TL;DR: A detailed evaluation of the results obtained by the numerous investigators gave us no definitive clue as to the nature of the discrepancies and decided to run similar studies with greater emphasis on placebo and time controls with respect to steady-state concentrations and rates of synthesis of serotonin and 5-HIAA.
Abstract: Serotonin levels in rabbit brain were reported to be decreased by single doses of ethanol in viv0.'~~~~~25 Subsequently, several groups were unable to confirm this finding in rabbit brain12J3.21,29 or in rat brain.8,9.31,33 Other groups reported an increase in rat brain serotonin levels under the influence of ethanol and other anesthetic~.2,3,~6,~~ Recent studies of the effect of single doses of ethanol on serotonin steady-state concentrations and rates of biosynthesis as determined by the MAO-inhibitorinduced increase in serotonin are just as contradictory. Tyce and colleague^^^-^^ first reported that the concentration and turnover of serotonin in brain was normal in ethanol-intoxicated rats; but, later, Tyce and associates38 qualified the statement to indicate that although the steady-state concentration was not altered, the rate of serotonin accumulation after pargyline was decreased by ethanol. Palaic and colleaguesz7 reported that the levels of serotonin in rat brain were markedly increased at one hour and six hours after ethanol administration and still elevated at 24 hours after the single dose and that the rate of serotonin accumulation after pargyline was increased by ethanol. Reichle and c o w ~ r k e r s ~ ~ also reported that acute amounts of ethanol increased brain serotonin levels. Kuriyama and associatesz3 found no difference in brain serotonin levels in mice after ethanol and a slight but not significant decrease in the pargyline induced serotonin accumulation. They also reported that single doses of ethanol had no significant effect on mouse brain tryptophan-5hydroxylase consistent with the observation that ethanol had no effect on serotonin synthesis. Tyce and colleagues38 reported that ethanol did not alter the brain concentration of 5-HIAA and slightly but significantly blocked the pargylineinduced decrease in 5-HIAA. Palaic and associates27 reported that ethanol induced a decrease in the brain 5-HIAA levels and an acceleration of the pargylineinduced decrease in 5-HIAA. A detailed evaluation of the results obtained by the numerous investigators gave us no definitive clue as to the nature of the discrepancies. We therefore decided to run similar studies with greater emphasis on placebo and time controls with respect to steady-state concentrations and rates of synthesis of serotonin and 5-HIAA.
TL;DR: Evidence is now provided for the presence of free endogenous 5-HTOL in the mouse whole brain, as identified by a GC-MS procedure.
Abstract: THE PRODUCTION of 5-hydroxytryptophol (5-HTOL) from exogenous 5-HT has been shown to occur in homogenates of rat and human brain tissue (ECCLESTON et a/., 1966: FELDSTEIN & WILLIAMSON, 1968) and in the cat spinal cord in cico (BULAT et a/.. 1970). Endogenous 5-HTOL has been isolated by paper chromatography and tlc from bovine pineal gland (MCISAAC rt ul., 1965) and from human CSF. using the dipentafluoroproprionate derivative of the alcohol for gas chromatography-mass spectrometry (GC-MS) (CURTIL‘S et a/.. 1975; TAKAHASHI rt (11.. 1978). However. the presence of endogenously-formed 5-HTOL in brain tissue has not yet been demonstrated. Evidence is now provided for the presence of free endogenous 5-HTOL in the mouse whole brain, as identified by a GC-MS procedure.
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