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C Pu

Publications and source records attributed to C Pu.

22 records · Page 2Linked to original sources

Developmental dissociation of methamphetamine-induced depletion of dopaminergic terminals and astrocyte reaction in rat striatum.

In 60- and 80-day-old rats, TH-positive terminal depletion occurred simultaneously with increased glial fibrillary acid protein (GFAP)-containing astrocytes in the caudate-putamen nucleus following four 10 or 20 mg/kg methamphetamine treatments. At 40 days, astrocytes were increased without depletion of TH-positive terminals. At younger ages (20 days old) neither marker was altered. Processes leading to methamphetamine-induced gliosis and TH-positive terminal depletion may not be present in rats prior to 40 and 60 days, respectively. The data suggest that factors other than degenerated dopaminergic terminals, such as increased glutamate release and/or production of free radicals may be involved in triggering striatal gliosis.

Animals↗

The effect of radix Salviae Miltiorrhizae (RSM) on substance P in cerebral ischemia--animal experiment.

The levels of substance P (SP) in rat brains were assayed in 64 rats. Bilateral common carotid artery ligation was done in 49 rats. Half an hour before ligation, 25 rats were given 10 g/kg of RSM; 24 rats were given the same volume of normal saline as controls. Sham operation was done in 15 rats. Half an hour and 3 hours after cerebral ischemia, the rats were quickly decapitated. SP concentration was assayed in the cerebral cortex, caudate nucleus and brain stem. In saline-treated animals, the SP level of caudate nucleus at 3-hour group was significantly decreased as compared with the 0.5-hour group and sham-operated group respectively. No significances were found among RSM-treated groups and sham-operated groups. The SP levels were shown: brain stem greater than caudate nucleus greater than cerebral cortex. The preliminary results suggest that SP may be involved in the pathophysiologic procedures of cerebral ischemia and RSM may attenuate the dysfunction of SP during cerebral ischemia.

Animals↗

Long-term learning deficits and changes in unlearned behaviors following in utero exposure to multiple daily doses of cocaine during different exposure periods and maternal plasma cocaine concentrations.

Although the possible behavioral neurotoxic effects of in utero exposure to cocaine have been the subject of numerous experiments, only a limited number of different types of animal models of cocaine exposure, critical periods, or long-term effects of such exposures have been investigated. In the present experiment, the effects of multiple daily SC exposures to cocaine (20 mg/kg/dose x 5 doses per day) were investigated when administered to gravid Sprague-Dawley CD rats on embryonic days E7-12 or E13-18 compared to weight-matched, vehicle injected, pair-fed controls. Effects of exposure were assessed on general development, olfactory orientation behavior, early locomotion, startle reactivity, spontaneous motor activity, and learning on two different tasks (Morris and Cincinnati water mazes). The multiple cocaine dosing regimen produced maternal peak serum concentrations of cocaine 3 times higher than that of a single dose (approximately 1550 vs. approximately 550 ng/mL). Early-exposed cocaine offspring had lower olfactory orientation scores and reduced postweaning rearing and hole-poke motor activity, whereas late-exposed cocaine offspring had increased postweaning locomotor, rearing, and hole-poke activity. On the Morris hidden platform maze, the cocaine early-exposed females had longer latencies on acquisition than controls. On the Cincinnati multiple-T water maze, the early-exposed cocaine females and the late-exposed cocaine males had increased errors, whereas the early-exposed cocaine males had reduced errors. The effects on measures of learning, when taken together, and in light of their being in the early-exposed group, suggest that embryonic cocaine exposure may have subtle effects on cognition in the offspring as adults. Such effects represent a form of neurotoxicity not previously associated with prenatal cocaine exposure.

Animals↗

Evaluation of neonatal exposure to cocaine on learning, activity, startle, scent marking, immobility, and plasma cocaine concentrations.

Prenatal cocaine treatment produces equivocal effects on spatial learning and memory; however, no data are available on neonatal treatment as a model of human third-trimester exposure. Sprague-Dawley rats were treated on postnatal days (P) 1-10 or 11-20 with cocaine (15 mg/kg x 4 per day at 2-h intervals) or saline (P1-P20) and evaluated as adults in the Morris water maze and on tests of activity, startle, scent marking, swimming immobility, and sequential learning. Neonatal cocaine had no effect on mortality; however, early treatment reduced body weight, whereas later treatment did not. Neonatal cocaine had no effects on exploratory activity, swimming ability, sequential learning, multiday activity rhythms, scent marking, or swimming immobility, but augmented acoustic startle amplitude in the early-treated group. Neonatal cocaine also produced an interaction on spatial learning in which the cocaine early-treated males performed slightly more efficiently than controls. Plasma cocaine concentrations were significantly higher in the early-treated group than the later-treated group despite receiving the same weight-adjusted doses. It was concluded that neonatal cocaine, when administered during a stage of brain development analogous to human third trimester, induces few behavioral effects based on the assessments used in this study.

Animals↗