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Early cognitive deficit characteristic of early Alzheimer's disease seems to be produced by the soluble forms of β-amyloid protein. Such cognitive deficit correlates with neuronal network dysfunction that is reflected as alterations in the electroencephalogram of both Alzheimer patients and transgenic murine models of such disease. Correspondingly, recent studies have demonstrated that chronic exposure to βAP affects hippocampal oscillatory properties. However, it is still unclear if such neuronal network dysfunction results from a direct action of βAP on the hippocampal circuit or it is secondary to the chronic presence of the protein in the brain. Therefore, we aimed to explore the effect of acute exposure to βAP25-35 on hippocampal network activity both in vitro and in vivo, as well as on intrinsic and synaptic properties of hippocampal neurons. We found that βAP25-35, reversibly, affects spontaneous hippocampal population activity in vitro. Such effect is not produced by the inverse sequence βAP35-25 and is reproduced by the full-length peptide βAP1-42. Correspondingly βAP25-35, but not the inverse sequence βAP35-25, reduces theta-like activity recorded from the hippocampus in vivo. The βAP25-35-induced disruption in hippocampal network activity correlates with a reduction in spontaneous neuronal activity and synaptic transmission, as well as with an inhibition in the subthreshold oscillations produced by pyramidal neurons in vitro. Finally, we studied the involvement of Fyn-kinase on the βAP25-35-induced disruption in hippocampal network activity in vitro. Interestingly, we found that such phenomenon is not observed in slices obtained from Fyn-knockout mice. In conclusion, our data suggest that βAP acutely affects proper hippocampal function through a Fyn-dependent mechanism. We propose that such alteration might be related to the cognitive impairment observed, at least, during the early phases of Alzheimer's disease. © 2009 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Oleamide is a recently described lipid obtained from the cerebrospinal fluid (CSF) of total sleep-deprived cats. It has been suggested that oleamide possesses several biological effects such as sleep induction, immunological suppression, as well as serotonin and GABA receptor activation; also oleamide binds to cannabinoid receptors. Objective: To determine if oleamide affects the memory processes. Material and methods: Oleamide was tested by a passive avoidance paradigm. It was assessed the effect of oleamide on locomotor activity, core temperature and pain perception in rats. Results: We observed that oleamide hastened memory extinction, oleamide is also capable of impairing cAMP production by hippocampal cells. In an in vitro preparation In addition, oleamide reduced locomotor activity, core temperature, and pain perception as has been observed in mice. Conclusions: These results suggest that oleamide modulates memory processes. Since these effects are also induced by marihuana, it is very likely that oleamide may be affecting the cerebral cannabinoid system. [ABSTRACT FROM AUTHOR]