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Open Access The Effects of Analgesic Supplements on Neural Activity in the Main Olfactory Bulb of the Mouse

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We evaluated ketoprofen, a nonsteroidal anti-inflammatory drug (NSAID), as an antinociceptive supplement to chloral hydrate anesthesia in mouse. Effects of ketoprofen on main olfactory bulb (MOB) neuronal spontaneous activity were investigated using extracellular recordings in mouse in vivo. These effects were compared with those of another nociceptive supplement, the -opioid agonist buprenorphine. Ketoprofen (100 or 200 mg/kg) did not significantly alter MOB single-unit spontaneous rates in either ICR or C57BL/6J mice. In contrast, buprenorphine, at doses of 0.02, 0.05, and 0.20 mg/kg, inhibited MOB neuronal spontaneous rates by 19%, 49%, and 57%, respectively. Neither drug altered the temporal patterning of single-unit spike trains, as measured by the interspike interval (ISI) coefficient of variation (CV). We also investigated the ability of ketoprofen and buprenorphine to induce antinociception in the anesthetized mouse. The electroencephalogram (EEG) was used to measure the anesthetic plane. Both ketoprofen and buprenorphine altered the EEG trace and ketoprofen altered the power spectrum in a manner consistent with deepening anesthesia. Lastly, when applied at the time of anesthesia induction, ketoprofen decreased the amount of chloral hydrate necessary to maintain a defined anesthetic plane during the rest of the experiment. These results suggest that ketoprofen induces antinociception under chloral hydrate anesthesia without significantly inhibiting spontaneous activity of MOB neurons. Ketoprofen is therefore suitable as an antinociceptive supplement to chloral hydrate anesthesia during in vivo electrophysiologic recordings of the mouse MOB.

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Document Type: Miscellaneous

Publication date: 2007-04-01

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  • Comparative Medicine (CM), an international journal of comparative and experimental medicine, is the leading English-language publication in the field and is ranked by the Science Citation Index in the upper third of all scientific journals. The mission of CM is to disseminate high-quality, peer-reviewed information that expands biomedical knowledge and promotes human and animal health through the study of laboratory animal disease, animal models of disease, and basic biologic mechanisms related to disease in people and animals.

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