Raccoon poxvirus as a mucosal vaccine vector for domestic cats.

In the present study, we evaluated both the immunogenicity and safety of recombinant raccoon poxvirus (RCN) as a mucosal vaccine vector for domestic cats. RCN is an orthopoxvirus that was isolated from healthy raccoons and has been used experimentally as a vaccine vector for rabies and other antigens in a variety of species, including raccoons, skunks, foxes, bobcats, rabbits, domestic cats, piglets, sheep and non-human primates. We evaluated the antibody response induced by a recombinant RCN vaccine expressing the rabies-G glycoprotein (RCN/rabies-G) administered to cats by the oral (PO), intranasal (IN), conjunctival (CO) or intranasal/conjunctival (IN/CO) route (dose: 10 plaque forming units or PFU).

Nitric oxide and the neurotoxic effects of methamphetamine and 3,4-methylenedioxymethamphetamine.

The role of nitric oxide (NO) in the long-term, amine-depleting effects of methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA) was investigated in the rodent central nervous system. The NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) antagonized the dopamine- and serotonin-depleting effects of both METH and MDMA. The protective actions of L-NAME in METH-treated mice were reversed by prior administration of the NO generator isosorbide dinitrate.

The late chlamydial inclusion membrane is not derived from the endocytic pathway and is relatively deficient in host proteins.

Chlamydiae are obligate intracellular parasites which multiply within infected cells in a membrane-bound structure termed an inclusion. Newly internalized bacteria are surrounded by host plasma membrane; however, the source of membrane for the expansion of the inclusion is unknown. To determine if the membrane for the mature inclusion was derived by fusion with cellular organelles, we stained infected cells with fluorescent or electron-dense markers specific for organelles and examined inclusions for those markers.

Effects of glutamate antagonists on methamphetamine and 3,4-methylenedioxymethamphetamine-induced striatal dopamine release in vivo.

Several amphetamine analogues are reported to increase striatal glutamate efflux in vivo, whereas other data indicate that glutamate is capable of stimulating the efflux of dopamine (DA) in the striatum via a glutamate receptor-dependent mechanism. Based on these findings, it has been proposed that the ability of glutamate receptor-blocking drugs to antagonize the effects of amphetamine may be explained by their capacity to inhibit DA release induced by glutamate. To examine this possibility further, we investigated in vivo the ability of glutamate antagonists to inhibit DA release induced by either methamphetamine (METH) or 3,4-methylenedioxymethamphetamine (MDMA).