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ABSTRACT: Stress associated with transportation has widespread effects on physiological systems in laboratory animals, including changes in the cardiovascular, endocrine, immune, central nervous, and reproductive systems. Although short-lived, these changes can confound research if animals are utilized before homeostasis is restored and physiological measures return to normal. Therefore, some period of acclimatization following transportation is generally suggested to restore homeostasis. The following two questions should be considered to establish an adequate period for acclimatization: (1) Will anticipated physiological changes confound the research to be conducted? (2) What is the length of time necessary for confounding physiological changes to normalize? Finding answers to those questions in the literature can be a challenge. Most literature on the physiological impact of transportation involves agricultural animals, although the limited literature in common laboratory animal species generally parallels changes documented in agricultural animals. The literature documents elevated heart rate and weight loss, as well as elevated concentrations of adrenaline, noradrenaline, glucose, cortisol, free fatty acids, and beta-hydroxybutyrate. Carbohydrate, protein, and lipid metabolism (both lipolysis and lipogenesis) are altered, and plasma osmolality, albumen, protein, and pack-cell volume increase. Neutrophilia and lymphopenia are also evident. These measures generally return to baseline within 1 to 7 days of transportation, although animals that are young, severely stressed, and have stress-sensitive genotypes may show altered physiological measures for several weeks. Other measures such as circadian rhythm and reproductive performance may take several weeks to months to normalize.
ILAR journal / National Research Council, Institute of Laboratory Animal Resources 02/2006; 47(4):364-9. · 2.33 Impact Factor
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Jennifer A Obernier
Contemporary topics in laboratory animal science / American Association for Laboratory Animal Science 06/2004; 43(3):64, 66, 68. · 0.82 Impact Factor
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ABSTRACT: Impairments of learning and memory are common neuropsychological sequelae of chronic alcohol abuse. Alcoholics often have impairments of anterograde memory, including spatial memory dysfunction, and a tendency toward response perseveration. This study was designed to assess the effects of binge ethanol exposure on neurodegeneration and cognitive function. Rats were given ethanol three times daily for 4 days. Silver staining revealed neurodegeneration in the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and dentate gyrus. After withdrawal, behavioral testing in the Morris water maze revealed significant differences in reversal learning between treatment groups. Ethanol-treated animals required more trials to learn the reversal task, entered the previously trained quadrant more often, and spent more time there than controls. [3H]PK-11195 binding, an index of CNS damage, was elevated in the piriform cortex of ethanol-treated animals. Thus, binge ethanol exposure resulted in neurodegeneration of a corticolimbic circuit with common excitatory inputs from the olfactory bulb and was associated with perseverative responding on a spatial learning task. These studies suggest that a single binge drinking episode could cause neurodegeneration and cognitive dysfunction in humans. The perseverative nature of the behavioral deficit could be related to both cognitive dysfunction and the behavioral components of the addiction process.
Pharmacology Biochemistry and Behavior 07/2002; 72(3):521-32. · 2.53 Impact Factor
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ABSTRACT: Impairments of learning and memory are common neuropsychological sequelae of chronic alcohol abuse. Alcoholics often have impairments of anterograde memory, including spatial memory dysfunction, and a tendency toward response perseveration. This study was designed to assess the effects of binge ethanol exposure on neurodegeneration and cognitive function. Rats were given ethanol three times daily for 4 days. Silver staining revealed neurodegeneration in the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and dentate gyrus. After withdrawal, behavioral testing in the Morris water maze revealed significant differences in reversal learning between treatment groups. Ethanol-treated animals required more trials to learn the reversal task, entered the previously trained quadrant more often, and spent more time there than controls. [3H]PK-11195 binding, an index of CNS damage, was elevated in the piriform cortex of ethanol-treated animals. Thus, binge ethanol exposure resulted in neurodegeneration of a corticolimbic circuit with common excitatory inputs from the olfactory bulb and was associated with perseverative responding on a spatial learning task. These studies suggest that a single binge drinking episode could cause neurodegeneration and cognitive dysfunction in humans. The perseverative nature of the behavioral deficit could be related to both cognitive dysfunction and the behavioral components of the addiction process.
Pharmacology Biochemistry and Behavior.
