Home About us Contact
|
Home About us Contact | ||
|
|
||
Adult Male Sprague-Dawley Rats (adult + male_sprague-dawley_rat)
Selected AbstractsChanges in rat hippocampal CA1 synapses following imipramine treatmentHIPPOCAMPUS, Issue 7 2008Fenghua Chen Abstract Neuronal plasticity in hippocampus is hypothesized to play an important role in both the pathophysiology of depressive disorders and the treatment. In this study, we investigated the consequences of imipramine treatment on neuroplasticity (including neurogenesis, synaptogenesis, and remodelling of synapses) in subregions of the hippocampus by quantifying number of neurons and synapses. Adult male Sprague-Dawley rats were injected with imipramine or saline (i.p.) daily for 14 days. Unbiased stereological methods were used to quantify the number of neurons and synapses. No differences in the volume and number of neurons of hippocampal subregions following imipramine treatment were found. However, the number and percentage of CA1 asymmetric spine synapses increased significantly and, conversely, the percentage of asymmetric shaft synapses significantly decreased in the imipramine treated group. Our results indicate that administration of imipramine for 14 days in normal rats could significantly increase the excitatory spine synapses, and change the relative distribution of spine and shaft synapses. We speculate that the present findings may be explained by the establishment of new synaptic connections and by remodelling or transformation of existing synapses. © 2008 Wiley-Liss, Inc. [source] Comparison of extratemporal and intratemporal facial nerve injury models,THE LARYNGOSCOPE, Issue 12 2009Nijee Sharma BS Abstract Objectives/Hypothesis: The purpose of this study was to compare functional recovery and motor nerve conduction following a distal extratemporal crush injury of the facial nerve to a more proximal intratemporal crush injury. Study Design: Prospective, controlled animal study. Methods: Adult male Sprague-Dawley rats were divided into four experimental groups: 1) extratemporal crush, 2) extratemporal sham-operated, 3) intratemporal crush, and 4) intratemporal sham-operated. Each group had an n of 4,9. The facial nerve was crushed near its exit from the stylomastoid foramen for extratemporal facial nerve injuries and within the facial canal in the temporal bone for intratemporal facial nerve injuries. Recovery times for the return of facial nerve functional parameters were compared between the two injury models. Motor nerve conduction studies were also done weekly to quantify the changes in peak amplitude and latency of evoked response. Results: Rats receiving the extratemporal facial nerve injury recovered full facial function by ,2 weeks postoperative (wpo) and displayed normal peak amplitude and latency recordings by 4 wpo. In comparison, rats receiving the intratemporal facial nerve injury failed to reach complete functional recovery at the end of 8 wpo. Although latency of evoked response returned to normal by 2 weeks following the intratemporal injury, peak amplitude remained ,70% below normal at the end of 8 wpo. Conclusions: An intratemporal crush of the facial nerve leads to significantly delayed functional recovery and decreased motor nerve conduction as compared to an extratemporal crush, indicating that the location of injury strongly influences the recovery outcome. Laryngoscope, 2009 [source] Lycopene, a Carotenoid, Attenuates Cyclosporine-Induced Renal Dysfunction and Oxidative Stress in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2007Ahmet Ate, ahin Adult male Sprague-Dawley rats were randomly divided into four groups. The control group received physiological saline; animals in the lycopene group received only lycopene (10 mg/kg); animals in the cyclosporine A group received only cyclosporine A (15 mg/kg) and animals in cyclosporine plus lycopene group received cyclosporine and lycopene for 21 days. The effects of lycopene on cyclosporine A-induced nephrotoxicity were evaluated by plasma creatinine, urea, sodium and calcium concentrations; kidney tissue thiobarbituric acid reactive species, reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and catalase activities and histopatological examinations. Administration of cyclosporine A to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. Cyclosporine A also induced oxidative stress as indicated by increased kidney tissue concentrations of thiobarbituric acid reactive species and GSH, and reduced activities of GSH-Px and catalase. Moreover, the kidneys of cyclosporine A-treated rats showed tubular necrosis, degeneration, dilatation, thickened basement membranes, luminal cast formation and inter-tubular fibrosis. Lycopene markedly reduced elevated plasma creatinine, urea levels and counteracted the deleterious effects of cyclosporine A on oxidative stress markers. In addition, lycopene ameliorated cyclosporine A-induced pathological changes including tubular necrosis, degeneration, thickened basement membranes and inter-tubular fibrosis when compared to the alone cyclosporine A group. These data indicate that the natural antioxidant lycopene might have protective effect against cyclosporine-induced nephrotoxicity and oxidative stress in rat. [source] PRECLINICAL STUDY: Changes in leptin, ghrelin, growth hormone and neuropeptide-Y after an acute model of MDMA and methamphetamine exposure in ratsADDICTION BIOLOGY, Issue 1 2008Firas H. Kobeissy ABSTRACT Club drug abuse is a growing problem in the United States. Beyond addiction and toxicity are endocrine effects which are not well characterized. Specifically, the changes in appetite following exposure to drugs of abuse are an interesting but poorly understood phenomenon. Serum hormones such as leptin, ghrelin, growth hormone (GH), and neuropeptide-Y (NP-Y) are known to affect appetite, but have not been studied extensively with drugs of abuse. In this work, we examine the effects of club drugs 3,4-methylenedioxymethamphetamine (MDMA) (ecstasy) and methamphetamine (METH) (doses of 5, 20 and 40 mg/kg) on serum concentrations of these hormones in adult male Sprague-Dawley rats 6, 12, 24 and 48 hours after drug administration. In a dose-dependent manner, MDMA was shown to cause transient significant decreases in serum leptin and GH followed by a base line recovery after 24 hours. Conversely, serum ghrelin increased and normalized after 24 hours. Interestingly, serum NP-Y showed a steady decrease in both treatment of MDMA and METH at different time points and dosages. In humans, abuse of these drugs reduces eating. As evident from these data, acute administration of METH and MDMA had significant effects on different serum hormone levels involved in appetite regulation. Future studies should be performed to see how chronic, low dose drug administration would affect hormone levels and try to answer questions about the physiological mechanisms involved in the anorexic paradigm observed in drug use. [source] Spectral analysis of electrocorticographic activity during pharmacological preconditioning and seizure induction by intrahippocampal domoic acidHIPPOCAMPUS, Issue 8 2010P.M. Sawant Abstract Previously we have shown that low-dose domoic acid (DA) preconditioning produces tolerance to the behavioral effects of high-dose DA. In this study, we used electrocorticography (ECoG) to monitor subtle CNS changes during and after preconditioning. Young adult male Sprague-Dawley rats were implanted with a left cortical electrode, and acute recordings were obtained during preconditioning by contralateral intrahippocampal administration of either low-dose DA (15 pmoles) or saline, followed by a high-dose DA (100 pmoles) challenge. ECoG data were analyzed by fast Fourier transformation to obtain the percentage of baseline power spectral density (PSD) for delta to gamma frequencies (range: 1.25,100 Hz). Consistent with previous results, behavioral analysis confirmed that low-dose DA preconditioning 60 min before a high-dose DA challenge produced significant reductions in cumulative seizure scores and high level seizure behaviors. ECoG analysis revealed significant reductions in power spectral density across all frequency bands, and high-frequency/high-amplitude spiking in DA preconditioned animals, relative to saline controls. Significant correlations between seizure scores and ECoG power confirmed that behavioral analysis is a reliable marker for seizure analysis. The reduction ofpower in delta to gamma frequency bands in contralateral cortex does not allow a clear distinction between seizure initiation and seizure propagation, but does provide objective confirmation that pharmacological preconditioning by DA reduces network seizure activity. © 2009 Wiley-Liss, Inc. [source] Melatonin attenuates kainic acid-induced hippocampal neurodegeneration and oxidative stress through microglial inhibitionJOURNAL OF PINEAL RESEARCH, Issue 2 2003Seung-Yun Chung Abstract:,The antioxidant and anti-inflammatory effects of melatonin on kainic acid (KA)-induced neurodegeneration in the hippocampus were evaluated in vivo. It has been suggested that the pineal secretory product, melatonin, protects neurons in vitro from excitotoxicity mediated by kainate-sensitive glutamate receptors, and from oxidative stress-induced DNA damage and apoptosis. In this study, we injected 10 mg/kg kainate intraperitoneally (i.p.) into adult male Sprague-Dawley rats. This results in selective neuronal degeneration accompanied by intense microglial activation and triggers DNA damage in the hippocampus. We tested the in vivo efficacy of melatonin in preventing KA-induced neurodegeneration, oxidative stress and neuroinflammation in the hippocampus. Melatonin (2.5 mg/kg, i.p.) was given 20 min before, immediately after, and 1 and 2 hr after KA administration. Rats were killed 72 hr later and their hippocampi were examined for evidence of DNA damage (in situ dUTP end-labeling, i.e. TUNEL staining), cell viability (hematoxylin and eosin staining), and microglial (isolectin-B4 histochemistry) and astroglial responses (glial fibrillary acidic protein immunohistochemistry), as well as lipid peroxidation (4-hydroxynonenal immunohistochemistry). A cumulative dose of 10 mg/kg melatonin attenuates KA-induced neuronal death, lipid peroxidation, and microglial activation, and reduces the number of DNA breaks. A possible mechanism for melatonin-mediated neuroprotection involves its antioxidant and anti-inflammatory actions. The present data suggest that melatonin is potentially useful in the treatment of acute brain pathologies associated with oxidative stress-induced neuronal damage such as epilepsy, stroke, and traumatic brain injury. [source] The effects of activated protein C and prostacyclin on arterial oxygenation and protein leakage in the lung and the gut under endotoxaemia in the ratACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2008M. DUBNIKS Background: Based on the anti-adhesive/anti-aggregatory and permeability-reducing properties of activated protein C (APC) and prostacyclin (PGI2), we analysed and compared these substances regarding their efficacy in counteracting transcapillary leakage of albumin in the lung and the gut, and in improving arterial oxygenation under a condition of inflammation. Methods: The randomized and blinded study was performed on 31 adult male Sprague-Dawley rats. Inflammation was induced by continuous infusion of Escherichia coli endotoxin (lipopolysaccharide, LPS). Six hours after the start of the LPS infusion (240,000 U/kg/h), a simultaneous infusion of saline (control group) or 8 ,g/kg/min of human recombinant APC or 2 ng/kg/min of PGI2 was started and continued for 24 h (n=8 per group). The study also included a sham group. Transcapillary leakage of albumin was measured from the ratio between tissue radioactivity [counts per minute (cpm)/g tissue] and actual amount of radioactivity given (cpm/g body weight of 125I-albumin). Oxygenation was assessed from arterial and central venous blood samples. Results: LPS induced albumin leakage in the gut and the lung, and impaired blood oxygenation. In the lung, the leakage was lower in the PGI2 group than in the APC and the control groups (P<0.05). In the gut, it was lower in the APC and the PGI2 groups than in the control group (P<0.05). Oxygenation was better in the APC and PGI2 groups than in the control group. Conclusion: Our data suggest that both APC and low-dose PGI2 are beneficial in LPS-induced inflammation in the rat, by reducing albumin leakage and improving blood oxygenation. [source] FK506 and Sildenafil Promote Erectile Function Recovery after Cavernous Nerve Injury Through Antioxidative MechanismsTHE JOURNAL OF SEXUAL MEDICINE, Issue 4i 2007Gwen Lagoda MS ABSTRACT Introduction., Immunophilin ligands and phosphodiesterase type 5 (PDE5) inhibitors are touted to promote erectile function recovery after cavernous nerve (CN) injury. However, the mechanisms for their effects remain unclear. Aim., To compare the erection recovery effects of the immunophilin ligand FK506 and the PDE5 inhibitor sildenafil after CN injury and determine whether they involve antioxidative and/or antiapoptotic mechanisms. Methods., Initial experiments established conditions of our CN injury model in adult male Sprague-Dawley rats. Subsequently, we evaluated treatment effects 14 days after: (i) unilateral CN injury (UNI) + saline (vehicle control); (ii) UNI + FK506 (5 mg/kg once daily, subcutaneous ×5 days); (iii) UNI + sildenafil (20 mg/kg every 8 hours, subcutaneous ×7 days); (iv) UNI + FK506/sildenafil; and (v) sham surgery. Main Outcome Measures., Intracavernous pressure (ICP) measurement after CN electrical stimulation to assess erectile function and Western blot analysis of expressions of glutathione peroxidase (GPX; antioxidant enzyme), nitrotyrosine (NT; oxidative stress marker), and phosphorylated and total Akt (antiapoptotic factor) in penes. Results., In the UNI model, GPX expression was increased at Days 1 and 7, while p-Akt expression decreased at Day 1 and returned to baseline at Day 7. GPX expression was significantly higher in the UNI + FK506 group compared with the saline-treated group (P < 0.05). ICP increased in all treatment groups compared with that of the saline-treated group (P < 0.05). NT levels were increased after saline treatment (P < 0.05) but not after FK506 and sildenafil treatment, alone or in combination. GPX was localized to nerves coursing through the penis and to smooth muscle and endothelium of the dorsal vein and arteries. Conclusions., Both FK506 and sildenafil protect erectile function after CN injury by decreasing oxidative stress-associated tissue damage. FK506 may act through increased GPX activity. Further research is required to elucidate mechanisms associated with the beneficial effect of sildenafil. Lagoda G, Jin L, Lehrfeld TJ, Liu T, and Burnett AL. FK506 and sildenafil promote erectile function recovery after cavernous nerve injury through antioxidative mechanisms. J Sex Med 2007;4:908,916. [source] Combinatorial treatments enhance recovery following facial nerve crush,,THE LARYNGOSCOPE, Issue 8 2010Nijee Sharma BS Abstract Objectives/Hypothesis: To investigate the effects of various combinatorial treatments, consisting of a tapering dose of prednisone (P), a brief period of nerve electrical stimulation (ES), and systemic testosterone propionate (TP) on improving functional recovery following an intratemporal facial nerve crush injury. Study Design: Prospective, controlled animal study. Methods: After a right intratemporal facial nerve crush, adult male Sprague-Dawley rats were divided into the following eight treatment groups: 1) no treatment, 2) P only, 3) ES only, 4) ES + P, 5) TP only, 6) TP + P, 7) ES + TP, and 8) ES + TP + P. For each group n = 4,8. Recovery of the eyeblink reflex and vibrissae orientation and movement were assessed. Changes in peak amplitude and latency of evoked response, in response to facial nerve stimulation, was also recorded weekly. Results: Brief ES of the proximal nerve stump most effectively accelerated the initiation of functional recovery. Also, ES or TP treatments enhanced recovery of some functional parameters more than P treatment. When administered alone, none of the three treatments improved recovery of complete facial function. Only the combinatorial treatment of ES + TP, regardless of the presence of P, accelerated complete functional recovery and return of normal motor nerve conduction. Conclusions: Our findings suggest that a combinatorial treatment strategy of using brief ES and TP together promises to be an effective therapeutic intervention for promoting regeneration following facial nerve injury. Administration of P neither augments nor hinders recovery. Laryngoscope, 2010 [source] The acute hypoxic ventilatory response under halothane, isoflurane, and sevoflurane anaesthesia in rats,ANAESTHESIA, Issue 3 2010N. Karanovic Summary The relative order of potency of anaesthetic agents on the hypoxic ventilatory response has been tested in humans, but animal data are sparse. We examined the effects of 1.4, 1.6, 1.8, and 2.0 MAC halothane, isoflurane, and sevoflurane on phrenic nerve activity in euoxia (baseline) and during acute normocapnic hypoxia (inspired oxygen fraction 0.09) in adult male Sprague-Dawley rats. With halothane, all animals became apnoeic even in euoxia, and the hypoxic response was completely abolished at all anaesthetic levels. With isoflurane, 5 of 14 animals exhibited phrenic nerve activity in euoxia at 1.4 MAC and demonstrated a hypoxic response (302% of baseline activity), but all became apnoeic and lost the hypoxic response at higher doses. With sevoflurane, phrenic nerve activity and a hypoxic response was preserved in at least some animals at all doses (i.e. even the highest dose of 2.0 MAC). Similar to the rank order of potency previously observed in humans, the relative order of potency of depression of the hypoxic ventilatory response in rats was halothane (most depressive) > isoflurane > sevoflurane (p = 0.01 for differences between agents). [source] Uncontrolled Hemorrhage in Insulin-dependent Diabetic RatsACADEMIC EMERGENCY MEDICINE, Issue 8 2009Eric J. Morley MD Abstract Objectives:, Diabetes mellitus (DM) is a known risk factor for higher morbidity and mortality after trauma. The authors tested the hypothesis that there is a difference in the response to uncontrolled hemorrhage between normal euglycemic rats and insulin-dependent diabetic rats. Methods:, Thirty-one adult male Sprague-Dawley rats were used in this study. Fifteen streptozocin (STZ)-injected rats became diabetic (DM+) 2 weeks after treatment. Sixteen rats served as nondiabetic controls (DM,). All rats were anesthetized with Althesin and their femoral arteries were catheterized via cutdown, allowing continuous monitoring of vital signs. Sixteen (eight DM,, eight DM+) rats underwent uncontrolled hemorrhage by 75% tail amputation. Fifteen (eight DM,, seven DM+) rats served as nonhemorrhage controls. The mean arterial pressure (MAP), lactate, and cumulative hemorrhage volume per 100 g were measured prehemorrhage and then every 15 minutes posthemorrhage for 2 hours. Data were reported as mean ± standard deviation. Interval data were analyzed by analysis of variance (two tails, , = 0.05). Results:, Prehemorrhage glucose was significantly higher (p < 0.001) in the DM+ (357.9 ± 22.2 mg/dL) versus DM, (125.7 ± 9.7 mg/dL) rats. At baseline, there was no significant difference in weight, MAP, or lactate between DM+ and DM, rats. Body-weight-adjusted mean cumulative hemorrhage volume was significantly greater (p < 0.04) in diabetic rats (2.52 ± 0.15 cm3/100 g body weight) than the nondiabetic rats (1.86 ± 0.25 cm3/100 g body weight). Conclusions:, Compared to nondiabetic rats, diabetic rats suffered a greater blood loss after the same uncontrolled vascular injury. [source] | |||||||||||||