The Influence of Lithium on Water Binding Ability, Consistency and Macromolecules in the Rat Brain

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Rats were treated with lithium added to the diet for five weeks (40 mmol LiCl/kg diet). The mean plasma lithium concentration was 0.48 mmol/l plasma, and the blood was drawn at 8 a.m. The brains were removed and synaptosomes were prepared according to the method of Gray & Whittaker (1962) and Bradford (1972). The synaptosomes were incubated for 120 min. with 32P‐orthophosphate, either in a lithium‐containing medium or in a lithium‐free medium. The 32P‐incorporation was lower in the synaptosomes from lithium‐treated rats than the 32P‐incorporation in synaptosomes from control rats regardless of the medium chosen. The results indicate that lithium treatment in vivo decreases the 32P‐incorporation into synaptosomal phospholipids and that the effect remains after the removal of the lithium ion.

Section: Discussionsupporting

confidence: 55%

The Effect of Lithium on the Incorporation of ³²P‐Orthophosphate into Synaptosomal Phospholipids from Rat Brain

Edelfors

1980

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“…Lithium, however, is known to have an effect on multiple neuronal systems, an effect which is partly on hormone-sensitive adenylate cyclase systems (Geisler & Klysner 1981), partly on the calcium-inositol system (Hallcher & Sherman 1980), and partly a more general membrane "stabilizing" effect (Edelfors 1977;Andersen et al 1984).…”

Section: Discussionmentioning

confidence: 99%

No Change in Rat Cerebral Cortex Calmodulin Content Following Chronic Treatment with Lithium, Reserpine, Imipramine, and Lithium Combined with Reserpine or Imipramine

Andersen

Geisler

Klysner

1984

Rats were treated 2-3 weeks with lithium, reserpine, imipramine, and combinations of lithium with reserpine or imipramine. Lithium was given in the diet, while the other drugs were dissolved in 0.9% saline and given intraperitoncally twice daily. The control and lithium groups received only vehicle injections. Twenty-four hours after the last injection the rats were decapitated and the cerebral cortex dissected. The tissue was sliced and the noradrenaline-stimulated cyclic AMP accumulation determined or the tissue was homogenized and centrifuged at 10,000 x g for 30 min. and the calmodulin content determined in the pellet and the supernatant. Reserpine treatment was found to cause an 50% increase in the noradrenaline-stimulated cyclic AMP accumulation, while treatment with imipramine and the combination lithium-imiprdmine decreased the noradrenaline-stimulated cyclic AMP accumulation by 40%. The tissue content of calmodulin was, however, found unaltered by all treatments.

“…So far there have been no investigations as to the glycopeptide content in the cerebrospinal fluid from manic-depressive patients, but schizophrenia and manicdepressive psychosis are both endogenous disorders where abnormal function of the central nervous system can be expected. The increased content of sialogangliosides and sialoglycopeptides may be another expression of general membrane changes caused by the lithium treatment and which may be of importance for the therapeutical effect (Wagner et al 1970;Edelfors 1977Edelfors & 1980.…”

Section: Controlsmentioning

confidence: 99%

The Effect of Chronic Lithium Treatment on the Sialic Acid Content in Rat Brain Synaptosomes

Edelfors

1981

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Rats were fed a lithium‐containing diet for five weeks (40 mmol LiCl/kg fodder). Plasma lithium concentration was 0.44 mmol Li+/1 plasma. The synaptosomes were isolated and incubated with 3H‐glucosamine for 60 min. The glycopeptides and the gangliosides were extracted and the sialic acid content and the 3H‐sialic acid content were measured. The lithium treatment produced an increase in the synaptosomal glycopeptide content. The sialic acid content was simultaneously increased in glycopeptides as well as gangliosides. The specific activity of sialic acid was reduced to 75% of the control value in the sialoglycopeptide fraction.