The synaptolytic effect of thiamine related to its interaction with neurotransmitters

Galzigna, L

doi:10.1016/0006-2952(69)90364-5

Cited by 13 publications

(1 citation statement)

References 8 publications

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“…On the other hand, there is a possibility that (3) the oxythiamine effect concerned the mechanism of release in a more direct manner. Thiamine has been shown to form complexes with ACh, and the stability of these complexes increases as the ratio of ACh to thiamine is increased (Galzigna, 1969). It might be that a certain amount of intraterminal thiamine is attached to the presynaptic membrane and can bind a given amount of cytoplasmic ACh.…”

Section: Oxythiaminementioning

confidence: 99%

Thiamine and Cholinergic Transmission in the Electric Organ of Torpedo

Eder

Dunant²,

Loctin³

1980

Journal of Neurochemistry

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The electrogenic tissue of Torpedo was found to phosphorylate in vitro external [14C]thiamine by a saturable process. The rate of this metabolisaton was increased when acetate, an efficient precursor of acetylcholine (ACh) synthesis in this tissue, was added to the incubation medium, thus increasing the turnover of ACh. Nerve stimulation did not release significant amounts of the previously accumulated [14C]thiamine. Exogenous thiamine modified the size of the electroplaque potential (e.p.p.). At concentrations higher than 10(-3)M the nerve-electroplaque transmission was depressed after a transient increase of the e.p.p. Such a depression was due to a strong decrease of the ACh release. At concentrations equal to or lower than 10(-3)M, thiamine affected transmission in a rather complex fashion. ACh release was decreased or increased depending on concentration, time of application, and mode of stimulation. Oxythiamine, a structural antimetabolite of thiamine, affected the transmission in a very characteristic manner at 10(-5)M and higher concentrations. The amplitude of the e.p.p. was increased and, more strikingly, its duration was prolonged. These changes were not due to an inhibition of cholinesterase activity but to an enhancement of the evoked release of ACh either on single-impulse or repetitive stimulation. Another antimetabolite, pyrithiamine, had no effect on the transmission nor on ACh release. From this and our previous work, it is proposed that thiamine is involved, directly or indirectly, in the process of ACh release. The possible mechanisms of this involvement are discussed.

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Section: Oxythiaminementioning

confidence: 99%

Thiamine and Cholinergic Transmission in the Electric Organ of Torpedo

Eder

Dunant²,

Loctin³

1980

Journal of Neurochemistry

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Indoleamine neurons and their processes in the normal rat brain and in chronic diet‐induced thiamine deficiency demonstrated by uptake of ³H‐Serotonin

Chan‐Palay

1977

J of Comparative Neurology

220

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Indoleamine structures in the brains of normal, pair-fed control, and thiamine deficient rats are selectively localized by autoradiography following monoamine oxidase inhibition and simultaneous intraventricular infusion of 3H-5HT M). The locations of indoleamine neurons and their plexuses are comparable in the normal and control animals and are enumerated and mapped in detail. In addition to numerous labeled neurons in the raphe and reticular formation of pons and medulla, there are indoleamine neurons in several hypothalamic nuclei, in the mammillary, habenular, and interpeduncular nuclei. Labeled axonal plexuses occur in almost all areas of the brain but certain regions in spinal cord, medulla, midbrain, diencephalon, basal ganglia, and hippocampus are particularly rich. Thiamine deficiency causes lack of label in almost all indoleamine neurons and their processes in the midbrain and medulla; only a few dystrophic cells with hypertrophied axons are seen. In the diencephalon more indoleamine neurons and their axonal plexuses are visualized in these uptake studies. The periventricular regions of spinal cord, medulla, midbrain and diencephalon, the mammillary nuclei, habenular nuclei, and cerebellum -areas richly innervated by indoleamine axons in the normal brain -are the most severely affected. The ventricular and leptomeningeal indoleamine structures are preserved, however, and individual axons may hypertrophy. I t remains to be resolved whether these changes reflect disturbances in the ability of certain indoleamine neurons to take up and retain 3H-5HT or true neuronal degeneration. MI and cold d-1 norepinephrineThe mammalian central nervous system is supplied by a vast plexus of indoleamine-containing structures generated by a relatively small number of neurons collected in distinct groups. These indoleamine systems were first demonstrated in the brainstem of rat by histo- It is generally accepted that with monoamine oxidase inhibition and appropriate dosages of the labeled transmitter substance, indoleamine systems can be selectively localized by these methods. Biochemical approaches for measuring the amounts of 5HT in well localized regions of the brain have also been developed (Palkovits et al., '74; Saavedra et al., '74; Zivin et al., '75) thus providing excellent means for correlation between anatomical location and biochemical content. The present studies utilize continuous intraventricular infusion of 3H-5HT and cold d-1 norepinephrine (NE) followed by autoradiography in order to demonstrate the indoleamine neurons 467

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The Molecular Structures of the Phenothiazine Derivatives, Chlorpromazine, Thiethylperazine and Thioridazine, and a Discussion Of The Mechanism Of Action

McDowell

1974

The Jerusalem Symposia on Quantum Chemistry and Biochemistry

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The synaptolytic effect of thiamine related to its interaction with neurotransmitters

Cited by 13 publications

References 8 publications

Thiamine and Cholinergic Transmission in the Electric Organ of Torpedo

Thiamine and Cholinergic Transmission in the Electric Organ of Torpedo

Indoleamine neurons and their processes in the normal rat brain and in chronic diet‐induced thiamine deficiency demonstrated by uptake of ³H‐Serotonin

The Molecular Structures of the Phenothiazine Derivatives, Chlorpromazine, Thiethylperazine and Thioridazine, and a Discussion Of The Mechanism Of Action

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The synaptolytic effect of thiamine related to its interaction with neurotransmitters

Cited by 13 publications

References 8 publications

Thiamine and Cholinergic Transmission in the Electric Organ of Torpedo

Thiamine and Cholinergic Transmission in the Electric Organ of Torpedo

Indoleamine neurons and their processes in the normal rat brain and in chronic diet‐induced thiamine deficiency demonstrated by uptake of 3H‐Serotonin

The Molecular Structures of the Phenothiazine Derivatives, Chlorpromazine, Thiethylperazine and Thioridazine, and a Discussion Of The Mechanism Of Action

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Indoleamine neurons and their processes in the normal rat brain and in chronic diet‐induced thiamine deficiency demonstrated by uptake of ³H‐Serotonin