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 * Stonefish / Jellyfish Sting Antivenom info, sting treatments

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http://www.ncbi.nlm.nih.gov/pubmed/19041336 Minocycline reduced craving for cigarettes but did not affect smoking or intravenous nicotine responses in humans. Sofuoglu M, Waters AJ, Mooney M, O'Malley SS.

Yale University, School of Medicine, Department of Psychiatry, West Haven, CT, USA. Mehmet.Sofuoglu@yale.edu Abstract In recent preclinical studies, the role of nitric oxide (NO) in nicotine dependence has become increasingly evident. Inhibition of NO synthesis blocks acquisition of conditioned place preference, and attenuates the nicotine abstinence syndrome in rodents. These findings have not been followed up in human studies. In order to obtain preliminary data on NO inhibition in human smokers, we conducted a randomized, double-blind, crossover study (N=12) of minocycline, a tetracycline derivative antibiotic, that inhibits the neuronal nitric oxide (NO) synthase enzyme with resultant inhibition of NO production. Medication effects were assessed through a smoking choice procedure as well as subjective and physiological responses to nicotine administered via the intravenous route (IV). Minocycline treatment did not affect smoking self-administration in our choice procedure and did not affect most of the subjective responses to IV nicotine or sample smoking. Following IV nicotine administration, there was a greater reduction in craving for cigarettes under minocycline, compared to placebo. Similarly, smokers had greater reduction in their craving for cigarettes following sample smoking under minocycline treatment. These findings provide limited support for the potential use of minocycline as a treatment of nicotine dependence.

http://jpet.aspetjournals.org/content/early/2009/12/15/jpet.109.158543?cited-by=yes&legid=jpet;jpet.109.158543v1 histamine potentiates nmda

Abstract The ability of histamine to facilitate the N-methyl-d-aspartate (NMDA) induced depolarization of cortical projection neurones was examined by use of grease-gap recording.

Histamine (1 to 15 μm) reversibly facilitated the NMDA-induced depolarization yielding a bell-shaped concentration-response relationship. The peak enhancement was 167% above the control at 10 μm histamine. Desensitization was present in 4 out of 5 slices on second exposure 40 min following the first exposure.

Histamine did not alter the depolarization induced by 10 μm kainate.

The histamine-induced facilitation persisted in the presence of tetrodotoxin, but was reduced in a concentration-dependent manner by diphenhydramine (IC50=7.6 nm). Cyproheptadine (10 nm) also reduced the facilitation, whereas ranitidine (200 nm) and thioperamide (10 nm) were ineffective in this regard.

Histamine (10 μm) facilitated the NMDA (25 μm)-induced depolarization in nominally Mg2+-free medium. The magnitude of the facilitation was smaller than that observed in Mg2+-containing medium (17% above the control) and desensitization was not observed. This facilitation was not reduced by cyproheptadine (10 nm) or diphenhydramine (1 μm).

We conclude that histamine facilitates the NMDA depolarization at cortical neurones via two distinct mechanisms. One mechanism involves activation of the histamine H1 receptor and is sensitive to Mg2+. The second mechanism is independent of histamine cell surface receptor activation and may reflect a direct action of histamine at the NMDA receptor.

http://onlinelibrary.wiley.com/doi/10.1038/sj.bjp.0701123/full