Urethane modestly affects multiple neurotransmitter systems at an anesthetic concentration. Our findings suggest that these degenerate effects of urethane can produce anesthesia and that urethane has a potential to influence neuronal measurements made in in vivo preparations.

No abstract

The effects of alpha-cyclodextrin-horseradish oil complex (CD-HR) on methane production and ruminal fermentation were studied in vitro and in steers. In the in vitro study, diluted ruminal fluid (30 mL) was incubated anaerobically at 38 degrees C for 6 h with or without CD-HR, using cornstarch as substrate. The CD-HR was added at various concentrations (0, 0.17, 0.85 and 1.7 g/L). Treatment affected neither the pH of the medium nor the number of protozoa. Total VFA increased in a linear manner (P = 0.02), and NH3-N decreased quadratically (P = 0.04) as the concentration of CD-HR increased from 0.17 g/L to 1.7 g/L. Molar proportions of acetate decreased in a linear manner (P = 0.03), and propionate increased linearly (P = 0.008) with increasing concentrations of CD-HR. Production of methane was inhibited up to 90%, whereas accumulation of dihydrogen was increased 36-fold by 1.7 g/L of CD-HR supplementation relative to controls. The effect of CD-HR on methane production, ruminal fermentation and microbes, and digestibility was further investigated in vivo using four Holstein steers in a crossover design. The CD-HR supplement was mixed into the concentrate portion of a (1.5:1) Sudangrass hay plus concentrate mixture that was fed twice daily to the steers. Ruminal samples were collected 0, 2, and 5 h after the morning feeding. No effects of CD-HR supplementation on ruminal pH (P = 0.63) or protozoal numbers (P = 0.44) were observed. Molar proportion of acetate was decreased (P = 0.04) and propionate was increased (P = 0.005) by CD-HR treatment. Molar proportion of butyrate was increased (P = 0.05) in CD-HR-supplemented steers. Ruminal NH3-N was decreased (P = 0.05) by treatment. Blood plasma glucose concentration was increased (P = 0.02) and urea-N was decreased (P = 0.04) with CD-HR supplementation. Daily DMI was decreased (P = 0.04), and apparent digestibility of DM (P = 0.13), NDF (P = 0.14), and CP tended (P = 0.14) to be increased by treatment. Methane production was decreased (P = 0.03) by 19%, and the number of methanogens was also decreased (P = 0.03). Although N retention (P = 0.11), total viable bacteria (P = 0.15), and sulfate-reducing bacteria (P = 0.17) were not significantly altered by treatment, tendencies for increases were noted with CD-HR supplementation. The number of cellulolytic (P = 0.38) and acetogenic bacteria (P = 0.32) remained unchanged by treatment. These results indicate that CD-HR supplementation can be used to decrease methane production in steers.

We assessed the effects of tramadol, a centrally acting analgesic, and its major metabolite, on neurotransmitter-gated ion channels. Tramadol binds to mu-opioid receptors with low affinity and inhibits reuptake of monoamines in the central nervous system. These actions are believed to primarily contribute to its antinociceptive effects. However, little is known about other sites of tramadol's action. We tested the effects of tramadol and its M1 metabolite (0.1-100 microM) on human recombinant neurotransmitter-gated ion channels, including glycine, gamma-aminobutyric acid(A) (GABA(A)), and N-methyl-D-aspartate (NMDA) receptors, expressed in Xenopus oocytes. Tramadol and M1 metabolite did not have any effects on glycine receptors. GABA(A) receptors were significantly inhibited only at large concentrations (100 microM). NMDA receptors were inhibited in a concentration-dependent manner. Tramadol and M1 metabolite inhibited the glutamate-concentration response curve without changing the half-maximal effective concentration or the Hill coefficient, indicating a noncompetitive inhibition. This study suggests that glycine receptors do not provide the antinociceptive effect of tramadol and that the inhibition of GABA(A) receptors at large concentration might correlate with convulsions. The inhibitory effect on NMDA receptors may contribute to the antinociceptive effect of tramadol at relatively large concentrations.