Molecular mechanisms mediating gastrin-releasing peptide receptor modulation of memory consolidation in the hippocampus.

Although the gastrin-releasing peptide-preferring bombesin receptor (GRPR) has been implicated in memory formation, the underlying molecular events are poorly understood. In the present study, we examined interactions between the GRPR and cellular signaling pathways in influencing memory consolidation in the hippocampus. Male Wistar rats received bilateral infusions of bombesin (BB) into the dorsal hippocampus immediately after inhibitory avoidance (IA) training. Intermediate doses of BB enhanced, whereas a higher dose impaired, 24-h IA memory retention. The BB-induced memory enhancement was prevented by pretraining infusions of a GRPR antagonist or inhibitors of protein kinase C (PKC), mitogen-activated protein kinase (MAPK) kinase and protein kinase A (PKA), but not by a neuromedin B receptor (NMBR) antagonist. We next further investigated the interactions between the GRPR and the PKA pathway. BB-induced enhancement of consolidation was potentiated by coinfusion of activators of the dopamine D1/D5 receptor (D1R)/cAMP/PKA pathway and prevented by a PKA inhibitor. We conclude that memory modulation by hippocampal GRPRs is mediated by the PKC, MAPK, and PKA pathways. Furthermore, pretraining infusion of BB prevented beta-amyloid peptide (25-35)-induced memory impairment, supporting the view that the GRPR is a target for the development of cognitive enhancers for dementia.

Glycerol as substrate for the production of biosurfactant by Pseudomonas aeruginosa UCP0992.

In this work the influence of the carbon source concentration, of the type and concentration of the nitrogen source and of the cultivation conditions (temperature, aeration and agitation speed) in mineral medium formulated with glycerol was studied for biosurfactant production by Pseudomonas aeruginosa UCP0992. The kinetics of microorganism growth and biosurfactant production have been described for the medium supplemented with 3% glycerol and 0.6% NaNO(3), at 28 degrees C during 120 h under 200 rpm, showing a growth-associated production. The isolated biosurfactant corresponded to a concentration of 8.0 g/l after 96 h. The medium surface tension was reduced to 27.4 mN/m and the emulsification index of hexadecane reached 75-80% after 72 h. A CMC of 700 mg/l and an interfacial tension against hexadecane of 2 mN/m were obtained. The biosurfactant showed stability when submitted at 90 degrees C during 2 h, and thermal (4-120 degrees C) and pH (4-12) stability regarding the surface tension reduction and the emulsification capacity of vegetable oils and hydrocarbons, and tolerance under high salt concentrations (2-10%). The biosurfactant was characterized as a group of rhamnolipids with anionic nature. The crude biosurfactant did not show toxicity against the microcrustacean Artemia salina and the cabbage (Brassica oleracea), while the isolated biosurfactant showed toxicity against the microcrustacean at the CMC. The application of the biosurfactant in diesel recovery from sand was demonstrated by removal percentiles above 85%. The results obtained in this work are noteworthy for possible biosurfactant production from glycerol with potential of application in the environment.

Ketamine impairs recognition memory consolidation and prevents learning-induced increase in hippocampal brain-derived neurotrophic factor levels.

The non-competitive N-methyl-d-aspartate (NMDA) glutamate receptor antagonist ketamine has been shown to produce cognitive deficits. However, the effects of ketamine on the consolidation phase of memory remain poorly characterized. Here we show that systemic administration of ketamine immediately after training dose-dependently impairs long-term retention of memory for a novel object recognition (NOR) task in rats. Control experiments showed that the impairing effects of ketamine could not be attributed to an influence on memory retrieval or sensorimotor effects. In addition, ketamine prevented the increase in hippocampal brain-derived neurotrophic factor (BDNF) levels induced by NOR learning. Our results show for the first time that ketamine disrupts the consolidation phase of long-term recognition memory. In addition, the findings suggest that the amnestic effects of ketamine might be at least partially mediated by an influence on BDNF signaling in the hippocampus.