Effect of dietary protein and fat on prothrombin time of chickens at different environmental temperatures.
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Age Factors↗
Biomedical subjects
K F Soliman
Publications and source records attributed to K F Soliman.
Behavioral and neurochemical changes in the dopaminergic system after repeated cocaine administration.
In order to determine whether repeated cocaine administration produced persistent changes in dopamine (DA) receptor binding and release consistent with behavioral sensitization, rats were treated with either cocaine (25 mg/kg ip) or saline twice daily for 14 consecutive days followed by a 3-d withdrawal period. The DA transporter site was assayed using [3H]GBR 12935, whereas D1 and D2 sites were assayed using [3H]SCH 23390 and [3H]spiperone, respectively. The density (Bmax) of the DA transporter binding sites in the ST of the cocaine-treated group increased significantly (p < 0.05) over controls 3 d after the last injection, whereas the density of striatal D1 and D2 binding sites remained unchanged. The DA transporter in the nucleus accumbens (NA) was also studied with [3H]GBR 12935 and was unchanged following drug treatment. D1 and D2 binding parameters for the NA were not determined in this study. Furthermore, cocaine administration did not affect the affinities (Kd) of the radioligands used to label the transporter, D1, or D2 sites in any of the studies performed. In addition, striatal DA release was measured using in vivo microdialysis in anesthetized rats. Linear regression analysis on maximal decreases in DA release after apomorphine (0.02, 0.2, and 2.0 mg/kg sc) injection showed no difference in the functional capacity of the ST to modulate DA transmission between control and treated groups. Moreover, animals pretreated with cocaine showed a significant (p < 0.01) decrease in locomotor activity (LA) after a presynaptic, autoregulating dose of apomorphine (0.03 mg/kg sc) was given. These results suggests that the effects seen after repeated exposure to cocaine may be regulated, in part, by changes in striatal DA transporter binding site densities and not necessarily by DA-releasing mechanisms or D1 and D2 receptor modification.
Animals↗
Hypothermic effect of ethanol in mice selected for differential sleep-time response to pentobarbital.
The hypothermic action of ethanol was investigated in genetically distinct lines of mice selected for sleep-time response to pentobarbital for six generations. Ethanol (3 g/kg, intraperitoneally) was administered to alcohol-naive males and females from each of the unselected control, long-, and short-sleep mouse lines. Rectal temperatures were measured immediately before, and at 15, 30, 60, 90, 120, and 240 min after ethanol injection. Eight female and eight male mice from each line were sacrificed at each time point, and trunk blood was collected for plasma ethanol analysis. The results show that short-sleep mice were less hypothermic (p < 0.05) compared to long-sleep mice at 15 and 30 min after ethanol administration. However, plasma ethanol concentrations were not significantly different between the mouse lines at any time point. Therefore, the line-dependent differential ethanol-induced hypothermia observed may be a result of differences in "brain sensitivity" rather than in the rates of ethanol metabolism among the mouse lines.
Animals↗
The role of inducible nitric oxide synthase in cocaine-induced locomotor sensitization.
Experimentally naive male Sprague-Dawley rats (weighing 85-110 g) were used to examine the role of inducible nitric oxide synthase (iNOS) in cocaine-induced locomotor sensitization. Repeated administration of cocaine (15 mg/kg, ip) for 7 consecutive days produced locomotor sensitization. Pretreatment with iNOS inhibitors, L-N(6)-(1-iminoethyl) lysine (NIL) or (-)-epigallocatechin gallate (EGCG; 10 mg/kg, ip), 30 min before cocaine (15 mg/kg, ip) administration totally blocked the development of cocaine-induced locomotor sensitization. Dopamine (DA) receptor binding in the nucleus accumbens (NAC) showed a significant decrease in the density of D(2) receptor and the affinity of D(1) receptor after cocaine treatment. Pretreatment with EGCG or NIL abolished the cocaine-induced changes in these parameters. These results suggest that iNOS may participate in the process of development of locomotor sensitization through the modulation of DA receptors in the NAC.
Animals↗
The role of NMDA receptors in neonatal cocaine-induced neurotoxicity.
The present study assessed the ability of N-methyl-D-aspartate (NMDA) receptor antagonist, dizocilpine (MK-801), to modulate neonatal cocaine-induced neurobehavioral changes in the rat. Sprague-Dawley rats were randomly assigned on postnatal day 0 (PND 0) to one of four treatment groups. Treatments began on PND 4 and continued until PND 10. Treatments consisted of an oral bolus of either cocaine HCl (40 mg/kg), (+)MK-801 (0.4 mg/kg), (+)MK-801 (0.4 mg/kg) followed 30 min later with cocaine HCl (40 mg/kg) or 0.9% saline. On PND 21, 30, 40 and 60, males and females were examined for stress response using the cold-water swim test. Cocaine-treated male and female rats exhibited significantly diminished tolerance to cold-water stress compared to control and MK-801/cocaine-treated groups. In addition, neonatal exposure to cocaine was associated with increased severity of motor symptoms (tail twitches, wet dog shaking and convulsions) following the administration of NMDA (35 mg/kg). Treatment groups were also tested for pain sensitivity using the tail flick (TF) and hot plate (HP) methods. The results indicated that neonatal cocaine exposure altered pain sensitivity in both tests. NMDA receptor binding studies showed a significant increase in receptor densities in the hippocampus and hypothalamus of the cocaine-treated group compared to control. MK-801 administered to rat pups before cocaine treatment blocked the increase in receptor density. The results indicated that neonatal cocaine exposure was associated with altered responses to NMDA, stress tolerance and pain sensitivity. Moreover, the pretreatment with NMDA receptor antagonist, MK-801, abolished or attenuated these cocaine-induced neurobehavioral changes.
Adrenocorticotropic Hormone↗
Involvement of the brain cholinergic system in the rapid development of tolerance to glucose-induced analgesia.
In this study, male Sprague-Dawley rats (150-230 g), maintained under controlled lighting and temperature conditions, were used. In one experiment, glucose administration (10 g/kg) was found to be associated with profound analgesia which could be blocked by prior administration of atropine (0.5 mg/kg). In another experiment, when two doses of glucose were given at 24 hr interval, the second injection of glucose was associated with tolerance to glucose-induced analgesia. In an attempt to correlate changes in the cholinergic enzymes with glucose-induced analgesia, choline acetyltransferase and acetylcholinesterase activities were determined in the cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata in control rats and rats treated with a single dose of glucose (10 g/kg) or two doses of glucose. The second administration of glucose was accompanied with tolerance in the level of acetylcholinesterase in the bulbus olfactorius, midbrain, cerebral cortex, cerebellum and pons. There were no significant changes in choline acetyltransferase activities between the groups studied. The results obtained indicate that the cholinergic system may be involved in glucose-induced analgesia and that the rapid development of tolerance to glucose-induced analgesia is associated with the tolerance in the response of brain acetylcholinesterase activity.
Acetylcholinesterase↗
Effect of morphine on the rat gastrointestinal cholinergic enzymes.
Male Sprague-Dawley rats weighing approximately 225 g and maintained under controlled lighting and temperature conditions, were used in this experiment. Animals were given morphine (10 mg/kg, i.p.) either at 10:00 hr or at 22:00 hr. One hour later, treated animals with their proper control were sacrificed and the mucosa of the stomach, duodenum, ileum and colon were separated and assayed for acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities. Data obtained indicate that morphine administration during the light phase resulted in a significant increase (p less than 0.01) in AChE activity in the colon, with no significant effect on the stomach, duodenum or the ileum. There was also significant increase (p less than 0.05) in ChAT activity in the stomach and the duodenum as a result of morphine administration during the light phase, with no effect on other tissues studied. During the dark phase, there were no significant changes observed in AChE activity of all tissues examined following morphine administration. However, the determination of ChAT activity during the dark phase, following morphine treatment, showed a significant increase (p less than 0.01) in the duodenum and the ileum, with a significant decline (P less than 0.05) in the colon. Results obtained from this study indicate that gastrointestinal changes seen after morphine administration could be due to changes in the activity of the cholinergic enzymes and these changes may be diurnally controlled.
Acetylcholinesterase↗