Neuronal Injuries Induced by Perinatal Hypoxic-Ischemic Insults Are Potentiated by Prenatal Exposure to Lipopolysaccharide: Animal Model for Perinatally Acquired Encephalopathy

2005 ◽  
Vol 27 (2-4) ◽  
pp. 134-142 ◽  
Author(s):  
A. Larouche ◽  
M. Roy ◽  
H. Kadhim ◽  
A.M. Tsanaclis ◽  
D. Fortin ◽  
...  
2016 ◽  
Vol 20 (6) ◽  
pp. 343-350 ◽  
Author(s):  
Kamila Castro ◽  
Diego Baronio ◽  
Ingrid Schweigert Perry ◽  
Rudimar dos Santos Riesgo ◽  
Carmem Gottfried

2011 ◽  
Vol 1408 ◽  
pp. 8-16 ◽  
Author(s):  
Victorio Bambini-Junior ◽  
Leticia Rodrigues ◽  
Guilherme Antônio Behr ◽  
José Cláudio Fonseca Moreira ◽  
Rudimar Riesgo ◽  
...  

2018 ◽  
Vol 25 (5-6) ◽  
pp. 285-299 ◽  
Author(s):  
Iohanna Deckmann ◽  
Gustavo Brum Schwingel ◽  
Mellanie Fontes-Dutra ◽  
Victorio Bambini-Junior ◽  
Carmem Gottfried

2012 ◽  
Vol 33 (8) ◽  
pp. 652-661 ◽  
Author(s):  
Federica Laudisi ◽  
Manolo Sambucci ◽  
Francesca Nasta ◽  
Rosanna Pinto ◽  
Rossella Lodato ◽  
...  

2008 ◽  
Vol 33 (6) ◽  
pp. 728-740 ◽  
Author(s):  
Tomasz Schneider ◽  
Adam Roman ◽  
Agnieszka Basta-Kaim ◽  
Marta Kubera ◽  
Bogusława Budziszewska ◽  
...  

2013 ◽  
Vol 1495 ◽  
pp. 52-60 ◽  
Author(s):  
Roberta Bristot Silvestrin ◽  
Victorio Bambini-Junior ◽  
Fabiana Galland ◽  
Larissa Daniele Bobermim ◽  
André Quincozes- Santos ◽  
...  

2015 ◽  
Vol 292 ◽  
pp. 361-369 ◽  
Author(s):  
Romana Šlamberová ◽  
Marie Pometlová ◽  
Eva Macúchová ◽  
Kateryna Nohejlová ◽  
Aleš Stuchlík ◽  
...  

2021 ◽  
Author(s):  
◽  
Michaela Pettie

<p>Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder, characterised by deficits in verbal and non-verbal communication, social interaction and repetitive behaviours (APA, 2013). The aetiology of ASD is mostly unknown, with continued research identifying a multitude of genetic and non-genetic factors. However, it is the interaction between environmental factors and the genetic background of an individual which leads to the development of ASD. There is an urgent need for improved animal models of ASD to further our understanding of the aetiology and particularly its pathophysiology, as this will aid in the development of much needed pharmaceutical treatments to alleviate the impact of adverse symptoms for individuals with ASD. Current animal models of ASD examine the genetic (e.g. serotonin transporter knock out rats) or the environmental (e.g. prenatal exposure to Valproate) contributions to the disorder, and very rarely a combination of the two.  This thesis aimed to improve the Valproate (VPA) induced ASD animal model with a genetic × environmental interaction approach, as well as optimising chronic administration of the VPA to pregnant rats. To this aim, a non-invasive method of delivering VPA was used, which allowed genetically normal rats to voluntarily consume VPA throughout pregnancy. The prenatal exposure to VPA led to ASD-like behaviours in the offspring (communication delays, increased social behaviour, and social aversion). Next, rats with a genetic deficit in SERT (SERT+/-) exposed to VPA throughout gestation, with an optimised administration method using gelatine pellets, which allowed for voluntary non-invasive consumption, and a more accurate administration of increased VPA doses. Overall, the chronic prenatal exposure to VPA in SERT+/- rats led to a mild ASD-like phenotype, with rats exhibiting communication delays, abnormal play behaviour, disrupted social preference, and to some extent increased anxiety-like behaviour. The brains of the adult offspring were examined for neuronal changes in the GABA interneurons in brain regions associated with social behaviour (amygdala and hippocampus). However, no significant effects of prenatal VPA exposure, genotype, or sex were found. Thus, the variations GABAergic system is unlikely to underlie the earlier identified behavioural alterations. Ultimately, this thesis has furthered the VPA induced ASD animal model with a genetic × environmental interaction approach, as well as optimising the chronic administration method for pregnant rats.</p>


2021 ◽  
Vol 8 (03) ◽  
pp. e104-e113
Author(s):  
Rick Wilhiam de Camargo ◽  
Marina Goulart da Silva ◽  
Guilherme Cabreira Daros ◽  
Fabiana Durante de Medeiros ◽  
Naiana da Rosa ◽  
...  

Abstract p-Cymene is a monoterpene found in over 100 plant species. It shows a range of biological activity, including anti-inflammatory and antimicrobial effects. It is possibly a new therapeutic alternative for autism spectrum disorder characterized by deficits in interaction and behavioral abnormalities. These symptoms can occur in response to maternal immune activation through prenatal exposure to lipopolysaccharide. Thus, this study aimed to evaluate the behavioral, memory, and biochemical effects of chronic administration of p-cymene in an animal model of autism by prenatal maternal exposure to lipopolysaccharide. Twenty-four pregnant Wistar rats were used, who received 100 μg/kg of lipopolysaccharide or saline intraperitoneally (i.p.) on the 9.5 gestational day. After birth, the male offspring remained with the mothers until weaning and underwent model validation tests on postnatal day 30. From postnatal day 31 on, chronic administration, via i.p., of saline (1 mL/kg), risperidone (0.2 mg/kg), or p-cymene (100 mg/kg) for 22 days was performed. The animals were submitted to behavioral (postnatal day 52) and memory tests (postnatal days 52–53) and subsequently sacrificed (postnatal day 54) when their brain structures were removed for quantification of proinflammatory cytokines (TNF-α, interleukin 1β, and interleukin 6). Prenatal exposure to lipopolysaccharide significantly increased episodes of stereotyped movement (p=0.0001) and decreased parameters of social interaction in offspring, including sniffing, following, mounting, and allowing mounting (p=0.0043, p<0.0001, p=0.0009, and p=0.0200, respectively). Chronic p-cymene treatment was not significant for behavioral, memory, and biochemical tests. However, due to their pharmacokinetic characteristics, p-cymene nanomaterials’ formulation may be an exciting alternative to be tested for further results.


2011 ◽  
Vol 45 (11) ◽  
pp. 1497-1503 ◽  
Author(s):  
Daiane B. Fraga ◽  
Pedro F. Deroza ◽  
Fernando V. Ghedim ◽  
Amanda V. Steckert ◽  
Renata D. De Luca ◽  
...  

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