Transmitter release in hippocampal slices from rats with limbic seizures produced by systemic administration of kainic acid

The systemic injection of kainic acid (KA) has been shown to destroy neurons in the hippocampus and to induce limbic-type seizure activity. However, little is known on the neurochemical events that are associated with this convulsant effect. In the present work we studied the spontaneous and the K⁺-stimulated release of labeled -aminobutyric acid (GABA), glutamate, serotonin and dopamine, in hippocampal slices of KA-treated rats, at the moment of clinical seizures (2 h) and 72 h later. At the onset of convulsions we found a 40–45% decrease in the K⁺-stimulated release of GABA. The release of the other neurotransmitters was not significantly affected by KA treatment. After 72 h GABA release was still reduced by 30–40%. It is concluded that the epileptogenic effect of KA in the hippocampus is probably related to a diminished inhibitory GABAergic neurotransmission.     

Minor components in food plants--Note I. Flavonol glycosides from Ullucus tuberosus.

This work deals with the isolation and characterization in Ullucus tuberosus of flavonoids, a class of natural products influencing potentially the taste and nutritional value of the plant food. The three flavonoids, rutin, narcissin and kaempferol 3-O-(2",6"-di-O-alpha-L-rhamnopyranosil)-beta-D-glucopyranoside, isolated, are devoid of taste, but appear to possess health promoting effects.     

Differential Calcium Dependence of γ-Aminobutyric Acid and Acetylcholine Release in Mouse Brain Synaptosomes

The dependence of gamma-aminobutyric acid (GABA) and acetylcholine (ACh) release on Ca2+ was comparatively studied in synaptosomes from mouse brain, by correlating the influx of 45Ca2+ with the release of the transmitters. It was observed that exposure of synaptosomes to a Na+-free medium notably increases Ca2+ entry, and this condition was used, in addition to K+ depolarization and the Ca2+ ionophore A23187, to stimulate the influx of Ca2+ and the release of labeled GABA and ACh. The effect of ruthenium red (RuR) on these parameters was also investigated. Of the three experimental conditions used, the absence of Na+ in the medium proved to be the most efficient in increasing Ca2+ entry. RuR inhibited by 60-70% the influx of Ca2+ stimulated by K+ depolarization but did not affect its basal influx or its influx stimulated by the absence of Na+ or by A23187. The release of ACh was stimulated by K+ depolarization, absence of Na+ in the medium, and A23187 in a strictly Ca2+-dependent manner, whereas the release of GABA was only partially dependent on the presence of Ca2+ in the medium. The extent of stimulation of ACh release was related to the extent of Ca2+ entry, whereas no such correlation was observed for GABA. In the presence of Na+, RuR did not affect the release of the transmitters induced by A23187. In the absence of Na+, paradoxically RuR notably enhanced the release of both ACh and GABA induced by A23187, in a Ca2+-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determination by capillary gas liquid chromatography of nitrosamine in partially altered food

The nitrosamines have been extensively studied for their toxicity. Their formation in the foods containing nitrous and nitric derivatives is favoured by the presence of suitable substrata. In the present work have been used column and capillari GL Chromatography for the determination of some nitrosamines in altered foods. The results obtained by applying the suggested procedure to a number of altered samples have been very encouraging.     

Inhibition of Brain Glutamate Decarboxylase Activity Is Related to Febrile Seizures in Rat Pups

Because previous work showed that in the newborn brain, but not in the adult brain, glutamate decarboxylase (GAD) is notably susceptible to heat, we have studied the possible involvement of GAD inhibition in febrile convulsions and the related changes in gamma-aminobutyric acid (GABA) content. Rats of different ages were subjected to hyperthermia, and GAD activity was determined in brain homogenates by measuring the release of 14CO2 from labeled glutamate and by measuring the formation of GABA. The latter method gave considerably lower values than the former in the youngest rats, and was considered more reliable. With this method, we found a 37-48% inhibition of GAD activity in rat pups 2-5 days old, which showed febrile seizures at progressively higher body temperatures, whereas in 10- and 15-day-old animals, which did not show convulsions, GAD activity was not affected by hyperthermia. Whole-brain GABA levels, however, did not change at any age. In contrast to GAD, choline acetyltransferase and lactic dehydrogenase activities were not altered by hyperthermia at any of the ages studied. These results suggest that a decreased efficiency of the inhibitory neurotransmission mediated by GABA, consequent to the inhibition of GAD activity, may be a factor related to febrile convulsions.     

Selective Stimulation of Neurotransmitter Release from Chick Retina by Kainic and Glutamic Acids

The excitatory action of kainic and glutamic acids in chick whole retina was demonstrated as an immediate stimulation of the release of labeled gamma-aminobutyric acid (GABA) and glycine in a superfusion system. This stimulatory effect was 3-10 times greater than that produced by a depolarizing K+ concentration; in addition, it was independent of Ca2+ in the medium, but notably inhibited when Na+ was omitted from the medium. Under identical experimental conditions, neither kainic nor glutamic acid had any effect on the release of labeled dopamine or alpha-aminoisobutyric acid, thus indicating that their effect is not unspecific or due to cell damage. Similar although less marked stimulation of labeled GABA and glycine release by kainic acid was obtained in subcellular retinal fractions, particularly in fraction P1, which contained photoreceptor terminals and outer segments. This stimulation was also Ca2+ independent and greatly reduced when Na+ was omitted from the medium. It is suggested that the stimulation of GABA release by kainic and glutamic acids is probably due to a Na+-dependent, carrier-mediated mechanism that responds to the entry of Na+ produced by the interaction of glutamic and kainic acids with retinal membranes. In cortical or striatal slices from mouse brain, these acids had a negligible stimulatory effect on GABA and dopamine release.     

Highways are a threat for giant armadillos that underpasses can mitigate

We report 24 records of giant armadillo roadkill on Brazilian highways in the Cerrado, Pantanal and Amazon biomes illustrating that highways are a threat to this species. However, we also documented the species using underpasses, demonstrating that these structures could help to reduce the risk of roadkill for giant armadillos.     

Palmitic Acid-Induced NAD+ Depletion is Associated with the Reduced Function of SIRT1 and Increased Expression of BACE1 in Hippocampal Neurons

Increased levels of circulating fatty acids, such as palmitic acid (PA), are associated with the development of obesity, insulin resistance, type-2 diabetes and metabolic syndrome. Furthermore, these diseases are linked to an increased risk of cancer, cardiovascular diseases, mild cognitive impairment and even Alzheimer’s disease (AD). However, the precise actions of elevated PA levels on neurons and their association with neuronal metabolic disruption that leads to the expression of pathological markers of AD, such as the overproduction and accumulation of the amyloid-β peptide, represent an area of intense investigation. A possible molecular mechanism involved in the effects of PA may be through dysfunction of the NAD⁺ sensor enzyme, SIRT1. Therefore, the aim of the present study was to analyze the relationship between the effects of PA metabolism on the function of SIRT1 and the upregulation of BACE1 in cultured hippocampal neurons. PA reduced the total amount of NAD⁺ in neurons that caused an increase in p65 K310 acetylation due to inhibition of SIRT1 activity and low protein content. Furthermore, BACE1 protein and its activity were increased, and BACE1 was relocated in neurites after PA exposure.

     

Chagas disease in Mexico

Mexico - the northernmost country of Latin America - has long been thought to have an unusually low prevalence of Chagas disease compared with other Latin American countries. This has seemed unusual because of the large number of vector species and subspecies reported from the country, and the social and ecological conditions that seem to parallel those in other countries where Chagas disease is recognized as a major public health priority. This review seeks to clarify the question, and suggests that the epidemiological, parasitological, and entomological pattern of Chagas disease in Mexico may also parallel that of other endemic regions, but has been masked by poor awareness of the disease both at local and institutional levels.