In addition, loss of AC5 compromises the ability of both contextual and discrete cues to modulate instrumental behavior.”
“We investigated whether an inflammation-dependent activation of the brain occurs in response to systemic intraperitoneal
(i.p.) or local injections of macrophage-activating lipopeptide-2 (MALP-2) into a subcutaneous Fosbretabulin (s.c.) air pouch, and whether local (peripheral) or central cyclooxygenase (COX)-2-dependent formations of prostaglandin E(2) (PGE(2)) are involved in MALP-2-induced illness responses. Body temperature, activity, food and water intake were measured telemetrically. Local (s.c.) and circulating levels of PGE(2) were measured by an ELISA. Inflammatory activation of the CP-690550 in vivo brain in response to MALP-2 was determined by immunohistochemical detection of the transcription factors NF kappa B and STAT3
in cell nuclei as well as the appearance of COX-2 at the same sites. S.c. treatment with the preferential COX-2 inhibitor meloxicam attenuated, but not abolished fever induced by local injections of MALP-2 into the pouch. Local MALP-2-induced formation of PGE(2) was blunted by treatment with meloxicam. In the brain, i.p. stimulation with MALP-2-induced nuclear STAT3- and NF kappa B-translocation in the vasculature and the sensory circumventricular organs, which was accompanied by an increase
in COX-2 immunoreactivity (IR) in endothelial cells. Local MALP-2-treatment induced a moderate STAT3 activation and a small but significant increase in COX-2 IR while no NF kappa B-activation could be observed in the brains of these animals. We demonstrated that the activation of the brain STAT3 (NF kappa ID-8 B)-COX-2 singling cascade seems to be involved in the manifestation of brain-controlled illness symptoms induced by systemic and local inflammatory stimulation with MALP-2. The present data further suggest a contribution of peripherally produced PGE(2) to MALP-2-induced activation of brain sites implicated in fever. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Research on the role of the hippocampus in object recognition memory has produced conflicting results. Previous studies have used permanent hippocampal lesions to assess the requirement for the hippocampus in the object recognition task. However, permanent hippocampal lesions may impact performance through effects on processes besides memory consolidation including acquisition, retrieval, and performance. To overcome this limitation, we used an intrahippocampal injection of the GABA agonist muscimol to reversibly inactivate the hippocampus immediately after training mice in two versions of an object recognition task.