Age at Puberty and First Litter Size in Early and Late Paired Rats12

Evans, Alida M.

doi:10.1095/biolreprod34.2.322

Cited by 31 publications

(20 citation statements)

References 13 publications

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“…Rats from 35–55 days old are adolescent or pubertal aged rats [25]. In this study, 90 SD rats (50-day-old), which are equivalent to 10–15 years old human subjects, were used.…”

Section: Discussionmentioning

confidence: 99%

Impact of Ketamine on Learning and Memory Function, Neuronal Apoptosis and Its Potential Association with miR-214 and PTEN in Adolescent Rats

Zhou

Wang

et al. 2014

PLoS ONE

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Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, is used as a general pediatric anesthetic and anti-depressive drug. Recent studies suggest that ketamine enhances neuronal apoptosis in developing rats. The goal of this study is to explore whether ketamine could result in learning and memory impairment and neurodegeneration in adolescent rats, and if so, whether the effects of ketamine are associated with miR-214 and PTEN expression. Fifty-day-old SD rats were randomly divided into three groups receiving ketamine at 30, or 80 mg/kg, i.p. or saline for seven consecutive days. Twenty-four hours after the last treatment, learning and memory function were tested by the Morris water maze. The rats were then decapitated, and the brains were isolated for detection of neuronal apoptosis and protein PTEN expression by TUNEL and immunohistochemistry respectively. Expression levels of the miR-214 and PTEN in the hippocampus were measured by qRT-PCR and western blot analysis respectively. Ketamine administered to the adolescent rats at a dose of 80 mg/kg rather than the lower dose of 30 mg/kg caused learning and memory impairment, increased the number of apoptotic cells in the hippocampal CA1 region, cerebral cortex and subcortical region, decreased the miR-214 levels and increased PTEN protein expression in hippocampus. The results suggest that ketamine at a dose of 80 mg/kg in the adolescent rats is able to induce the learning and memory impairment and neurodegeneration, in which the down-regulation of miR-214 and high expression of PTEN protein may be involved.

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“…Rats from 35–55 days old are adolescent or pubertal aged rats [25]. In this study, 90 SD rats (50-day-old), which are equivalent to 10–15 years old human subjects, were used.…”

Section: Discussionmentioning

confidence: 99%

Impact of Ketamine on Learning and Memory Function, Neuronal Apoptosis and Its Potential Association with miR-214 and PTEN in Adolescent Rats

Zhou

Wang

et al. 2014

PLoS ONE

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“…The experimental design, depicted below (Table 1), illustrates the sequence of procedures, for which the PND was appropriately chosen. The choice of PND 33 considered the adolescence stage, when the animals present intense social and motor activities (Semple et al, 2013), and also considered the estrous cycle that starts between PND 37 to 52 (Evans, 1986; Suckow et al, 2005), which we tried to avoid.…”

Section: Methodsmentioning

confidence: 99%

Behavioral, cognitive and histological changes following neonatal anoxia: Male and female rats' differences at adolescent age

Kumar

Motta-Teixeira

Takada

et al. 2018

Intl J of Devlp Neuroscience

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Neonatal anoxia induces long‐term brain injury that may underlie neurobehavioral deficits at adolescence. Neonatal anoxia, induced by exposure of 30‐hour old pups to 100% nitrogen, represents a non‐invasive and global stimulus, which simulates clinical conditions of human pre‐term babies (around 6 gestational months). Previous studies showed that neonatal anoxia induced impairments of spatial memory and altered anxiety‐like behaviors in male rats tested at adult age. This study evaluated if neonatal anoxia induces similar behavioral effects in female rats, as compared to males, by testing the animals at adolescence, and also searched for possible cell losses in hippocampal subfields. Results in the Elevated Plus Maze test showed that anoxic females spent proportionally more time within the open arms as compared to anoxic males, suggesting a less anxious‐like behavior. In the Morris Water Maze Test, latencies and path lengths of the anoxic subjects were longer as compared to control subjects, thus indicating that anoxia disrupted the cognitive functions required for spatial mapping. In addition, results showed that anoxia‐induced disruption was greater in male rats as compared to female rats. Stereological analysis revealed that anoxic male rats exhibited significant cell losses in the dorsal hippocampus dentate gyrus and CA1 subfields, but not in CA3‐2 subfield. Similar results were observed in the ventral hippocampus, but now with cell loss in the male CA3‐2 subfield. There were also significant cell loss differences of anoxic male rats as compared to anoxic female rats. In conclusion, neonatal anoxia induces deleterious and long lasting behavioral and cognitive disruptions, and these effects were stronger in male rats as compared to female rats. These changes are congruent with the pattern of cell losses observed in hippocampal subfields. Together, these results emphasize the relevance of scientific research, aiming at clinical strategies and treatments, consider the sex differential patterns of response to neonatal injury.

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“…Electrophysiological experiments were performed using different groups of rats at 35 to 37 days of age. Successful testosterone treatments and masculization of female rats were verified by inspection of the vagina opening and vaginal smears, which occur normally in females during puberty (Evans,1986).…”

Section: Methodsmentioning

confidence: 99%

Sex difference in stress‐induced enhancement of hippocampal CA1 long‐term depression during puberty

Huang¹,

Chen²,

Yeh³

2012

Hippocampus

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Females and males react differently to stress. Our previous studies revealed that acute stress facilitates the induction of long-term depression (LTD) in hippocampal CA1 region. However, it remains unknown whether sex difference exists in the effect of stress on LTD. Using an acute unpredictable and inescapable restraint-tailshock stress paradigm, we report here that hippocampal slices from stressed male rats expressed larger LTD by low-frequency stimulation (LFS) than controls, whereas such effect was not observed in female rats during puberty. The facilitatory effect of stress on LTD was prevented when animals were submitted to bilateral adrenalectomy. However, no sex difference in the magnitudes of LTD induced by direct application of N-methy-D-aspartate or a combination of LFS with the glutamate uptake inhibitor D,L-threo-β-benzyloxyaspartate was observed in slices from naive rats. Female rats exhibited significantly higher basal but not stress-evoked levels of plasma corticosterone than male rats. In addition, the expression levels of glucocorticoid receptors in hippocampal CA1 region were significantly lower in female than male rats. Moreover, female rats showed less responsiveness to stress- or dexamethasone-induced suppression of glutamate uptake in hippocampal synaptosomal preparations than male rats. Importantly, female rats that were masculinized with testosterone at birth responded to stress like male rats did, demonstrating an enhancement of LTD. In contrast, ovariectomized female rats failed to restore the ability of stress to facilitate LTD. These results reveal an obvious sex difference in stress-induced modification of hippocampal synaptic plasticity, which depends on organizational effect of testosterone during early development.

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Age at Puberty and First Litter Size in Early and Late Paired Rats12

Cited by 31 publications

References 13 publications

Impact of Ketamine on Learning and Memory Function, Neuronal Apoptosis and Its Potential Association with miR-214 and PTEN in Adolescent Rats

Impact of Ketamine on Learning and Memory Function, Neuronal Apoptosis and Its Potential Association with miR-214 and PTEN in Adolescent Rats

Behavioral, cognitive and histological changes following neonatal anoxia: Male and female rats' differences at adolescent age

Sex difference in stress‐induced enhancement of hippocampal CA1 long‐term depression during puberty

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