucinations and delusions) of schizophrenia. Roth and Meltzer [5] have provided a review of the literature and have concluded a role for serotonin as well in the pathophysiology and treatment of schizophrenia. The basic premise of their work stems from the known interaction between the serotonergic and dopaminergic systems. 

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