Prenatal exposure to restraint or predator stresses attenuates field excitatory postsynaptic potentials in infant rats

Developmental Psychobiology

Roshan‐Milani

et al. 2014

Self Cite

Prenatal exposure to stress and morphine has complicated effects on epileptic seizure. Many reports have shown an interaction between morphine- and stress-induced behavioral changes in adult rats. In the present study, effect of prenatal forced-swim stress and morphine co-administration on pentylentetrazole (PTZ)-induced epileptic behaviors was investigated in rat offspring to address effect of the interaction between morphine and stress. Pregnant rats were divided to four groups of control-saline, control-morphine, stressed-saline and stressed-morphine. In the stressed group, the rats were placed in 25 °C water on 17-19 days of pregnancy. In the morphine/saline group, the rats received morphine/saline on the same days. In the morphine/saline-stressed group, they were exposed to stress and received morphine/saline simultaneously. On postnatal day 15 (P15), blood samples were collected to determine corticosterone (COS) level. On P15 and P25, PTZ was injected to the rest of pups to induce seizure. Then, epileptic behaviors of each rat were individually observed. Latency of tonic-colonic seizures decreased in control-morphine and stressed-saline groups while increasing in stressed-morphine rats compared to control-saline group on P15. Duration of tonic-colonic seizures significantly increased in control-morphine and stressed-saline rats compared to stressed-morphine and control-saline rats on P15, but not P25. COS levels increased in stressed-saline group but decreased in control-morphine group compared to control-saline rats. Body weight was significantly higher in morphine groups than saline treated rats. Prenatal exposure to forced-swim stress potentiated PTZ-induced seizure in the offspring rats. Co-administration of morphine attenuated effect of stress on body weight, COS levels, and epileptic behaviors.

Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Effect of prenatal forced‐swim stress and morphine co‐administration on pentylentetrazol‐induced epileptic behaviors in infant and prepubertal rats

Ebrahimi

Developmental Psychobiology

Roshan‐Milani

et al. 2014

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“…Predator stimuli are stressful for rats and mice. Exposure to natural predators and their odors elevate monoaminergic and stress hormone release in rats (Adamec et al, 1998; Saboory et al, 2011) and mice (Belzung et al, 2001). Therefore, to obtain more accurate results, both types of stress were applied in this study.…”

Section: Discussionmentioning

confidence: 99%

Effect of prenatal stress on density of NMDA receptors in rat brain

Tavassoli

Intl J of Devlp Neuroscience

Teshfam

et al. 2013

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N-methyl-D-aspartate (NMDA) receptors are important excitatory receptors which contribute to many brain functions. Altered NMDA receptor levels cause maldevelopment of corticostriatal and corticolimbic pathways, which is a neurobiological predisposing factor for development of epilepsy, schizophrenia and other idiopathic psychotic disorders. It was hypothesized that prenatal stress could play a role in pathophysiology of these disorders by affecting expression of the receptors through releasing corticosterone. Sixty-eight virgin female Wistar rats were selected and mated with male rats with the same genotype. Then, the pregnant rats were subjected to restraint or predator stress on 15th, 16th and 17th gestation days. Prenatal stress consisted of restraint or predator stresses of the dams under normal room conditions. After parturition, the pups were studied in terms of density of NMDA receptors in brain at different time points. Meanwhile, blood sample was obtained and corticosterone blood level (CBL) was measured. The pups were then compared with the pups born to unstressed dams. Stress induced significant rise in CBL and NMDA receptors in brain of the offspring. CBL was significantly higher among the stressed rats compared to the control ones; there was significant difference between the two stresses and between the two sexes. The male pups were affected more severely. Stressful events during gestation had important effects on NMDA receptors of the offspring. It can be concluded that stress-induced elevation of NMDA receptors and corticosterone might mediate altered susceptibility to epilepsy and decrease ability of learning and memory and other stress-induced neurologic disorders.

“…The potentiation of seizures by PS has been reported and is presumably caused by an imbalance between the excitatory and inhibitory systems. There are neurobiological bases for stress‐induced seizures: exposure to stressors evokes hippocampal plasticity (Saboory et al, 2011), induces noradrenergic neurotransmission, and facilitates adrenocortical hormone activation (Edwards et al, 2002; Sadaghiani and Saboory, 2010). Our current findings demonstrated that PS potentiated pilocarpine‐induced seizures.…”

Section: Discussionmentioning

confidence: 99%

“…After parturition, the mother and her pups were moved to a new cage and number of pups culled to 8 at each litter. On the P14 and P21 (Hashemi et al, 2016; Saboory et al, 2011; Tavassoli et al, 2013), a male (n = 6 in each group) and a female (n = 6 in each group) from each litter were decapitated under ether anesthesia and entire hippocampus was removed quickly and placed inside the normal saline ice. Then, 50 mg tissues were homogenized in one ml RiboEX (Gene all, South Korea) solution, which is a protective solution of RNA.…”

Section: Methodsmentioning

confidence: 99%

Effect of prenatal stress on ɑ5 GABA_A receptor subunit gene expression in hippocampus and pilocarpine induced seizure in rats

Nejatbakhsh

Intl J of Devlp Neuroscience

Bagheri

2018

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The GABAergic synapses go through structural and functional maturation during early brain development. Maternal stress alters GABAergic synapses in developing brain, which are associated with the pathophysiology of neuropsychiatric disorders in adults. The present study aimed to investigate the effect of prenatal restraint stress (PS) on pilocarpine-induced seizure and ɑ5 subunit of γ-amino butyric acid type A (GABA) receptor expression in hippocampus. Pregnant Wistar rats were subjected to PS at gestational days 15-17 and the pups were examined for susceptibility to seizure and ɑ5 subunit of GABA receptor expression in hippocampus at postnatal days 14 and 21 (P14 and PND 21). Quantitative real-time PCR was used for evaluating the gene expression in the pups. Pilocarpine was injected intraperitoneally into the pups and seizure behaviors were recorded. The results showed that ɑ5 subunit mRNA expression significantly increased in hippocampus at both the P14 and P21 in the stressed rats. However, ɑ5 subunit level was greater at the P21 than at the P14 in both the groups. Latency of first tonic-clonic seizure significantly decreased in the PS group compared to the control pups. Number and duration of tonic-clonic seizures increased in the PS rats compared to the controls. PS led to an increase in total score of seizure at the P14 and P21. It can be concluded that PS increases the seizure susceptibility and GABA receptor ɑ5 subunit gene expression in offspring; it is likely that the mechanism of increased seizure susceptibility by PS, at least in part, can increase the GABA receptor ɑ5 subunit gene expression in hippocampus.