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  • 2000-2004  (2)
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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have previously shown that behavioral changes induced by cannabinoid were due to an elevation of prostaglandin E2 (PGE2) via the arachidonic acid cascade in the brain. In the present study, we investigated the participation of the prostanoid EP3 receptor, the target of PGE2 in the brain, in behavioral suppression induced by Δ8-tetrahydrocannabinol (Δ8-THC), an isomer of the naturally occurring Δ9-THC, using a one-lever operant task in rats. Intraperitoneal administration of Δ8-THC inhibited the lever-pressing behavior, which was significantly antagonized by both the selective cannabinoid CB1 receptor antagonist SR141716A and the cyclooxygenase inhibitor diclofenac. Furthermore, intracerebroventricular (i.c.v.) administration of PGE2 significantly inhibited the lever-pressing performance similar to Δ8-THC. Prostanoid EP3 receptor antisense-oligodeoxynucleotide (AS-ODN; twice a day for 3 days, i.c.v.) significantly decreased prostanoid EP3 receptor mRNA levels as determined by the RT-PCR analysis in the cerebral cortex, hippocampus and midbrain. AS-ODN also antagonized the PGE2-induced suppression of the lever pressing. In the same way, the suppression of lever-pressing behavior by Δ8-THC was significantly improved by AS-ODN. It is concluded that the suppression of lever-pressing behavior by cannabinoid is due to activation of the prostanoid EP3 receptor through an elevation of PGE2 in the brain.
    Type of Medium: Electronic Resource
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