Caffeine, like malnutrition, can produce behavioral and electrophysiological alterations. However, the interaction of both factors remains unclear. Here this interaction has been studied in male Wistar rats previously malnourished during the lactation period by feeding their dams the "regional basic diet" of Northeast Brazil, containing about 8% protein, predominantly from vegetable sources (RBD(8)). At 70-75days of life, a subset of the pups was treated intraperitoneally with 30mg/kg caffeine for 4days while being tested according to the behavioral model of latent inhibition. Another group was subjected to an electrophysiological recording of the phenomenon known as cortical spreading depression, and the effects of caffeine injected during the recording session were evaluated. Caffeine did not affect cortical spreading depression, but antagonized latent inhibition in both the RBD(8)-malnourished rats and in the well-nourished control group fed a chow diet with 22% protein. This effect of caffeine was not seen in malnourished rats fed a protein-supplemented RBD (protein increased to 22% by increasing the proportion of foodstuffs from vegetable origin; RBD(22) group), suggesting that the amino acid imbalance of this diet may modulate the caffeine effects on latent inhibition. The results indicate a differential effect of caffeine in the latent inhibition behavioral model, as compared to the cortical spreading depression phenomenon, and this effect is influenced by the early nutritional status of the animal. We suggest that caffeine may modulate dopaminergic subcortical receptors participating in attention processes, but does not interact at the cortical level, in a way that would affect cortical spreading depression.

The purpose of this investigation was to verify the role of dopamine and serotonin receptors in the effect of fencamfamine (FCF) on latent inhibition. FCF is a psychomotor stimulant with an indirect dopaminergic action. Latent inhibition is a model of attention. Latent inhibition is blocked by dopaminergic agents and facilitated by dopamine receptor agonists. FCF has been shown to abolish latent inhibition. The serotonergic system may also participate in the neurochemical mediation of latent inhibition. The selective dopamine D(1) receptor antagonist SCH 23390 (7-chloro-3-methyl-1-phenyl-1,2,4,5-tetrahydro-3-benzazepin-8-ol), D(2) receptor antagonists pimozide (PIM) and methoclopramide (METH), and serotonin 5-HT(2A/C) receptor antagonist ritanserin (RIT) were used in the present study. Latent inhibition was evaluated using a conditioned emotional response procedure. Male Wistar rats that were water-restricted were subjected to a three-phase procedure: preexposure to a tone, tone-shock conditioning, and a test of the effect of the tone on licking frequency. All of the drugs were administered before the preexposure and conditioning phases. The results showed that FCF abolished latent inhibition, and this effect was clearly antagonized by PIM and METH and moderately attenuated by SCH 23390. At the doses used in the present study, RIT pretreatment did not affect latent inhibition and did not eliminate the effect of FCF, suggesting that the FCF-induced abolition of latent inhibition is not mediated by serotonin 5-HT(2A/C) receptors. These results suggest that the effect of FCF on latent inhibition is predominantly related to dopamine D(2) receptors and that dopamine D(2) receptors participate in attention processes.

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Lithium salts exert electrophysiological and behavioral effects in animals and humans and have been used clinically in the treatment of bipolar disorders. Little is known about the lithium/nutrition interaction in the developing brain. This work aimed to determine, in adult rats, whether treatment with a single dose of lithium chloride (LiCl) would influence the propagation of the brain excitability-related phenomenon known as cortical spreading depression (CSD). Male well-nourished (W; fed a lab chow diet with 22% protein; n=22) and previously protein-malnourished rats (M; fed a low-quality 8% protein diet; proteins mostly from vegetable source; n=20) were treated at 75-80 days of age with a single intraperitoneal injection of either 50 mg/kg LiCl (n=9 W and 10 M rats) or saline (n=13 W and 10 M rats). When the pups were 90-110 days, CSD was elicited at the frontal cortex and recorded during 4 hours at two cortical parietal points. In malnourished, but not in well-nourished rats, lithium treatment lowered CSD velocities (P < 0.05), in comparison with saline-injected animals. In a third group (n=23), in which the low-protein diet was quantitatively corrected to 22%, the lithium effect disappeared (n=12), compared to saline (n=11). Our results demonstrate a facilitating effect of malnutrition on the CSD-impairing action of a single lithium administration, suggesting a lithium/nutrition interaction.

This article thematizes treatments in children affected by Acute Lymphocytic Leukemia. For this, treatment in patients from low-risk and high-risk groups will be addressed to the importance of diagnosis, bringing the expected results. Aiming at the process that the child patient receives, from the diagnostic to the treatments developed to reach the cure. This study was conducted from a literature review perspective, which consists of developing a theoretical basis, in the treatment of a research problem that can be answered in the analysis of a published literature. Therefore, this article is based on obtaining the study about articles that described several cases of acute lymphocytic leukemia. During this study it was possible to understand the results through treatment of patients with different degrees of the disease, each with its peculiarities, symptoms and treatment 2