Ability Of Adult Rats Research Articles

ApoE transiently regulates hippocampus amyloid-beta deposition to stable learning and memory ability in adult rats exposed in sevoflurane.

Post-operative cognitive dysfunction (POCD) is a common central nervous system complication after surgery. Inhaled anesthetic sevoflurane is thought to have harmful effects on the developing and aged nerves, but its effects on adults' nervous system are less studied and the mechanism is not clear. Male adult rats were divided into control group and sevoflurane group. Rats from sevoflurane group were received 3.2% sevoflurane + carrier gas (1L/min O2+1L/min air) for 2h, while control group received carrier gas for 2h. Each group was subsequently divided into 3 subgroups according to the Day 1, Day 3, Day 7 after sevoflurane anesthesia. Morris Water Maze, amyloid-beita (Abeta) and apolipoprotein E (ApoE) mRNA in hippocampus were analyzed. Then, adult ApoE-/- rats were also divided into control group and sevoflurane group. Each group was divided into 3 subgroups according to Day 1, Day 3 and Day 7. Abeta mRNA and protein expression in hippocampus were analyzed. Compared with the control group, hippocampal Abeta mRNA and protein expression in rats from sevoflurane group significantly increased in hippocampus on Day 7, while ApoE mRNA and protein expression increased on Day 1 and Day 3. There was no difference in times of crossing platforms, time during platform, times across platform quadrant and time percent during platform quadrant between each group. Compared with the control group, hippocampal Abeta and ApoE-/- rats in sevoflurane group did not change. ApoE modulates hippocampal Abeta deposition and stabilizes learning and memory ability in adult rats after sevoflurane exposure, but this effect is not constant.

Effects of Transient Restraint Stress on the Plasticity of the Cortical Areas of the Brain and Cognitive Functions in Adult Rats with Normal and Disturbed Embryogenesis

The aim of the present work was to analyze changes in the numbers of labile synaptopodin-positive dendritic spines in the parietal cortex and hippocampal field CA1 and the ability of adult rats to remember after repeated transient restraint stress (5 min daily for 10 days). These parameters were compared in animals with normal development and in those subjected to hypoxia during embryogenesis (E14, 7% O2, 3 h). Shortterm and long-term memory were degraded in adult rats with normal embryogenesis subjected to restraint stress, and the number of labile spines was decreased in hippocampal field CA1 (by 17.3 ± 10.4%, p ≤ 0.05) and increased in the molecular layer of the parietal cortex (by 36.9 ± 9.2%) compared with intact control animals. Rats subjected to prenatal hypoxia, regardless of whether or not they had been subjected to restraint stress at the adult stage or not, showed impairments to both short-term and long-term memory, along with decreases in the numbers of labile spines in the hippocampus (by 22.9 ± 10.5%) and the parietal cortex (by 28.1 ± 9.3%). These results lead to the conclusion that increases in plasticity, supporting adaptive behavior in the animals, occur in neural networks in the neocortex in response to repeated transient stress only after normal brain formation during embryogenesis, while impairments to embryogenesis led to decreases in plasticity and the adaptive potentials of the nervous system in further ontogeny.

Long-lasting effects of prenatal dietary choline availability on object recognition memory ability in adult rats

Choline is an essential nutrient required for early development. Previous studies have shown that prenatal choline availability influences adult memory abilities depending on the medial temporal lobe integrity. The relevance of prenatal choline availability on object recognition memory was assessed in adult Wistar rats. Three groups of pregnant Wistar rats were fed from E12 to E18 with choline-deficient (0 g/kg choline chloride), standard (1.1 g/kg choline chloride), or choline-supplemented (5 g/kg choline chloride) diets. The offspring was cross-fostered to rat dams fed a standard diet during pregnancy and tested at the age of 3 months in an object recognition memory task applying retention tests 24 and 48 hours after acquisition. Although no significant differences have been found in the performance of the three groups during the first retention test, the supplemented group exhibited improved memory compared with both the standard and the deficient group in the second retention test, 48 hours after acquisition. In addition, at the second retention test the deficient group did not differ from chance. Taken together, the results support the notion of a long-lasting beneficial effect of prenatal choline supplementation on object recognition memory which is evident when the rats reach adulthood. The results are discussed in terms of their relevance for improving the understanding of the cholinergic involvement in object recognition memory and the implications of the importance of maternal diet for lifelong cognitive abilities.

Development of novel behavioral toxicity tests in rodents aimed for application to health risks in humans

We here introduce characteristic features of the novel behavioral tests, named Flavor Map and IntelliCage, recently developed to elucidate how maternal exposure to environmental chemicals affects executive brain functions in rats and mice. Flavor Map test requires rats to learn the existence of a schema of paired-associate of flavor and location, and enables to examine the short-term memory, long-term memory and paired-associative learning ability in adult rats. We have found that maternal exposure to a low dose of dioxin causes deficit in the paired-associative memory formation. Using the IntelliCage system, we have developed our own test protocol in mice. IntelliCage is versatile in terms of accommodation of as many as 16 mice at a time to monitor and record their basic physical activities and learning function. Our protocol successfully increases the efficiency of detection of the learning behavior with minimal variations between individual mice. We found that male mice born to dioxin-administered dams develop less behavioral flexibility. We believe that these behavioral tests can be used to study the executive functions in rats and mice, in biomedical research fields not only in toxicological study but also in animal psychology.

Neonatal ventral hippocampal lesions disrupt set-shifting ability in adult rats

Set-shifting in a T-maze task was assessed in rats with a neonatal ventral hippocampal lesion (NVHL), a proposed animal model of schizophrenia. NVHL animals tested as adults were impaired in shifting to a new rule; an increase in perseverative errors suggested that this impairment stemmed from an inability to suppress the previously learned strategy. The NVHL animals’ performance is reminiscent of humans with prefrontal damage and patients with schizophrenia.

Polychlorinated Biphenyls PCB 153 and PCB 126 Impair the Glutamate–Nitric Oxide–cGMP Pathway in Cerebellar Neurons in Culture by Different Mechanisms

Polychlorinated biphenyls (PCBs) are persistent organic pollutants present in human blood and milk. Exposure to PCBs during pregnancy and lactation leads to cognitive impairment in children. Perinatal exposure to PCB 153 or PCB 126 impairs the glutamate-nitric oxide-cGMP pathway in cerebellum in vivo and learning ability in adult rats. The aims of this work were: (1) to assess whether long-term exposure of primary cultures of cerebellar neurons to PCB 153 or PCB 126 reproduces the impairment in the function of the glutamate-nitric oxide-cGMP pathway found in rat cerebellum in vivo; (2) to provide some insight on the steps of the pathway affected by these PCBs; (3) to assess whether the mechanisms of interference of the pathway are different for PCB 126 and PCB 153. Both PCB 153 and PCB 126 increase basal levels of cGMP by different mechanisms. PCB 126 increases the amount of soluble guanylate cyclase while PCB 153 does not. PCB 153 reduces the amount of calmodulin while PCB 126 does not. Also both PCBs impair the function of the glutamate-nitric oxide-cGMP pathway by different mechanisms, PCB 153 impairs nitric oxide-induced activation of soluble guanylate cyclase and increase in cGMP while PCB 126 does not. PCB 126 reduces NMDA-induced increase in calcium while PCB 153 does not. When PCB 153 and PCB 126 exhibit the same effect, PCB 126 was more potent than PCB 153, as occurs in vivo.

Neonatal exposure to monosodium glutamate disrupts place learning ability in adult rats

The activation of glutamatergic NMDA receptors of the hippocampus is closely associated with expression of place learning. Neonatal exposure to monosodium glutamate leads to abnormal expression of NMDA receptor subunits in the hippocampus, but its effect on place learning is unknown. Place learning acquisition and retrieval were assessed in mature adult rats after subcutaneous injection of monosodium glutamate (4 mg/g body weight) in eight neonatal rat pups at postnatal days one, three, five, and seven. Eight untreated rats were used as controls. At four months of age, the rats were challenged over a period of nine days with a place learning task. The task used an acquisition–retrieval paradigm in a Morris maze. Place learning acquisition was impaired in the experimental rats, which were unable to reduce their escape latencies during the nine training days. Controls improved between the fifth and ninth days of training. Test trials showed that retrieval of spatial information was also impaired in the experimental animals. These results show that both place learning acquisition and retrieval abilities in mature rats are impaired by neonatal treatment with monosodium glutamate. These findings may be related to the abnormal expression of NMDA receptor subunits in the hippocampus.

Effects of Environmental Enrichment on Rate of Contextual Processing and Discriminative Ability in Adult Rats

The effect of environmental enrichment on conditioned freezing to contextual cues in adult Sprague-Dawley rats was examined. The freezing of both enriched-and standard-reared rats increased with the time spent in the chamber prior to shock. Both groups of rats showed equally low levels of contextual conditioning following a preshock period of 4 s and equally high levels following a 120-s preshock period. However, following a preshock period of 16 s enriched rats displayed more contextual conditioning than standard rats. That is, enriched rats appeared to process contextual information faster than their standard-reared counterparts. Enriched- reared rats also showed a greater ability to discriminate between the conditioning context and a similar but distinctive context. Hence, in addition to forming a representation of the context in memory more rapidly than standard-reared rats, enriched-reared rats also appear to form a more complex representation.

Mechanisms of impaired urinary concentrating ability in adult rats treated neonatally with enalapril.

Neonatal angiotensin-converting enzyme inhibition or angiotensin II type-1 receptor blockade induces irreversible renal histological abnormalities and an impaired urinary concentrating ability in the rat. The aim of the present study was to determine the pathophysiological mechanisms underlying the defect in urine concentration in adult rats treated neonatally with enalapril. Male Wistar rats received daily intraperitoneal injections of enalapril (10 mg kg(-1)) or saline vehicle from 3 to 24 days of age. Assessments of fluid handling and maximal urine osmolality (Uosm(max)), renal function and tubular free water reabsorption (T(c)H2O) under pentobarbital anaesthesia, renal tissue solute concentrations, renal aquaporin-2 (AQP2) expression, and kidney histology, were performed in 12-16-week-old rats. Uosm(max) (1488 +/- 109 vs. 2858 +/- 116 mosm kg(-1), P < 0.05) and maximal T(c)H2O were reduced in enalapril- vs. vehicle-treated rats after administration of 1-desamino-8-D-arginine vasopressin. Neonatally enalapril-treated rats showed marked papillary atrophy, a decrease in medullary tissue solute concentrations, and a reduction in AQP2 expression specifically in the inner medulla. Glomerular filtration rate, renal plasma flow and urinary excretion rates of sodium, potassium and chloride did not differ between groups. In conclusion, adult rats treated neonatally with enalapril showed a urinary concentrating defect of renal origin which primarily could be explained by the papillary atrophy. However, an impaired ability to generate medullary interstitial hypertonicity, and a decrease in inner medullary AQP2 expression, also seem to contribute to this defect.

Effects of Teeth Loss on Learning and Memory Ability in Adult Rats

Effects of Teeth Loss on Learning and Memory Ability in Adult Rats