Brain Aromatase in Control Versus Castrated Norway Brown, Sprague-Dawley and Wistar Adult Rats

Abstract Background Preclinical and clinical studies have indicated that impaired endogenous synthesis of glutathione during early postnatal development plays a significant role in the pathophysiology of schizophrenia. Moreover, some studies have suggested that antidepressants are able to increase the activity of atypical antipsychotics which may efficiently improve the treatment of negative and cognitive symptoms of schizophrenia. Methods In the present study, we investigated the influence of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behavior and BDNF mRNA expression in adult rats exposed to glutathione deficit during early postnatal development. Male pups between the postnatal days p5–p16 were treated with the inhibitor of glutathione synthesis, BSO (L-buthionine-(S,R)-sulfoximine) and the dopamine uptake inhibitor, GBR 12,909 alone or in combination. Escitalopram and aripiprazole were given repeatedly for 21 days before the tests. On p90–92 rats were evaluated in the behavioral and biochemical tests. Results BSO given alone and together with GBR 12,909 induced deficits in the studied behavioral tests and decreased the expression of BDNF mRNA. Repeated aripiprazole administration at a higher dose reversed these behavioral deficits. Co-treatment with aripiprazole and an ineffective dose of escitalopram also abolished the behavioral deficits in the studied tests. Conclusion The obtained data indicated that the inhibition of glutathione synthesis in early postnatal development induced long-term deficits corresponding to schizophrenia-like behavior and decreased the BDNF mRNA expression in adult rats, and these behavioral deficits were reversed by repeated treatment with a higher dose of aripiprazole and also by co-treatment with aripiprazole and ineffective dose of escitalopram.

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Effects of adolescent caffeine consumption on cocaine self-administration and reinstatement of cocaine seeking

Journal of Psychopharmacology ◽

10.1177/0269881118812098 ◽

2018 ◽

Vol 33 (1) ◽

pp. 132-144

Author(s):

Tracey A Larson ◽

Casey E O’Neill ◽

Michaela P Palumbo ◽

Ryan K Bachtell

Keyword(s):

Dose Response ◽

Extinction Training ◽

Schedules Of Reinforcement ◽

Sprague Dawley ◽

Self Administration ◽

Caffeine Consumption ◽

Adult Rats ◽

Sprague Dawley Rats ◽

Cocaine Seeking ◽

Administration Procedure

Background: Caffeine consumption by children and adolescents has risen dramatically in recent years, yet the lasting effects of caffeine consumption during adolescence remain poorly understood. Aim: These experiments explore the effects of adolescent caffeine consumption on cocaine self-administration and seeking using a rodent model. Methods: Sprague-Dawley rats consumed caffeine for 28 days during the adolescent period. Following the caffeine consumption period, the caffeine solution was replaced with water for the remainder of the experiment. Age-matched control rats received water for the duration of the study. Behavioral testing in a cocaine self-administration procedure occurred during adulthood (postnatal days 62–82) to evaluate how adolescent caffeine exposure influenced the reinforcing properties of cocaine. Cocaine seeking was also tested during extinction training and reinstatement tests following cocaine self-administration. Results: Adolescent caffeine consumption increased the acquisition of cocaine self-administration and increased performance on different schedules of reinforcement. Consumption of caffeine in adult rats did not produce similar enhancements in cocaine self-administration. Adolescent caffeine consumption also produced an upward shift in the U-shaped dose response curve on cocaine self-administration maintained on a within-session dose-response procedure. Adolescent caffeine consumption had no effect on cocaine seeking during extinction training or reinstatement of cocaine seeking by cues or cocaine. Conclusions: These findings suggest that caffeine consumption during adolescence may enhance the reinforcing properties of cocaine, leading to enhanced acquisition that may contribute to increased addiction vulnerability.

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Serotonin2 receptors mediate respiratory recovery after cervical spinal cord hemisection in adult rats

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.6.2665 ◽

2001 ◽

Vol 91 (6) ◽

pp. 2665-2673 ◽

Cited By ~ 46

Author(s):

Shi-Yi Zhou ◽

Gregory J. Basura ◽

Harry G. Goshgarian

Keyword(s):

Spinal Cord ◽

Receptor Antagonist ◽

Phrenic Nerve ◽

Cervical Spinal Cord ◽

Sprague Dawley ◽

Related Activity ◽

Adult Rats ◽

Cord Injury ◽

Respiratory Recovery ◽

Spinal Cord Hemisection

The aim of the present study was to specifically investigate the involvement of serotonin [5-hydroxytryptamine (5-HT2)] receptors in 5-HT-mediated respiratory recovery after cervical hemisection. Experiments were conducted on C2 spinal cord-hemisected, anesthetized (chloral hydrate, 400 mg/kg ip), vagotomized, pancuronium- paralyzed, and artificially ventilated female Sprague-Dawley rats in which CO2 levels were monitored and maintained. Twenty-four hours after spinal hemisection, the ipsilateral phrenic nerve displayed no respiratory-related activity indicative of a functionally complete hemisection. Intravenous administration of the 5-HT2A/2C-receptor agonist (±)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) induced respiratory-related activity in the phrenic nerve ipsilateral to hemisection under conditions in which CO2 was maintained at constant levels and augmented the activity induced under conditions of hypercapnia. The effects of DOI were found to be dose dependent, and the recovery of activity could be maintained for up to 2 h after a single injection. DOI-induced recovery was attenuated by the 5-HT2-receptor antagonist ketanserin but not with the 5-HT2C-receptor antagonist RS-102221, suggesting that 5-HT2A and not necessarily 5-HT2C receptors may be involved in the induction of respiratory recovery after cervical spinal cord injury.

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Protective effects of dietary fibre against manganese-induced neurobehavioral aberrations in rats

Archives of Industrial Hygiene and Toxicology ◽

10.2478/10004-1254-63-2012-2149 ◽

2012 ◽

Vol 63 (3) ◽

pp. 263-270 ◽

Cited By ~ 3

Author(s):

Xiu-Quan Shi ◽

Wei Yan ◽

Ke-Yue Wang ◽

Qi-Yuan Fan ◽

Yan Zou

Keyword(s):

Cerebral Cortex ◽

Animal Feed ◽

Oral Exposure ◽

Protective Effects ◽

Sprague Dawley ◽

Adult Rats ◽

Neurobehavioral Performance ◽

Sprague Dawley Rats ◽

Applied Dose ◽

Mn Concentrations

We tested the hypothesis that dietary fi bre (DF) has protective effects against manganese (Mn)-induced neurotoxicity. Forty-eight one-month old Sprague-Dawley rats were randomly divided into six groups: control, 16 % DF, Mn (50 mg kg-1 body weight), Mn+ 4 % DF, Mn+ 8 % DF, and Mn+ 16 % DF. After oral administration of Mn (as MnCl2) by intragastric tube during one month, we determined Mn concentrations in the blood, liver, cerebral cortex, and stool and tested neurobehavioral functions. Administration of Mn was associated with increased Mn concentration in the blood, liver, and cerebral cortex and increased Mn excretion in the stool. Aberrations in neurobehavioral performance included increases in escape latency and number of errors and decrease in step-down latency. Irrespective of the applied dose, the addition of DF in forage decreased tissue Mn concentrations and increased Mn excretion rate in the stool by 20 % to 35 %. All neurobehavioral aberrations were also improved. Our fi ndings show that oral exposure to Mn may cause neurobehavioral abnormalities in adult rats that could be effi ciently alleviated by concomitant supplementation of DF in animal feed.

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Kinetic impairment of nitrogen and muscle glutamine metabolisms in old glucocorticoid-treated rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1999.276.3.e558 ◽

1999 ◽

Vol 276 (3) ◽

pp. E558-E564 ◽

Cited By ~ 13

Author(s):

Regine Minet-Quinard ◽

Christophe Moinard ◽

Françoise Villie ◽

Stephane Walrand ◽

Marie-Paule Vasson ◽

...

Keyword(s):

Control Group ◽

Synthetase Activity ◽

Aged Rats ◽

Sprague Dawley ◽

Adult Rats ◽

Glucocorticoid Treatment ◽

Sprague Dawley Rats ◽

End Of Treatment ◽

Catabolic State ◽

Old Rats

Aged rats are more sensitive to injury, possibly through an impairment of nitrogen and glutamine (Gln) metabolisms mediated by glucocorticoids. We studied the metabolic kinetic response of adult and old rats during glucocorticoid treatment. The male Sprague-Dawley rats were 24 or 3 mo old. Both adult and old rats were divided into 7 groups. Groups labeled G3, G5, and G7 received, by intraperitoneal injection, 1.50 mg/kg of dexamethasone (Dex) for 3, 5, and 7 days, respectively. Groups labeled G3PF, G5PF, and G7PF were pair fed to the G3, G5, or G7 groups and were injected with an isovolumic solution of NaCl. One control group comprised healthy rats fed ad libitum. The response to aggression induced specifically by Dex (i.e., allowing for variations in pair-fed controls) appeared later in the aged rats (decrease in nitrogen balance from day 1 in adults but only from day 4 in old rats). The adult rats rapidly adapted to Dex treatment, whereas the catabolic state worsened until the end of treatment in the old rats. Gln homeostasis was not maintained in the aged rats; despite an early increase in muscular Gln synthetase activity, the Gln pool was depleted. These results suggest a kinetic impairment of both nitrogen and muscle Gln metabolisms in response to Dex with aging.

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Synergistic toxicity in an in vivo model of neurodegeneration through the co-expression of human TDP-43M337V and tauT175D protein

Acta Neuropathologica Communications ◽

10.1186/s40478-019-0816-1 ◽

2019 ◽

Vol 7 (1) ◽

Cited By ~ 2

Author(s):

Alexander J. Moszczynski ◽

Madeline Harvey ◽

Niveen Fulcher ◽

Cleusa de Oliveira ◽

Patrick McCunn ◽

...

Keyword(s):

Tau Protein ◽

Sensorimotor Gating ◽

In Vivo Model ◽

Motor Deficits ◽

Sprague Dawley ◽

Tau Pathology ◽

Adult Rats ◽

Sprague Dawley Rats ◽

Somatic Gene Transfer

Abstract Although it has been suggested that the co-expression of multiple pathological proteins associated with neurodegeneration may act synergistically to induce more widespread neuropathology, experimental evidence of this is sparse. We have previously shown that the expression of Thr175Asp-tau (tauT175D) using somatic gene transfer with a stereotaxically-injected recombinant adeno-associated virus (rAAV9) vector induces tau pathology in rat hippocampus. In this study, we have examined whether the co-expression of human tauT175D with mutant human TDP-43 (TDP-43M337V) will act synergistically. Transgenic female Sprague-Dawley rats that inducibly express mutant human TDP-43M337V using the choline acetyltransferase (ChAT) tetracycline response element (TRE) driver with activity modulating tetracycline-controlled transactivator (tTA) were utilized in these studies. Adult rats were injected with GFP-tagged tau protein constructs in a rAAV9 vector through bilateral stereotaxic injection into the hippocampus. Injected tau constructs were: wild-type GFP-tagged 2N4R human tau (tauWT; n = 8), GFP-tagged tauT175D 2N4R human tau (tauT175D, pseudophosphorylated, toxic variant, n = 8), and GFP (control, n = 8). Six months post-injection, mutant TDP-43M337V expression was induced for 30 days. Behaviour testing identified motor deficits within 3 weeks after TDP-43 expression irrespective of tau expression, though social behaviour and sensorimotor gating remained unchanged. Increased tau pathology was observed in the hippocampus of both tauWT and tauT175D expressing rats and tauT175D pathology was increased in the presence of cholinergic neuronal expression of human TDP-43M337V. These data indicate that co-expression of pathological TDP-43 and tau protein exacerbate the pathology associated with either individual protein.

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Relationship between preferred ambient temperature and autonomic thermoregulatory function in rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.252.6.r1130 ◽

1987 ◽

Vol 252 (6) ◽

pp. R1130-R1137 ◽

Cited By ~ 8

Author(s):

C. J. Gordon

Keyword(s):

Ambient Temperature ◽

Thermal Conductance ◽

Sprague Dawley ◽

Adult Rats ◽

Evaporative Water ◽

Longitudinal Temperature Gradient ◽

Longitudinal Temperature ◽

Thermoregulatory Function ◽

Colonic Temperature ◽

Experiment Individual

This study was designed to elucidate the relationships between behavioral and autonomic thermoregulation in three common strains of the laboratory rat. In one experiment eight adult rats of the Sprague-Dawley (SD), Long-Evans (LE), and Fischer (FCH) strains were repeatedly placed in a longitudinal temperature gradient while their preferred ambient temperature (Ta) was recorded. The mean preferred Ta's (+/- SE) for the SD, LE, and FCH strains were 24.9 +/- 0.4, 19.8 +/- 0.3, and 23.4 +/- 0.3 degrees C, respectively. In another experiment, individual adult rats of the same strains were placed in an environmental chamber thermostabilized at 2 degrees C intervals from 14 to 36 degrees C for 90 min while metabolic rate (MR), evaporative water loss (EWL), thermal conductance (C), and colonic temperature (Tcol) were determined. All three strains exhibited a minimal MR at a Ta of 30 degrees C. As Ta decreased below 30 degrees C, MR increased in a nonlinear fashion. EWL and C were minimal at cool Ta's and increased gradually with an elevation in Ta. All three strains maintained a normal Tcol between Ta's of 14 to 30 degrees C. The FCH strain exhibited the best control of Tcol at Ta's above 30 degrees C. Generally, one would predict that the preferred Ta would be associated with minimal thermoregulatory effort. However, the rat is unusual from other rodents (e.g., mouse, hamster, and guinea pig) in that the preferred Ta is well below the lower critical Ta for elevating MR.

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Cerebral cortex does not modulate “regulated” decrease in core temperature during hypoxemia in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.4.r1158 ◽

1998 ◽

Vol 274 (4) ◽

pp. R1158-R1161

Author(s):

Evvi-Lynn M. Rollins ◽

James E. Fewell

Keyword(s):

Cerebral Cortex ◽

Core Temperature ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Temperature Response ◽

Sprague Dawley ◽

Adult Rats ◽

The Core ◽

Sprague Dawley Rats ◽

Before And After

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.

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Potentiation of hypoxic ventilatory response by hyperoxia in the conscious rat: putative role of nitric oxide

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.1.129 ◽

1998 ◽

Vol 85 (1) ◽

pp. 129-132 ◽

Cited By ~ 31

Author(s):

David Gozal

Keyword(s):

Nitric Oxide ◽

Ventilatory Response ◽

Minute Ventilation ◽

Hypoxic Ventilatory Response ◽

Sprague Dawley ◽

Conscious Rat ◽

Adult Rats ◽

Hyperoxic Exposure ◽

Essential Components ◽

Oxide Synthase

In humans, the hypoxic ventilatory response (HVR) is augmented when preceded by a short hyperoxic exposure (Y. Honda, H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. J. Appl. Physiol. 81: 1627–1632, 1996). To examine whether neuronal nitric oxide synthase (nNOS) is involved in such hyperoxia-induced HVR potentiation, 17 male Sprague-Dawley adult rats underwent hypoxic challenges (10% O2-5% CO2-balance N2) preceded either by 10 min of room air (−O2) or of 100% O2(+O2). At least 48 h later, similar challenges were performed after the animals received the selective nNOS inhibitor 7-nitroindazole (25 mg/kg ip). In −O2 runs, minute ventilation (V˙e) increased from 121.3 ± 20.5 (SD) ml/min in room air to 191.7 ± 23.8 ml/min in hypoxia ( P< 0.01). After +O2,V˙e increased from 114.1 ± 19.8 ml/min in room air to 218.4 ± 47.0 ml/min in hypoxia (+O2 vs. −O2: P < 0.005, ANOVA). After 7-nitroindazole administration, HVR was not affected in the −O2 treatment group withV˙e increasing from 113.7 ± 17.8 ml/min in room air to 185.8 ± 35.0 ml/min in hypoxia ( P < 0.01). However, HVR potentiation in +O2-exposed animals was abolished (111.8 ± 18.0 ml/min in room air to 184.1 ± 35.6 ml/min in hypoxia; +O2 vs. −O2: P not significant). We conclude that in the conscious rat nNOS activation mediates essential components of the HVR potentiation elicited by a previous short hyperoxic exposure.

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