Prenatal exposure to noise stress: Anxiety, impaired spatial memory, and deteriorated hippocampal plasticity in postnatal life

Hippocampus ◽  
2014 ◽  
Vol 25 (2) ◽  
pp. 187-196 ◽  
Author(s):  
Marzieh Barzegar ◽  
Fatemeh Sadat Sajjadi ◽  
Sayyed Alireza Talaei ◽  
Gholamali Hamidi ◽  
Mahmoud Salami
Keyword(s):  
Spatial Memory ◽  
Prenatal Exposure ◽  
Postnatal Life ◽  
Hippocampal Plasticity ◽  
Noise Stress

scholarly journals Prenatal exposure to paracetamol/acetaminophen and precursor aniline impairs masculinisation of male brain and behaviour

Reproduction ◽  
2017 ◽  
Vol 154 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Anders Hay-Schmidt ◽  
Olivia T Ejlstrup Finkielman ◽  
Benjamin A H Jensen ◽  
Christine F Høgsbro ◽  
Jacob Bak Holm ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Sexual Behaviour ◽  
Reproductive Tract ◽  
Reproductive Behaviour ◽  
Postnatal Life ◽  
Similar Reduction ◽  
Foetal Development ◽  
Male Adult ◽  
Male Sexual Behaviour ◽  
Neuronal Number

Paracetamol/acetaminophen (N-Acetyl-p-Aminophenol; APAP) is the preferred analgesic for pain relief and fever during pregnancy. It has therefore caused concern that several studies have reported that prenatal exposure to APAP results in developmental alterations in both the reproductive tract and the brain. Genitals and nervous system of male mammals are actively masculinised during foetal development and early postnatal life by the combined actions of prostaglandins and androgens, resulting in the male-typical reproductive behaviour seen in adulthood. Both androgens and prostaglandins are known to be inhibited by APAP. Through intrauterine exposure experiments in C57BL/6 mice, we found that exposure to APAP decreased neuronal number in the sexually dimorphic nucleus (SDN) of the preoptic area (POA) in the anterior hypothalamus of male adult offspring. Likewise, exposure to the environmental pollutant and precursor of APAP, aniline, resulted in a similar reduction. Decrease in neuronal number in the SDN-POA is associated with reductions in male sexual behaviour. Consistent with the changes, male mice exposed in uteri to APAP exhibited changes in urinary marking behaviour as adults and had a less aggressive territorial display towards intruders of the same gender. Additionally, exposed males had reduced intromissions and ejaculations during mating with females in oestrus. Together, these data suggest that prenatal exposure to APAP may impair male sexual behaviour in adulthood by disrupting the sexual neurobehavioral programming. These findings add to the growing body of evidence suggesting the need to limit the widespread exposure and use of APAP by pregnant women.

scholarly journals Stress-induced alterations in hippocampal plasticity, place cells, and spatial memory

2007 ◽  
Vol 104 (46) ◽  
pp. 18297-18302 ◽  
Author(s):  
J. J. Kim ◽  
H. J. Lee ◽  
A. C. Welday ◽  
E. Song ◽  
J. Cho ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Place Cells ◽  
Hippocampal Plasticity

scholarly journals Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs

2009 ◽  
Vol 90 (3) ◽  
pp. 540-546 ◽  
Author(s):  
Pernille Tveden-Nyborg ◽  
Louise Kruse Johansen ◽  
Zindy Raida ◽  
Charlotte Krogh Villumsen ◽  
Jytte Overgaard Larsen ◽  
...  
Keyword(s):  
Vitamin C ◽  
Spatial Memory ◽  
Guinea Pigs ◽  
Hippocampal Neurons ◽  
Postnatal Life ◽  
Vitamin C Deficiency ◽  
Early Postnatal Life

Prenatal Exposure to Androgen Excess Increases LH Pulse Amplitude During Postnatal Life in Male Sheep

2012 ◽  
Vol 44 (09) ◽  
pp. 688-693 ◽  
Author(s):  
S. Recabarren ◽  
M. Recabarren ◽  
P. Rojas-Garcia ◽  
M. Cordero ◽  
C. Reyes ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Pulse Amplitude ◽  
Postnatal Life ◽  
Androgen Excess ◽  
Male Sheep

Effects of chronic noise stress on spatial memory of rats in relation to neuronal dendritic alteration and free radical-imbalance in hippocampus and medial prefrontal cortex

2006 ◽  
Vol 399 (1-2) ◽  
pp. 17-22 ◽  
Author(s):  
Sundaramahalingam Manikandan ◽  
Moorthy K Padma ◽  
Ramasundaram Srikumar ◽  
Narayanaperumal Jeya Parthasarathy ◽  
Arumugam Muthuvel ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Free Radical ◽  
Spatial Memory ◽  
Medial Prefrontal Cortex ◽  
Noise Stress

Prenatal exposure to testosterone masculinises the female gerbil and promotes the development of lesions in the prostate (Skene’s gland)

2015 ◽  
Vol 27 (7) ◽  
pp. 1000 ◽  
Author(s):  
Manoel F. Biancardi ◽  
Ana P. S. Perez ◽  
Cássia Regina Suzuki Caires ◽  
Rejane M. Góes ◽  
Patrícia S. L. Vilamaior ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Vaginal Wall ◽  
Experimental Models ◽  
Prostatic Tissue ◽  
Postnatal Life ◽  
Normal Prostate ◽  
Anogenital Distance ◽  
Morphological Alterations ◽  
Prostate Development ◽  
Prostatic Diseases

Androgenic imbalance may disrupt prostate development, leading to morphological alterations in adulthood and predisposing this gland to develop diseases during ageing. However, little is known about the endocrine disruption of the prostate that is caused by androgenic compounds, especially in female experimental models. Therefore, this study aimed to evaluate the prostates of aged female gerbils exposed to testosterone at certain periods in intrauterine and postnatal life, to determine whether exposure at a particular age increases susceptibility to prostatic lesions in these animals. To this end, morphological, stereological, immunohistochemical and immunofluorescence analyses were employed. It was found that females exposed to testosterone during intrauterine life were masculinised, showing increased anogenital distance, absence of the vaginal opening and ectopic development of prostatic tissue. Several areas of adenomatous hyperplasia, generally associated with inflammatory foci and mainly located in the ectopic prostatic tissue around the vaginal wall, were also observed. In conclusion, the results showed that abnormal prenatal exposure to testosterone severely affects the reproductive systems of female animals by disrupting normal prostate morphogenesis and increasing susceptibility to the development of prostatic diseases during ageing.

scholarly journals Morphogenesis of the thyroid gland of rats of the early period after the prenatal action of Dexamethasone

2021 ◽  
Vol 25 (1) ◽  
pp. 22-26
Author(s):  
О. V. Fedosieieva
Keyword(s):  
Thyroid Gland ◽  
Prenatal Exposure ◽  
Early Period ◽  
The Body ◽  
Control Group ◽  
Postnatal Life ◽  
Prenatally Exposed ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Compensatory Response

Annotation. The aim of the study was to establish the features of the morphogenesis of the thyroid gland of rats at an early age of normal postnatal ontogenesis and after prenatal exposure to dexamethasone. The study material was the thyroid gland of rats (54 animals) of the Wistar line at the age of 1 to 14 days of postnatal development, which experimentally operatively, through the membrane, intrauterinely injected a solution of dexamethasone at a dose of 0.05 ml at a dilution of 1:40 on the 18th day of pregnancy; control group – 0.05 ml of 0.9% NaCl. Sections were stained with haematoxylin and eosin, azan, immunohistochemically (ki-67). Statistically used Student's parametric t-test, the normality of the distribution was checked using the Shapiro-Wilk test, the reliability is not less than 95%, the reliability at p<0.05. In animals experimentally prenatally exposed to dexamethasone for 1-3 days, the gland was more functionally excited: the number of resorption vacuoles in the colloid, which was dense, increased, but the height of thyrocytes was almost no different from the control. There were more colloid-type follicles with ki-67-positive cells. On the 7th day of postnatal life, the structure of the gland changed in the direction of increasing the manifestations of the process of blocking the excretion of thyroid hormones, but the synthesis and excretion of components into the follicle cavity was preserved. Follicles increased throughout the body. On the 11th day of postnatal life in the thyroid glands of animals prenatally exposed to dexamethasone, the number of microfollicles decreased, and the proportion of proliferating ki-67-positive cells in the follicle wall decreased insignificantly compared to the previous period, but compared to the control of proliferating cells was less than 1.8 times. On 14th day, the thyroid gland of experimental animals was characterized by a mosaic arrangement of large follicles with flattened thyrocytes. Thus, the morphogenesis of the thyroid gland by hypofunctional type after prenatal exposure to dexamethasone in young rats indicates an adaptogenic compensatory response and morpho-functional immaturity of the organ during this period, which may be the basis for provoking the preservation of such morphogenetic factors under the influence of stressors.

scholarly journals Detection of vulnerable neurons damaged by environmental insults in utero

2017 ◽  
Vol 114 (9) ◽  
pp. 2367-2372 ◽  
Author(s):  
Masaaki Torii ◽  
Masanori Sasaki ◽  
Yu-Wen Chang ◽  
Seiji Ishii ◽  
Stephen G. Waxman ◽  
...  
Keyword(s):  
Heat Shock ◽  
Prenatal Exposure ◽  
Cellular Damage ◽  
Postnatal Life ◽  
Heat Shock Factor 1 ◽  
Reporter Assay ◽  
Reporter System ◽  
Essential Step ◽  
Reporter Mice ◽  
Prevention And Treatment

Development of prognostic biomarkers for the detection of prenatally damaged neurons before manifestations of postnatal disorders is an essential step for prevention and treatment of susceptible individuals. We have developed a versatile fluorescence reporter system in mice enabling detection of Heat Shock Factor 1 activation in response to prenatal cellular damage caused by exposure to various harmful chemical or physical agents. Using an intrautero electroporation-mediated reporter assay and transgenic reporter mice, we are able to identify neurons that survive prenatal exposure to harmful agents but remain vulnerable in postnatal life. This system may provide a powerful tool for exploring the pathogenesis and treatment of multiple disorders caused by exposure to environmental stress before symptoms become manifested, exacerbated, and/or irreversible.

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