Very mild stress of pregnant rats reduces volume and cell number in nucleus accumbens of adult offspring: some parallels to schizophrenia

2004 ◽  
Vol 149 (1) ◽  
pp. 21-28 ◽  
Author(s):  
William O. McClure ◽  
Armine Ishtoyan ◽  
Melvin Lyon
1986 ◽  
Vol 60 (5) ◽  
pp. 1704-1709 ◽  
Author(s):  
B. W. Craig ◽  
J. Treadway

The purpose of this investigation was to examine the relationship between an exercise program and fetal development to determine whether training could influence insulin sensitivity in the pregnant rat. Prior to impregnation one group of animals was exercise trained on a Quinton shock-stimulus rodent treadmill. The exercised group was trained to run 5 days/wk, for 2.0 h/day at 31 m/min up an 8 degree incline for 8 wk before mating. Following mating the training intensity was reduced to 27 m/min up a 5 degree incline, and the exercise period decreased to 1 h/day. On day 19 of gestation, 24 h postexercise for the trained mothers, the animals were killed in the fed state and the parametrial fat pads were removed. The parametrial depot of the trained mother was smaller than the sedentary control dam. This was due to a change in cell size and did not involve alterations in cell number. Isolated adipocytes of the parametrial fat pads were used to measure the rates of 2-deoxy-D-[3H]glucose uptake and D-[1–14C]glucose oxidation to 14CO2. The results indicated that the adipocytes from the dam trained prior to and during pregnancy were significantly (P less than 0.05) more responsive to insulin than those of animals remaining sedentary during the same period. At the maximal insulin concentration tested, the fat cells from trained mothers were able to take up and metabolize approximately twice as much glucose as the sedentary control dams. However, the increase in insulin responsiveness induced by the training program did not match the changes observed in trained nonpregnant rats of prior investigations.


Pharmaceutics ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 29
Author(s):  
Nair C. F. Castro ◽  
Izabelle S. Silva ◽  
Sabrina C. Cartágenes ◽  
Luanna M. P. Fernandes ◽  
Paula C. Ribera ◽  
...  

Psychoactive substances during pregnancy and lactation is a key problem in contemporary society, causing social, economic, and health disturbance. In 2010, about 30 million people used opioid analgesics for non-therapeutic purposes, and the prevalence of opioids use during pregnancy ranged from 1% to 21%, representing a public health problem. This study aimed to evaluate the long-lasting neurobehavioral and nociceptive consequences in adult offspring rats and mice exposed to morphine during intrauterine/lactation periods. Pregnant rats and mice were exposed subcutaneously to morphine (10 mg/kg/day) during 42 consecutive days (from the first day of pregnancy until the last day of lactation). Offspring were weighed on post-natal days (PND) 1, 5, 10, 15, 20, 30, and 60, and behavioral tasks (experiment 1) or nociceptive responses (experiment 2) were assessed at 75 days of age (adult life). Morphine-exposed female rats displayed increased spontaneous locomotor activity. More importantly, both males and female rats perinatally exposed to morphine displayed anxiety- and depressive-like behaviors. Morphine-exposed mice presented alterations in the nociceptive responses on the writhing test. This study showed that sex difference plays a role in pain threshold and that deleterious effects of morphine during pre/perinatal periods are nonrepairable in adulthood, which highlights the long-lasting clinical consequences related to anxiety, depression, and nociceptive disorders in adulthood followed by intrauterine and lactation morphine exposure.


2017 ◽  
Vol 102 (8) ◽  
pp. 1019-1036 ◽  
Author(s):  
Francine Gomes de Sá ◽  
Diego Barbosa de Queiroz ◽  
Fernanda Elizabethe Ramos-Alves ◽  
Juliana Santos-Rocha ◽  
Odair Alves da Silva ◽  
...  

2017 ◽  
Vol 169 ◽  
pp. 114-123 ◽  
Author(s):  
Camila Simonetti Pase ◽  
Karine Roversi ◽  
Katiane Roversi ◽  
Luciana Taschetto Vey ◽  
Verônica Tironi Dias ◽  
...  

2020 ◽  
Vol 295 (20) ◽  
pp. 6831-6848 ◽  
Author(s):  
Li Guo ◽  
Zhaoming Zhu ◽  
Guangyan Wang ◽  
Shan Cui ◽  
Meng Shen ◽  
...  

Major depression is a prevalent affective disorder characterized by recurrent low mood. It presumably results from stress-induced deteriorations of molecular networks and synaptic functions in brain reward circuits of genetically-susceptible individuals through epigenetic processes. Epigenetic regulator microRNA-15b inhibits neuronal progenitor proliferation and is up-regulated in the medial prefrontal cortex of mice that demonstrate depression-like behavior, indicating the contribution of microRNA-15 to major depression. Using a mouse model of major depression induced by chronic unpredictable mild stress (CUMS), here we examined the effects of microRNA-15b on synapses and synaptic proteins in the nucleus accumbens of these mice. The application of a microRNA-15b antagomir into the nucleus accumbens significantly reduced the incidence of CUMS-induced depression and reversed the attenuations of excitatory synapse and syntaxin-binding protein 3 (STXBP3A)/vesicle-associated protein 1 (VAMP1) expression. In contrast, the injection of a microRNA-15b analog into the nucleus accumbens induced depression-like behavior as well as attenuated excitatory synapses and STXBP3A/VAMP1 expression similar to the down-regulation of these processes induced by the CUMS. We conclude that microRNA-15b-5p may play a critical role in chronic stress-induced depression by decreasing synaptic proteins, innervations, and activities in the nucleus accumbens. We propose that the treatment of anti-microRNA-15b-5p may convert stress-induced depression into resilience.


2002 ◽  
Vol 12 (4) ◽  
pp. 229-239 ◽  
Author(s):  
Przemylaw Nowak ◽  
Ryszard Brus ◽  
Ryszard Szkilnik ◽  
Lukasz Labus ◽  
Halina Winiarska ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-26 ◽  
Author(s):  
Hui Qiao ◽  
Ming-Xing Li ◽  
Chang Xu ◽  
Hui-Bin Chen ◽  
Shu-Cheng An ◽  
...  

Depression, a severe psychiatric disorder, has been studied for decades, but the underlying mechanisms still remain largely unknown. Depression is closely associated with alterations in dendritic spine morphology and spine density. Therefore, understanding dendritic spines is vital for uncovering the mechanisms underlying depression. Several chronic stress models, including chronic restraint stress (CRS), chronic unpredictable mild stress (CUMS), and chronic social defeat stress (CSDS), have been used to recapitulate depression-like behaviors in rodents and study the underlying mechanisms. In comparison with CRS, CUMS overcomes the stress habituation and has been widely used to model depression-like behaviors. CSDS is one of the most frequently used models for depression, but it is limited to the study of male mice. Generally, chronic stress causes dendritic atrophy and spine loss in the neurons of the hippocampus and prefrontal cortex. Meanwhile, neurons of the amygdala and nucleus accumbens exhibit an increase in spine density. These alterations induced by chronic stress are often accompanied by depression-like behaviors. However, the underlying mechanisms are poorly understood. This review summarizes our current understanding of the chronic stress-induced remodeling of dendritic spines in the hippocampus, prefrontal cortex, orbitofrontal cortex, amygdala, and nucleus accumbens and also discusses the putative underlying mechanisms.


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