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At least 217 records · Page 12Linked to original sources
PubMed1997

The CCK-B agonist, BC264, increases dopamine in the nucleus accumbens and facilitates motivation and attention after intraperitoneal injection in rats.

Although it is known that panic attacks are triggered by the cholecystokinin fragment CCK4, the specific involvement of peripheral or central cholecystokinin CCK receptors in various adaptive processes such as emotion, memory and anxiety has yet to be demonstrated. With this aim, we have investigated the biochemical and pharmacological effects resulting from the administration of BC264, a highly potent and selective CCK-B agonist able to cross the blood-brain barrier. Very low doses of BC264 (microg/kg i.p.), increased the exploration of animals submitted to an unknown territory but were devoid of anxiogenic properties in the elevated plus maze. BC264 increased locomotion and rearings of rats newly placed in an open field and improved their spontaneous alternation in a Y-maze. The use of vagotomized animals showed that the increased alternation induced by BC264 did not require an intact vagus nerve, unlike the locomotor activation. These behavioural effects, prevented by the prior i.p. administration of the CCK-B antagonist L-365,260 but not by the CCK-A antagonist L-364,718, were shown to depend on dopaminergic systems, since they were blocked by D1 (SCH23390, 25 microg/kg i.p.) or D2 (sulpiride, 50 or 100 mg/kg i.p.) antagonists. In addition, bilateral perfusion in freely moving rats of BC264 at pharmacologically active doses, using a newly designed microdialysis system, was found to increase the extracellular levels of DA, DOPAC and HVA in the anterior part of the nucleus accumbens. These results show that activation of CCK-B receptors by BC264 does not produce anxiogenic-like effects but appears to improve motivation and attention, whereas other CCK-B agonists such as BocCCK4 induce anxiogenic responses. Several explanations, including the existence of different sub-sites of the CCK-B receptor, could account for these differential effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Intraperitoneal injection of synthetic bacterial lipopeptides does not cause a rise in circulating inflammatory cytokines.

The production of TNF-alpha, IL-1 and IL-6 was measured in mice after i.p. injections of the synthetic bacterial lipopeptide Pam3Cys-Ala-Gly, a potent macrophage and B cell activator in vitro. Only minor amounts of IL-6 and no TNF-alpha were detectable in the serum of mice injected with 10 or 100 micrograms of Pam3Cys-Ala-Gly. Lipopeptide concentrations up to 1000 micrograms failed to induce IL-1, and TNF-alpha production and serum IL-6 levels were only slightly elevated. In contrast to Pam3Cys-Ala-Gly, i.p. injections of LPS were accompanied by high levels of the inflammatory cytokines TNF-alpha, IL-1 and IL-6 suggesting fundamental differences of the mode of action of these two substances when applied in vivo.

Amino Acid Sequence↗
PubMed2005

The bisphosphonate zoledronic acid inhibits the development of plasmacytoma induced in BALB/c mice by intraperitoneal injection of pristane.

OBJECTIVES: Bisphosphonates (BPs) are mostly used in the palliative care of myeloma-associated osteolytic lesions. Recent studies have suggested that BPs may also exert direct antitumor effects on myeloma cells. We have investigated the effect of the potent bisphosphonate, zoledronic acid (ZOL), on the development of pristane (2,6,10,14-tetramethylpentadecane)-induced plasmacytoma (PCT) in six-week-old BALB/c mice. METHODS: Different groups of pristane-treated mice also received ZOL (100 microg/kg) commencing after the development of PCT or ZOL (20 microg/kg) from the first day. Control groups received pristane alone, ZOL alone (20 microg/kg), or phosphate-buffered saline. The study was terminated on day 300, and the remaining mice were autopsied and abdominal tissues were examined histologically for PCT. RESULTS AND CONCLUSIONS: Statistical analysis revealed a significant delay in PCT development in the group receiving pristane plus ZOL (20 microg/kg) from the first day compared to the groups receiving pristane alone and pristane combined with ZOL (100 microg/kg) after the appearance of PCT (Log-rank, P = 0.0001 and 0.0001; respectively). Kaplan-Meier analysis revealed a significant difference in survival between the group treated with pristane alone and the groups receiving pristane plus ZOL (20 microg/kg) from the first day or ZOL (100 microg/kg) after the appearance of PCT (Log-rank, P = 0.016 and 0.023; respectively). These results indicate a direct anti-tumor effect of ZOL in pristane-induced PCT development BALB/c mice, which may contribute to their significantly increased survival. This hypothesis should now be further investigated in clinical trials.

Animals↗