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INTRODUCTION: Social play behavior is crucial for acquiring social skills and the development of normal socioaffective responses. The repertoire of social play in rats changes throughout the life, peaking during the juvenile period and falling off around adolescence. The most characteristic postures in social plays of rodents are pinning and pouncing. In addition to playful activities during social play, rats also engage in non-playful behaviors including social exploration. The lack of ability to engage in social play with conspecifics is the main indicator of neuropsychiatric disorders like autism. There is strong evidence suggesting that maternal infection during pregnancy is correlated with increased risk of developing autism spectrum disorder (ASD) in the child. To model maternal immune activation, polyinosinic: polycytidylic acid (poly(I:C)) is used to induce inflammatory response in the maternal-placental-fetal axis. The resulting inflammation leads to perturbation of the brain development of pups and consequently may lead to development of the symptoms of autism. AIM(S): We performed the Social Play Test to study changes in social play behavior of rats in an ASD model induced by prenatal exposure to poly(I:C). METHOD(S): Pregnant Sprague-Dawley rat dams received a single intraperitoneal injection of poly(I:C) (5 mg/kg) or vehicle at gestational day 15. The 30 – 35 days-old rats were then tested using the Social Play Test. RESULTS: Rats that were prenatally exposed to poly(I:C) demonstrated a significant decrease in a number of episodes of pinning compared to the vehicle-treat ed controls. We also observed significantly diminished time of social exploration in the offspring of poly(I:C) treated females. CONCLUSIONS: The present study demonstrated that prenatal exposure to poly(I:C) results in social deficits in juvenile rats. Measures of social play behaviours in rats could be useful for quantifying abnormal levels of sociability associated with autism. FINANCIAL SUPPORT: Supported by NSC grant: 2016/23/B/NZ7/01131.
INTRODUCTION: Ketogenic diet (KD) results in mild to moderate ketosis, which in turn can significantly change the metabolic balance in the brain. The effects of KD are broadly studied in search of potential clinical uses, such as reducing seizure severity in epilepsy, or providing adjunctive therapy for cancer, Alzheimer’s or Parkinson’s disease. The exact mechanism of those putative neuroprotective effects of KD is, however, still poorly understood. AIM(S): Here, we have checked if prolonged ketogenic diet changed beta hydroxy butyrate(BHB) and epididymal fat levels. The crucial thing was to determine how the ketogenic diet affects brain volume and anatomy. METHOD(S): Male Wistar rats were assigned into two experimental groups: one was given KD for 4 months (n=10), the other (n=11) was fed normal laboratory chow (N). After 4 months, rats were sacrificed. Blood samples were collected and BHB levels measured with ELISA. T2-weighed ex vivo images of extracted brains, taken with a 9.4 T magnetic resonance scanner were obtained at the Institute of Nuclear Physics, at XY resolution of 0.025 mm and voxel depth of 0.25 mm. Using a computer-assisted Cavalieri method, the volumes of the entire brain, hippocampus and brainstem structures (midbrain, pons) were estimated. Volumes were compared between groups to show differentially affected regions. Student’s t‑tests was used for statystical analysis. RESULTS: We have observed increased epididymal fat and elevated BHB levels in KD in comparison to the N group (p<0,000001). Additionally we have found a significant reduction in overall pontine volume in the KD group after the 4-month feeding period. CONCLUSIONS: Our results indicate that the prolonged ketogenic feeding was successful in inducing metabolic changes in KD animals. Observed differences in pontine volume in rats fed a ketogenic diet may lead to modification of feeding behavior. These imapairments in food-intake process may be strictly involved with parabrachial structures which are engaged in regulating appetitive behavior. FINANCIAL SUPPORT: Supported by NCS GRANT: UMO-2015/17/B/NZ7/02953.
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