Long-term effects of feeding aflatoxin-contaminated market peanut oil to Sprague-Dawley rats

1981 ◽  
Vol 19 ◽  
pp. 179-183 ◽  
Author(s):  
L.Y.Y. Fong ◽  
W.C. Chan
2016 ◽  
pp. 133-143 ◽  
Author(s):  
I. STIPICA ◽  
I. PAVLINAC DODIG ◽  
R. PECOTIC ◽  
Z. DOGAS ◽  
Z. VALIC ◽  
...  

This study was undertaken to determine pattern sensitivity of phrenic nerve plasticity in respect to different respiratory challenges. We compared long-term effects of intermittent and continuous hypercapnic and hypoxic stimuli, and combined intermittent hypercapnia and hypoxia on phrenic nerve plasticity. Adult, male, urethane-anesthetized, vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats were exposed to: acute intermittent hypercapnia (AIHc or AIHcO2), acute intermittent hypoxia (AIH), combined intermittent hypercapnia and hypoxia (AIHcH), continuous hypercapnia (CHc), or continuous hypoxia (CH). Peak phrenic nerve activity (pPNA) and burst frequency were analyzed during baseline (T0), hypercapnia or hypoxia exposures, at 15, 30, and 60 min (T60) after the end of the stimulus. Exposure to acute intermittent hypercapnia elicited decrease of phrenic nerve frequency from 44.25±4.06 at T0 to 35.29±5.21 at T60, (P=0.038, AIHc) and from 45.5±2.62 to 37.17±3.68 breaths/min (P=0.049, AIHcO2), i.e. frequency phrenic long term depression was induced. Exposure to AIH elicited increase of pPNA at T60 by 141.0±28.2 % compared to baseline (P=0.015), i.e. phrenic long-term facilitation was induced. Exposure to AIHcH, CHc, or CH protocols failed to induce long-term plasticity of the phrenic nerve. Thus, we conclude that intermittency of the hypercapnic or hypoxic stimuli is needed to evoke phrenic nerve plasticity.


2021 ◽  
Author(s):  
Miguel Farinha-Ferreira ◽  
Nádia Rei ◽  
Jo&atildeo Fonseca-Gomes ◽  
Catarina Miranda-Lourenço ◽  
Paula Serr&atildeo ◽  
...  

Chronic adolescent cannabinoid receptor agonist exposure has been shown to lead to persistent increases in depressive-like behaviors. This has been a key obstacle to the development of cannabinoid-based therapeutics. However, most of the published work has been performed with only three compounds, namely ∆9-tetrahydrocannabinol, CP55,940 and WIN55,212-2. Hypothesizing that different compounds may lead to distinct outcomes, we herein used the highly potent CB1R/CB2R full agonist HU-210, and first aimed at replicating cannabinoid-induced long-lasting effects, by exposing adolescent female Sprague-Dawley rats to increasing doses of HU-210, for 11 days and testing them at adulthood, after a 30-day drug washout. Surprisingly, HU-210 did not significantly impact adult anxious- or depressive-like behaviors. We then tested whether chronic adolescent HU-210 treatment resulted in short-term (24h) alterations in depressive-like behavior. Remarkably, HU-210 treatment simultaneously induced marked antidepressant- and prodepressant-like responses, in the modified forced swim (mFST) and sucrose preference tests (SPT), respectively. Hypothesizing that mFST results were a misleading artifact of HU-210-induced behavioral hyperreactivity to stress, we assessed plasmatic noradrenaline and corticosterone levels, under basal conditions and following an acute swim-stress episode. Notably, we found that while HU-210 did not alter basal noradrenaline or corticosterone levels, it greatly augmented the stress-induced increase in both. Our results show that, contrary to previously studied cannabinoid receptor agonists, HU-210 does not induce persisting depressive-like alterations, despite inducing marked short-term increases in stress-induced reactivity. By showing that not all cannabinoid receptor agonists may induce long-term negative effects, these results hold significant relevance for the development of cannabinoid-based therapeutics.


2019 ◽  
Vol 41 (1-2) ◽  
pp. 44-55 ◽  
Author(s):  
Sarah A. Jablonski ◽  
Michael T. Williams ◽  
Charles V. Vorhees

Methamphetamine (MA) abuse is a worldwide issue that produces health and cognitive effects in the user. MA is abused by some women who then become pregnant and expose their developing child to the drug. Preclinical rodent models demonstrate cognitive deficits following developmental MA exposure, an effect observed in children exposed to MA in utero. To determine if the dopamine receptor D1 (DRD1) is involved in the learning and memory deficits following MA exposure, male Sprague-Dawley rats were treated 4 times daily at 2 h intervals with 0 (saline) or 10 mg/kg of MA from postnatal day (P)6–15, 30 min after 0.5, 1.0, or 2.0 mg/kg SCH23390. Cincinnati water maze testing began on P30, and the high dose of SCH23390 blocked the learning deficits induced by MA with no effect from the lower doses. Morris water maze (MWM) learning deficits following MA were not protected by SCH23390, although there was a non-dose dependent effect in the acquisition phase. Locomotor deficits induced by MA were reversed by all doses of SCH23390. There were no effects of MA on criterion to trial passive avoidance. Taken together, these data show that behaviors that are dependent on the striatum are better protected with the DRD1 antagonist during MA treatment than the hippocampally mediated spatial learning in the MWM. This suggests that multiple mechanisms exist for the deficits induced by neonatal MA administration.


1996 ◽  
Vol 271 (5) ◽  
pp. H1746-H1754 ◽  
Author(s):  
M. I. Heron ◽  
K. Rakusan

Neonatal hypo- and hyperthyroid effects on coronary arteriolar geometry were examined in newborn male Sprague-Dawley rats treated for 12 or 28 days with either triiodothyronine or propylthiouracil. Long-term effects were assessed in weaned rats 52 days after stopping treatment. Influence of both neonatal conditions was more pronounced after 28 days. Neonatal hyperthyroidism induced cardiac hypertrophy; neonatal hypothyroidism attenuated cardiac growth. Hyperthyroid rats had similar arteriolar and capillary numerical densities and arteriolar length density but significantly greater (P < 0.05) total arteriolar length than control. Hypothyroid rats had similar arteriolar numerical and length densities, greater capillary numerical density (P < 0.05), but markedly lower total arteriolar length (P < 0.01) than control. Results suggest that neonatal hyperthyroidism stimulates arteriolar and capillary growth, whereas neonatal hypothyroidism attenuates arteriolar but not capillary growth. After cessation of treatment, total arteriolar length in previously hyperthyroid rats did not change despite increased cardiac mass, whereas previously hypothyroid rats demonstrated marked increases in both cardiac mass and total arteriolar length (P < 0.01). These results indicate a lasting inhibitory effect of early hyperthyroidism on subsequent arteriolar growth.


2018 ◽  
pp. 975-983 ◽  
Author(s):  
Y. LI ◽  
W. ZHANG ◽  
R. SHI ◽  
M. SUN ◽  
L. ZHANG ◽  
...  

Prenatal exposure to caffeine can cause developmental problems. This study determined chronic influence of prenatal caffeine at relatively higher doses on cognitive functions in the rat offspring. Pregnant Sprague-Dawley rats (4-month-old) were exposed to caffeine (20 mg/kg, twice a day) for whole pregnancy from gestational day 4. Fetal and offspring body and brain weight was measured. Learning and memory were tested in adult offspring with Morris water maze. Learning and memory-related receptors were measured. The exposure to prenatal caffeine not only caused fetal growth restriction, but also showed long-term effects on learning and memory in the offspring. The caffeine offspring exhibited longer escape latency and path length in navigation testing. The number of passing the target was significantly reduced in those offspring. The expression of adenosine A1 and A2A receptors, nuclear PKA Cα, Cβ subunits, and pCREB were significantly increased in the fetal and neonatal brain, and suppressed in the hippocampus of the adult offspring. The expression of BDNF and TrkB were reduced regardless of various ages. The results suggest that intrauterine programming dysfunction of adenosine receptors and the down-stream of cAMP/PKA/pCREB system may play an important role in prenatal caffeine induced cognition disorders in the adult offspring.


2021 ◽  
pp. 1-20
Author(s):  
Juandré Lambertus Bernardus Saayman ◽  
Stephanus Frederik Steyn ◽  
Christiaan Beyers Brink

Abstract Objective: To investigate the long-term effects of juvenile sub-chronic sildenafil (SIL) treatment on the depressive-like behaviour and hippocampal brain-derived neurotrophic factor (BDNF) levels of adult Sprague-Dawley (SD) versus Flinders Sensitive Line (FSL) rats. Methods: SD and FSL rats were divided into pre-pubertal and pubertal groups, whereafter 14-day saline or SIL treatment was initiated. Pre-pubertal and pubertal rats were treated from postnatal day 21 (PND21) and PND35, respectively. The open field and forced swim tests (FST) were performed on PND60, followed by hippocampal BDNF level analysis one day later. Results: FSL rats displayed greater immobility in the FST compared to SD rats (p < 0.0001), which was reduced by SIL (p < 0.0001), regardless of treatment period. Hippocampal BDNF levels were unaltered by SIL in all treatment groups (p > 0.05). Conclusion: Juvenile sub-chronic SIL treatment reduces the risk of depressive-like behaviour manifesting during young adulthood in genetically susceptible rats.


2006 ◽  
Vol 82 (4) ◽  
pp. 285-291 ◽  
Author(s):  
H. J. Lee ◽  
S. H. Kim ◽  
S. Y. Choi ◽  
Y. M. Gimm ◽  
J. K. Pack ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document