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Other Rats (other + rat)
Selected AbstractsInteractions of Stress and CRF in Ethanol-Withdrawal Induced Anxiety in Adolescent and Adult RatsALCOHOLISM, Issue 9 2010Tiffany A. Wills Background:, Repeated stress or administration of corticotropin-releasing factor (CRF) prior to ethanol exposure sensitizes anxiety-like behavior in adult rats. Current experiments determined whether adolescent rats were more sensitive to these challenges in sensitizing ethanol withdrawal-induced anxiety and altering CRF levels in brain during withdrawal. Methods:, Male adult and adolescent Sprague,Dawley rats were restraint stressed (1 hour) twice 1 week apart prior to a single 5-day cycle of ethanol diet (ED; stress/withdrawal paradigm). Other rats received control diet (CD) and three 1-hour restraint stress sessions. Rats were then tested 5, 24, or 48 hours after the final withdrawal for anxiety-like behavior in the social interaction (SI) test. In other experiments, adolescent rats were given two microinjections of CRF icv 1 week apart followed by 5 days of either CD or ED and tested in social interaction 5 hours into withdrawal. Finally, CRF immunoreactivity was measured in the central nucleus of the amygdala (CeA) and paraventricular nucleus (PVN) after rats experienced control diet, repeated ethanol withdrawals, or stress/withdrawal. Results:, Rats of both ages had reduced SI following the stress/withdrawal paradigm, and this effect recovered within 24 hours. Higher CRF doses were required to reduce SI in adolescents than previously reported in adults. CRF immunohistochemical levels were higher in the PVN and CeA of CD-exposed adolescents. In adolescent rats, repeated ethanol withdrawals decreased CRF in the CeA but was not associated with decreased CRF cell number. There was no change in CRF from adult treatments. Conclusions:, In the production of anxiety-like behavior, adolescent rats have equal sensitivity with stress and lower sensitivity with CRF compared to adults. Further, adolescents had higher basal levels of CRF within the PVN and CeA and reduced CRF levels following repeated ethanol withdrawals. This reduced CRF within the CeA could indicate increased release of CRF, and future work will determine how this change relates to behavior. [source] Time-Course and Mechanisms of Restored Vascular Relaxation by Reduced Salt Intake and Angiotensin II Infusion in Rats Fed a High-Salt DietMICROCIRCULATION, Issue 3 2009SCOTT T. MCEWEN ABSTRACT Objective: This study determined the mechanisms and time-course of recovery of vascular relaxation in middle cerebral arteries (MCAs) of salt-fed Sprague-Dawley rats returned to a low-salt (LS) diet (0.4% NaCl) or infused with low-dose angiotensin II (ANG II). Methods: Rats were fed a high-salt (HS) diet (4% NaCl) for 3 days or 4 weeks before returning to an LS diet for various periods. Other rats fed a HS diet (HS+ANG II) received a chronic (3 days) intravenous (i.v.) infusion of a low dose of ANG II (5 ng kg,1 min,1) to prevent salt-induced ANG II suppression. Results: The HS diet eliminated the increase in cerebral blood flow in response to acetylcholine (ACh) infusion and the relaxation of MCA in response to ACh, iloprost, cholera toxin, and reduced PO2. Recovery of vascular relaxation was slow, requiring at least 2 weeks of the LS diet, regardless of the duration of exposure to a HS diet. Hypoxic dilation was mediated by cyclo-oxygenase metabolites and ACh-induced dilation was mediated via nitric oxide in LS rats and in HS rats returned to the LS diet or receiving ANG II infusion. Conclusions: Returning to a LS diet for 2 weeks or chronic 3-day ANG II infusion restores the mechanisms that normally mediate cerebral vascular relaxation. [source] Long-lasting hippocampal potentiation and contextual memory consolidationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2001Benedetto Sacchetti Abstract In order to ascertain whether there are hippocampal electrophysiological modifications specifically related to memory, exploratory activity and emotional stress, extracellular electrical activity was recorded in hippocampal slices prepared from the brains of male adult rats. Several groups of animals were employed: (i) rats which had freely explored the experimental apparatus (8 min exposure); (ii) rats which had been subjected, in the same apparatus, to a fear conditioning paradigm training entailing the administration of aversive electrical footshocks (8 min exposure); (iii) rats to which the same number of aversive shocks had been administered in the same apparatus, but temporally compressed so as to make difficult the association between painful stimuli and the apparatus (30 s exposure); (iv) naïve rats never placed in the apparatus. Half of the rats from each treatment group were used for retrieval testing and the other half for hippocampal excitability testing. The conditioned freezing response was exhibited for no less than 4 weeks. Hippocampal excitability was measured by means of input,output curves (IOC) and paired-pulse facilitation curves (PPF). Retrieval testing or brain slices preparation were performed at increasing delays after the training sessions: immediately afterwards or after 1, 7 or 28 days. Only the rats subjected to the fear conditioning training exhibited freezing when placed again in the apparatus (retrieval testing). It was found that IOCs, with respect to naïve rats, increased in the conditioned animals up to the 7-day delay. In free exploration animals the IOCs increased only immediately after the training session. In all other rats no modification of the curves was observed. IOC increases do not appear to imply presynaptic transmitter release modifications, because they were not accompanied by PPF modifications. In conclusion, a clear-cut correlation was found between the increase in excitability of the Schaffer collateral,CA1 dendrite synapses and freezing response consolidation. [source] Melatonin protects against endosulfan-induced oxidative tissue damage in ratsJOURNAL OF PINEAL RESEARCH, Issue 4 2008Gülden Z. Omurtag Abstract:, Endosulfan is a chlorinated cyclodiene insecticide which induces oxidative stress. In this study, we investigated the possible protective effect of melatonin, an antioxidant agent, against endosulfan (Endo)-induced toxicity in rats. Wistar albino rats (n = 8) were administered endosulfan (22 mg/kg/day orally) followed by either saline (Endo group) or melatonin (10 mg/kg/day, Endo + Mel group) for 5 days. In other rats, saline (control group) or melatonin (10 mg/kg/day, Mel group) was injected for 5 days, following corn oil administration (vehicle of endosulfan). Measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were performed in liver and kidney. Furthermore, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels, lactate dehydrogenase (LDH) activity were measured in the serum samples, while tumor necrosis factor-, (TNF-,), interleukin-, (IL-,) and total antioxidant capacity (AOC) were assayed in plasma samples. Endosulfan administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant rises in tissue MDA and collagen levels and MPO activity. Moreover, the proinflammatory mediators (TNF-, and IL-,), LDH activity, AST, ALT, creatinine and BUN levels were significantly elevated in the endosulfan-treated rats. On the other hand, melatonin treatment reversed all these biochemical alterations induced by endosulfan. Our results suggest that oxidative mechanisms play an important role in endosulfan-induced tissue damage and melatonin, by inhibiting neutrophil infiltration, balancing oxidant,antioxidant status and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury as a result of endosulfan toxicity. [source] Melatonin reduces dimethylnitrosamine-induced liver fibrosis in ratsJOURNAL OF PINEAL RESEARCH, Issue 2 2004Veysel Tahan Abstract:, Increased deposition of the extracellular matrix components, particularly collagen, is a central phenomenon in liver fibrosis. Stellate cells, the central mediators in the pathogenesis of fibrosis are activated by free radicals, and synthesize collagen. Melatonin is a potent physiological scavenger of hydroxyl radicals. Melatonin has also been shown to be involved in the inhibitory regulation of collagen content in tissues. At present, no effective treatment of liver fibrosis is available for clinical use. We aimed to test the effects of melatonin on dimethylnitrosamine (DMN)-induced liver damage in rats. Wistar albino rats were injected with DMN intraperitoneally. Following a single dose of 40 mg/kg DMN, either saline (DMN) or 100 mg/kg daily melatonin was administered for 14 days. In other rats, physiologic saline or melatonin were injected for 14 days, following a single injection of saline as control. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) levels were evaluated in blood and tissue homogenates. DMN caused hepatic fibrotic changes, whereas melatonin suppressed these changes in five of 14 rats (P < 0.05). DMN administration resulted in increased hydroxyproline and MDA levels, and decreased GSH and SOD levels, whereas melatonin reversed these effects. When melatonin was administered alone, no significant changes in biochemical parameters were noted. In conclusion, the present study suggests that melatonin functions as a potent fibrosuppressant and antioxidant, and may be a therapeutic choice. [source] Inflammation-induced leukocyte accumulation in injured skeletal muscle: Role of mast cellsMUSCLE AND NERVE, Issue 6 2008Claude H. Côt, e PhD Abstract Inflammation consequent to muscle damage is characterized by an accumulation of leukocytes. Our aim in this study was to determine whether mast cells can modulate inflammation-induced leukocyte trafficking. One approach consisted of giving rats a mast cell,degranulating agent, CMP 48/80, prior to a protocol of lengthening contractions inducing inflammation without neutrophil accumulation; in parallel, other rats were given the mast cell,stabilizing agent, cromolyn, prior to injecting muscle with bupivacaine, which induces neutrophil accumulation. Damage was evaluated through measurement of contractile force and inflammation using histochemical and immunohistochemichal methods. Stimulation with CMP 48/80 increased the proportion of degranulated mast cells significantly and neutrophil accumulation occurred with lengthening contractions. With bupivacaine, accumulation of neutrophils decreased by 70% when degranulation was inhibited. These results indicate that mast cells are important in the process governing leukocyte trafficking in skeletal muscle trauma and that targeting their inhibition could be an attractive alternative for control of inflammation. Muscle Nerve, 2008 [source] | |||||||||||||