Enhanced discriminated bar-press avoidance in the rat through appetitive preconditioning.

In 2 experiments with 57 male albino rats, an appetitive preconditioning procedure produced superior performance on a discriminated bar-press avoidance task. The technique was designed to minimize the number of shocks received early in training and consisted primarily of rewarding Ss with food pellets for an avoidance response in addition to terminating the warning stimulus. Ss so preconditioned were found to achieve sustained, high levels of avoidance. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Study of receptor-mediated neurotoxins released by HIV-1-infected mononuclear phagocytes found in human brain

Although there is growing evidence that neurotoxic molecules produced by HIV-1-infected mononuclear phagocytes damage neurons, the precise mechanisms of neuronal attack remain uncertain. One class of cytotoxin involves neuronal injury mediated via the NMDA receptor. We examined blood monocytes and brain mononuclear cells isolated at autopsy from HIV-1-infected individuals for the ability to release NMDA-like neuron-killing factors. We found that a neurotoxic amine, NTox, was produced by blood monocytes and by brain mononuclear phagocytes infected with retrovirus. In vivo injections of minute quantities of NTox produced selective damage to hippocampal pyramidal neurons. NTox can be extracted directly from brain tissues infected with HIV-1 and showed structural features similar to wasp and spider venoms. In contrast to NTox, HIV-1 infection did not increase the release of the NMDA excitotoxin quinolinic acid (QUIN) from mononuclear cells. Although we found modest elevations of QUIN in the CSF of HIV-1-infected individuals, the increases were likely attributable to entry through damaged blood-brain barrier. Taken together, our data pinpoint NTox, rather than QUIN, as a major NMDA receptor-directed toxin associated with neuro-AIDS.     

The HHQK domain of beta-amyloid provides a structural basis for the immunopathology of Alzheimer's disease

The beta-amyloid peptide 1-42 (Abeta1-42), a major component of neuritic and core plaques found in Alzheimer's disease, activates microglia to kill neurons. Selective modifications of amino acids near the N terminus of Abeta showed that residues 13-16, the HHQK domain, bind to microglial cells. This same cluster of basic amino acids is also known as a domain with high binding affinity for heparan sulfate. Both Abeta binding to microglia and Abeta induction of microglial killing of neurons were sensitive to heparitinase cleavage and to competition with heparan sulfate, suggesting membrane-associated heparan sulfate mediated plaque-microglia interactions through the HHQK domain. Importantly, small peptides containing HHQK inhibited Abeta1-42 cell binding as well as plaque induction of neurotoxicity in human microglia. In vivo experiments confirmed that the HHQK peptide reduces rat brain inflammation elicited after infusion of Abeta peptides or implantation of native plaque fragments. Strategies which exploit HHQK-like agents may offer a specific therapy to block plaque-induced microgliosis and, in this way, slow the neuronal loss and dementia of Alzheimer's disease.     

The study of the influence of industrial processing on the elemental composition of mate tealeaves (Ilex paraguariensis) using the PIXE technique

The influence of the industrial processing on the elemental composition of mate tealeaves was investigated using the Particle Induced X-ray Emission (PIXE) technique. Considerable changes were observed after the main steps of the industrial process. The concentration of Mg, P, S, K and Ca increased after the roasting (rapid contact of the leaves with wood flames and fog) and the drying processes, possibly due to the presence of contaminants in the hot gases (originated from burning wood) used in both steps, biomass burning and evaporation of water. Elements like Al, Si, Mn and Rb increase in concentration after the roasting but decrease after the drying process, while Fe and Ti were not affected by the drying step. Differences in concentration for several elements were observed due to the stationing period (waiting between the drying and the packaging of the leaf material). The mineral contents of leaves and twigs were also compared and results show that most of the elements are present in greater amounts in the leaves, except for Ca, Ti and Zn. These results highlight the importance of understanding the influence of the industrial process on the mineral content of mate tealeaves for the development of new products with controlled characteristics.     

Faster acquisition of discriminated lever-press avoidance by hippocampectomized rats.

Reports that 10 male albino rats with bilateral hippocampal destruction produced by aspiration acquired a discriminated lever-press avoidance task faster than, and exhibited avoidance levels consistently superior to 10 unoperated Ss and 10 Ss with neocortical destruction. Destruction of the hippocampus in Ss with extensive previous experience on the task resulted in improved avoidance performance, but the improvement was not significantly superior to the performance of controls. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Reactive glia as rivals in regulating neuronal survival

Reactive gliosis is a response noted after nearly every type of CNS injury and involves both activated microglia and astroglia. Although many investigators believe that reactive glia in some way regulate the survival of injured neurons, the influence of glial elements upon damaged neural tissues remains uncertain. To examine relationships between reactive glia and neurons, secretion products from both microglia and astroglia are tested for their effects upon the survival of cultured neurons. Microglia are found to secrete neurotoxic agents, while astroglia are a source of neuronotrophic factors. Similar patterns of soluble factor production are noted for astroglia-rich or microglia-rich regions of rat neocortex damaged by ischemia. These observations suggest that microglia and astroglia compete for control of neuronal survival. Importantly, microglial neurotoxins might hinder the recovery of neurologic function at sites of inflammation.