Serotonin levels

Also called adrenaline a hormone secreted by the adrenal gland that prepares the organism for "flight or fight.") (A hormone synthesized in the pineal gland. Certain mental disorders are believed to be related to serotonin levels in the brain.)... 

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. 

Gobert, A, Rivet, JM, Cistarelli, L, Melon, C and Millan, MJ (1997) Alpha2-adrenergic receptor blockade markedly potentiates duloxetine- and fluoxetine-induced increases in noradrenaline, dopamine and serotonin levels in the frontal cortex of freely moving rats. J. Neurochem. 69 2616-2619. 

Weiss, JM, Goodman, PA, Lostito, BG, Corrigan, S, Charry, JM and Bailey, WH (1981) Behavioral depression produced by an uncontrollable stressor relationship to norepinephrine, dopamine and serotonin levels in various regions of rat brain. Brain Res. Rev. 3 167-205. 

In contrast, following a treatment regimen of 20 mg/kg MDMA, there were no significant differences in the density of [3H]mazindol-labeled norepinephrine (NE) uptake sites (fmol/mg protein) in the frontal cerebral cortex between saline-treated (159 17) and MDMA-treated (152 5) animals. With respect to the dose of MDMA, serotonin levels appeared to be more readily decreased (45 percent reduction at 5 mg/kg), while comparable reductions in 5-HlAA levels and serotonin uptake sites were noted only at 10 or 20 mg/kg MDMA. This apparent discrepancy among the three serotonergic markers measured in the present study may relate to effects of lower doses of MDMA on synthetic enzyme activity (i.e., TPH), whereas the effects of higher doses of MDMA in reducing all three markers may relate in part to effects on TPH activity and in part to destruction of serotonin neurons as evidenced by decreases in serotonin uptake sites. 

It is also possible that axonal regeneration and collateral sprouting arc associated with considerably greater densities of uptake sites per neuron, thereby making it more difficult to assess neuronal recovery from this index. The fact that serotonin levels remain 40 to 50 percent below age-matched controls for up to 1 year in spite of normal levels of serotonin uptake sites indicates that, following lesion by MDMA, the serotonin... 

Fuller, R.W. Hines, C.W. and Mills, J. Lowering of brain serotonin level by chloroamphetamines. Biochem Pharmacol 14 483-488, 1965. 

Galantamine is a ChE inhibitor, which elevates acetylcholine in the cerebral cortex by slowing the degradation of acetylcholine.37 It also modulates the nicotinic acetylcholine receptors to increase acetylcholine from surviving presynaptic nerve terminals. In addition, it may increase glutamate and serotonin levels. The clinical benefit of action of these additional neurotransmitters is unknown. 

Against this backdrop, researchers reported evidence that iproniazid, the antitubercular drug that was to become the first antidepressant, might increase norepinephrine and serotonin levels in the brain. How did it have this effect Recall that some of the neurotransmitter molecules released by a neuron are destroyed by enzymes in the synaptic cleft between the sending presynaptic neuron and the receiving postsynaptic neuron. When the neurotransmitter is a monoamine - like norepinephrine and serotonin - this process is called monoamine oxidase (MAO). As early as 1952 researchers at the Northwestern University Medical School in Chicago reported that iproniazid inhibited the oxidation of monoamines. This meant that iproniazid was a... 

There are a few substances that can reduce serotonin, norepinephrine and/or dopamine rapidly and substantially, reducing them to levels thought to be lower than those of depressed patients.23 That is what reserpine was supposed to do and, as we have seen, it did not cause depression - despite the early clinical impression that it did. Other substances have been used in later studies, the most common of which are amino-acid mixtures that lack the essential amino acids needed by the body to produce these neurotransmitters. For example, having people drink a beverage that is rich in amino acids, but does not contain tryptophan (the amino acid needed to produce serotonin), lowers their serotonin levels within a couple of hours. 

Different types of antidepressants are supposed to work by different means. SSRIs (selective serotonin reuptake inhibitors) are supposed to increase serotonin levels. NDRIs (norepinephrine dopamine reuptake inhibitors) are supposed to increase norepinephrine and dopamine, rather than serotonin. These two types of antidepressants are supposed to be selective , affecting the... 

The risk of potentially serious side effects should be enough to preclude the prescription of antidepressants for their placebo benefit, but this is not the only hazard associated with these medications. On 19 July 2006 the FDA issued a public-health advisory warning that, when taken in conjunction with other drugs that can affect serotonin levels, antidepressants can induce a life-threatening disorder called the serotonin syndrome .5 The serotonin syndrome is caused by an excess of serotonin in a person s body. 

Inhibition of monoamine oxidase has been proposed as a possible mechanism underlying the hydrogen sulfide-mediated disruption of neurotransmission in brain stem nuclei controlling respiration (Warenycia et al. 1989a). Administration of sodium hydrosulfide, an alkali salt of hydrogen sulfide, has been shown to increase brain catecholamine and serotonin levels in rats. It has also been suggested that persulfide formation resulting from sulfide interaction with tissue cystine and cystinyl peptides may underlie some... 

Wilkinson, L. O., Auerbach, S. B. Jacobs, B. L. (1991). Extracellular serotonin levels change with behavioral state but not with pyrogen-induced hyperthermia. 

Hall, F.S., Devries, A.C., Fong, G.W., Huang, S., and Pert, A., Effects of 5,7-dihydroxytryptamine depletion of tissue serotonin levels on extracellular serotonin in the striatum assessed with in vivo microdialysis relationship to behavior, Synapse 33(1), 16-25, 1999. 

BMS-505130 (7) is a potent and selective serotonin transporter inhibitor (SERT K< = 0.18 nM, NET K< — 4.6 gM, DAT K< — 2.1 (tM). In brain microdialysis studies, 7 demonstrated a dose-dependent increase in cortical serotonin levels. Compound 7 was also active in the mouse tail suspension model [15]. Following oral administration, peak plasma concentration of 7 was reached at 1.6 h and then declined to a concentration less than 10% of Cmax within 6 h. The short half-life of 7 might be advantageous for the treatment of PE where an acute effect to delay ejaculation followed by a relatively rapid fall in SSRI plasma concentration might be desirable. 

Miller PE, Fink GB. 1973. Brain serotonin level and pentylenetetrazol seizure threshold in dieldrin and endrin treated mice. Proc West Pharmacol Soc 16 195-197. 

Serotonin reuptake channel (reduces synaptic serotonin levels)... 

Caffeine increases extracellular serotonin levels in the hippocampus (Okada et al. 1999). Enhanced release of dopamine and norepinephrine occurs at higher doses (Morgan and Vestal 1989). An inhibition of monoamine reuptake occurs, but only in the millimolar range, which would not matter at normal oral doses (Reith et al. 1987). 

Lumb AB. (1994). Effect of dried ginger on human platelet function. Thromb Haemost. 71(1) 110-1. Maione S, Palazzo E, Pallotta M, Leyva J, Berrino L, Rossi F. (1997). Effects of imipramine on raphe nuclei and prefrontal cortex extracellular serotonin levels in the rat. Psychopharmacology (Berlin). 134(4) 401-5. 

Role of extracellular serotonin levels in the effect of 5-HTlB receptor blockade. Psychopharmacology (Berl) 167(2) 153-158. 

Many commonly used medications also contain substances that are eliminated by the MAOIs and must not be taken by these patients. The list of medications to be avoided inclndes the narcotic pain reliever meperidine (Demerol), and many over-the-connter cold remedies containing dextromethorphan or pseudoephedrine. Finally, patients taking MAOIs must also avoid medications that elevate serotonin levels. This inclndes certain appetite snppressants and antidepressants including the SSRIs, venlafaxine, duloxetine, mirtazapine, nefazodone, and trazodone. Medications that interact with the MAOIs cannot be taken until at least 2 weeks after the MAOI has been stopped. 

Serotonin syndrome Some TCAs inhibit neuronal reuptake of serotonin and can increase synaptic serotonin levels (eg, clomipramine, amitriptyline). Either therapeutic or excessive doses of these drugs, in combination with other drugs that also increase synaptic serotonin levels (such as MAOIs), can cause a serotonin syndrome consisting of tremor, agitation, delirium, rigidity, myoclonus, hyperthermia, and obtundation. 

All drugs inducing a constantly increased serotonin level may induce pulmonary hypertension on the basis of a hypertrophic smooth muscle layer of small pulmonary arteries. 

Dopaminergic activity. Smoke was administered intranasally to mice for 20 minutes twice daily for 3 days before methamphet-amine treatment. The treatment significantly attenuated the neurotoxicity as judged by a lesser depletion of dopamine, dihydrophenylacetic acid, and homovanillic acid. The lesser effect of methamphetamine on the content of serotonin level was unaltered by prior inhalation of smoke h Tobacco glycoside, administered to mice, increased behavior via dopamine 2 neuronal activity but not dopamine 1 activity in a dose-dependent manner. The results indicated that smoking can affect the human brain function via not only the nicotinic cholinergic neuron but also the dopamine 2 neuron . 

I remember pondering questions of self the first time I read Peter Kramer s book Listening to Prozac. Some of the stories Kramer tells are both miraculous and disturbing. For instance, he describes a woman, once so incapacitated by social anxiety that she rarely left home, who became a social butterfly after boosting her serotonin level via... 

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