Effect of triperidol on processes involving acetylcholine in rat brain in vitro

Michałek, Hanna; Antal, J.; Gatti, G; Pocchiari, F.

doi:10.1016/0006-2952(71)90357-1

Cited by 14 publications

(3 citation statements)

References 17 publications

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“…LeFresne et al (1973) found that the initial rate of acetylcholine production was dependent on pyruvate concentration. Michalek et al (1971) observed that triperidol inhibited the oxidation of glucose and pyruvate and the synthesis of acetylcholine. These observations together suggest that acetylcholine synthesis may be closely linked to pyruvate oxidation, despite the differences in fluxes.…”

Section: Discussionmentioning

confidence: 99%

Decreased synthesis of acetylcholine accompanying impaired oxidation of pyruvic acid in rat brain minces

Gibson

Jope

Blass

1975

Biochemical Journal

235

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The relation between pyruvate utilization and acetylcholine synthesis was investigated in minces of adult rat brain. The flux of pyruvate to acetylcholine was less than 1% of that to CO2; nevertheless, a number of agents which inhibited conversion of [1-14C]-pyruvate or [2-14C]pyruvate into 14CO2 were associated with corresponding decreases in the conversion of [2-14C]pyruvate into acetylcholine. The amount of acetylcholine produced by minces of whole rat brain, measured by g.l.c.-mass spectrometry, decreased similarly. Among the inhibitory compounds tested were 3-bromopyruvate, an irreversible inhibitor of pyruvate dehydrogenase; 2-oxobutyrate, a competitive inhibitor of pyruvate dehydrogenase; other 2-oxo acids; and amobarbital and pentobarbital. Linear-regression equations relating CO2 production to acetylcholine synthesis gave correlation coefficients of 0.89-0.93 for the combined observations. The inhibition of acetylcholine synthesis could not be attributed to inhibition of choline acetyltransferase. Incorporation of [2-14C]pyruvate into lipids, proteins and nucleic acids was effected less than that into acetylcholine. Under these experimental conditions, it was shown that pyruvate utilization can limit acetylcholine synthesis.

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Section: Discussionmentioning

confidence: 99%

Decreased synthesis of acetylcholine accompanying impaired oxidation of pyruvic acid in rat brain minces

Gibson

Jope

Blass

1975

Biochemical Journal

235

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“…The reason for this disparity is that in the initial investigations of Mann et al (1939a,b) slices of the entire cerebrum, rather than those of the brain cortex, were taken. These included parts of the caudate nuclei, which are now known to be at least three or four times as active as brain cortex in synthesizing acetylcholine from glucose (Sattin, 1966;Michalek et al, 1972).…”

Section: Determination Of Acetylcholinementioning

confidence: 99%

Control of synthesis and release of radioactive acetylcholine in brain slices from the rat. Effects of neurotropic drugs

Grewaal

Quastel

1973

Biochemical Journal

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1. Studies of the synthesis and release of radioactive acetylcholine in rat brain-cortex slices incubated in Locke-bicarbonate-[U-(14)C]glucose media, containing paraoxon as cholinesterase inhibitor, revealed the following phenomena: (a) dependence of K(+)-or protoveratrine-stimulated acetylcholine synthesis and release on the presence of Na(+) and Ca(2+) in the incubation medium, (b) enhanced release of radioactive acetylcholine by substances that promote depolarization at the nerve cell membrane (e.g. high K(+), ouabain, protoveratrine, sodium l-glutamate, high concentration of acetylcholine), (c) failure of acetylcholine synthesis to keep pace with acetylcholine release under certain conditions (e.g. the presence of ouabain or lack of Na(+)). 2. Stimulation by K(+) of radioactive acetylcholine synthesis was directly proportional to the external concentration of Na(+), but some synthesis and release of radioactive acetylcholine occurred in the absence of Na(+) as well as in the absence of Ca(2+). 3. The Na(+) dependence of K(+)-stimulated acetylcholine synthesis was partly due to suppression of choline transport, as addition of small concentrations of choline partly neutralized the effect of Na(+) lack, and partly due to the suppression of the activity of the Na(+) pump. 4. Protoveratrine caused a greatly increased release of radioactive acetylcholine without stimulating total radioactive acetylcholine synthesis. Protoveratrine was ineffective in the absence of Ca(2+) from the incubation medium. It completely blocked K(+) stimulation of acetylcholine synthesis and release. 5. Tetrodotoxin abolished the effects of protoveratrine on acetylcholine release. It had blocking effects (partial or complete) on the action of high K(+), sodium l-glutamate and lack of Ca(2+) on acetylcholine synthesis and release. 6. Unlabelled exogenous acetylcholine did not diminish the content of labelled tissue acetylcholine, derived from labelled glucose, suggesting that no exchange with vesicular acetylcholine took place. In the presence of 4mm-KCl it caused some increase in the release of labelled acetylcholine. 7. The barbiturates (Amytal, pentothal), whilst having no significant effects on labelled acetylcholine synthesis in unstimulated brain except at high concentration (1mm), diminished or abolished (at 0.25 or 0.5mm) the enhanced release of acetylcholine, due to high K(+) or lack of Ca(2+). The fall in tissue content of acetylcholine, due to lack of Ca(2+), was diminished or abolished by pentothal (0.25 or 0.5mm) or Amytal (0.25mm).

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“…In rat brain cortex slices, TFP (0.2 mM) decreased 02 Uptake and CO2 production (9). In the same system acetylcholine synthesis was decreased 80%, but the activities of choline acetylase and acetylcholine esterase were not affected (8).…”

mentioning

confidence: 91%

Effects of the hypocholesteremic agent trifluperidol on the sterol, steryl ester, and fatty acid metabolism of Saccharomyces cerevisiae

Sobus¹,

Holmlund²,

Whittaker³

1977

J Bacteriol

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Trifluperidol (TFP), at a concentration of 100 ,M, inhibited the 24-h growth of Saccharomyces cerevisiae by about 30%. Effects on lipid metabolism were investigated by monitoring the incorporation of [1-14C]sodium acetate into various lipid fractions after 4 and 24 h of growth in the presence of several concentrations of TFP. Although little effect was noted on the amount of free sterols, 24-h incorporation of label into steryl esters was increased two-to fourfold by 100 ,M TFP. Major sterol components of the steryl ester fraction isolated from an untreated culture were zymosterol (48%) and ergosterol (24%), whereas from the TFP-treated culture A8 24(28)-ergostadienol (66.6%) and A8-ergostenol (14.7%) were most abundant. Free sterols present in the highest concentration in the untreated culture were ergosterol (78.2%) and lanosterol (13%); whereas A8'22_ ergostadienol (38.5%), A8-ergostenol (35.4%), and A8' 24(281-ergostadienol (25.4%) were the most abundant free sterols obtained from the TFP-treated culture. Thus, the major block in the sterol biosynthetic pathway in yeast appears to be A8-> A7 isomerization. In these same cultures the relative amounts of C12 and C14 acids isolated from both steryl ester and miscellaneous lipid fractions were increased more than threefold over controls.

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Effect of triperidol on processes involving acetylcholine in rat brain in vitro

Cited by 14 publications

References 17 publications

Decreased synthesis of acetylcholine accompanying impaired oxidation of pyruvic acid in rat brain minces

Decreased synthesis of acetylcholine accompanying impaired oxidation of pyruvic acid in rat brain minces

Control of synthesis and release of radioactive acetylcholine in brain slices from the rat. Effects of neurotropic drugs

Effects of the hypocholesteremic agent trifluperidol on the sterol, steryl ester, and fatty acid metabolism of Saccharomyces cerevisiae

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