scholarly journals Perinatal exposure to diesel exhaust origin secondary organic aerosol induces autism-like behavior in rats

2020 ◽  
Author(s):  
Tin Tin Win Shwe ◽  
Chaw Kyi Tha Thu ◽  
Yuji Fujitani ◽  
Shinji Tsukahara ◽  
Seishiro Hirano
Keyword(s):  
Prefrontal Cortex ◽  
Diesel Exhaust ◽  
Secondary Organic Aerosol ◽  
Organic Aerosol ◽  
Female Rats ◽  
Perinatal Exposure ◽  
Male And Female ◽  
Glutamate Concentration ◽  
Immunological Markers ◽  
Male And Female Rats

Abstract Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions and repetitive behaviors. The exact cause and mechanism of autism remains unknown. Both genetic and environmental factors may involve in ASD. In this study, we used diesel exhaust (DE) origin secondary organic aerosol (DE-SOA) as environmental pollutants. DE-SOA was generated by oxidative reaction of mixing DE with ozone. The aim of present study is to examine autism-like behaviors and related gene expressions in rats exposed to DE-SOA perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), DE and DE-SOA in the exposure chamber for 5 h per day (from 10:00 pm to 3:00 am), 5 days a week excluding weekends from gestational day 14 to postnatal day 21 with their pups. At postnatal day 21, the male and female offspring rats were allocated into three different groups as follows: 1) rats exposed to clean filtered air; 2) rats exposed to DE; 3) rats exposed to DE-SOA. Social behaviors were investigated at 10~13-weeks-old rats using a 3-chambered social behavior test, social dominance tube test and marble burying test. Prefrontal cortex was collected to examine neurological and immunological markers, and glutamate concentration, using real-time RT-PCR and ELISA methods. Results: DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior and increased repetitive behavior compared with the control rats. The mRNA expression levels of serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) were down-regulated whereas interleukin 1 b　(IL-b), and heme oxygenase 1 (HO-1) were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA compared to the control rats. Glutamate concentration was increased significantly in the prefrontal cortex of both male and female rats exposed to DE-SOA.Conclusion: Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior in rats by modulating neurological and immunological markers in the prefrontal cortex.

scholarly journals Perinatal exposure to diesel exhaust origin secondary organic aerosol induces autism-like behavior in rats

2020 ◽  
Author(s):  
Tin Tin Win Shwe ◽  
Chaw Kyi Tha Thu ◽  
Yuji Fujitani ◽  
Shinji Tsukahara ◽  
Seishiro Hirano
Keyword(s):  
Prefrontal Cortex ◽  
Diesel Exhaust ◽  
Secondary Organic Aerosol ◽  
Organic Aerosol ◽  
Female Rats ◽  
Perinatal Exposure ◽  
Male And Female ◽  
Glutamate Concentration ◽  
Immunological Markers ◽  
Male And Female Rats

Abstract Background Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, social interactions and repetitive behaviors. The etiology of autism remains unknown and its molecular basis is not well understood. Both genetic and environmental factors may contribute ASD. In this study, we used diesel exhaust origin secondary organic aerosol (DE-SOA) as environmental pollutants. The aim of present study is to examine autism-like behaviors and related gene expressions in rats exposed to DE-SOA perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), diesel exhaust (DE) and DE-SOA in the exposure chamber for 5 h per day, 5days a week from gestational day 8 to postnatal day 21. At postnatal day 21, the male and female offspring rats were allocated into three different groups as follows: 1) rats exposed to clean filtered air; 2) rats exposed to DE; 3) rats exposed to DE-SOA. Social behaviors were investigated at 10 ~ 13-weeks-old rats using a 3-chambered social behavior test, social dominance tube test and marble burying test. Prefrontal cortex was collected under deep anesthesia to examine neurological and immunological markers, glutamate concentration, mast cell and microglia activation using real-time RT-PCR method, ELISA method and immunohistochemical analysis. Results DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior and increased repetitive behavior compared with the control rats. The mRNA expression levels of serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) were down-regulated whereas interleukin 1 β (IL-β), and heme oxygenase 1 (HO-1) were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA compared to the control rats. In addition, the expression of mast cells and microglia marker ionized calcium-binding adapter molecule (Iba)1 were increased in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was increased significantly in the prefrontal cortex of both male and female rats exposed to DE-SOA. Conclusion Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior in rats by modulating neurological and immunological markers in the prefrontal cortex.

scholarly journals Perinatal exposure to diesel exhaust origin secondary organic aerosol induces autism-like behavior in rats

2020 ◽  
Author(s):  
Tin Tin Win Shwe ◽  
Chaw Kyi Tha Thu ◽  
Yuji Fujitani ◽  
Shinji Tsukahara ◽  
Seishiro Hirano
Keyword(s):  
Prefrontal Cortex ◽  
Diesel Exhaust ◽  
Secondary Organic Aerosol ◽  
Organic Aerosol ◽  
Female Rats ◽  
Perinatal Exposure ◽  
Male And Female ◽  
Glutamate Concentration ◽  
Immunological Markers ◽  
Male And Female Rats

Abstract Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions and repetitive behaviors. The exact cause and mechanism of autism remains unknown. Both genetic and environmental factors may involve in ASD. In this study, we used diesel exhaust origin secondary organic aerosol (DE-SOA) as environmental pollutants. The aim of present study is to examine autism-like behaviors and related gene expressions in rats exposed to DE-SOA perinatally. Sprague-Dawley pregnant rats were exposed to clean air (control), diesel exhaust (DE) and DE-SOA in the exposure chamber for 5 h per day, 5days a week from gestational day 8 to postnatal day 21. At postnatal day 21, the male and female offspring rats were allocated into three different groups as follows: 1) rats exposed to clean filtered air; 2) rats exposed to DE; 3) rats exposed to DE-SOA. Social behaviors were investigated at 10~13-weeks-old rats using a 3-chambered social behavior test, social dominance tube test and marble burying test. Prefrontal cortex was collected under deep anesthesia to examine neurological and immunological markers, glutamate concentration, mast cell and microglia activation using real-time RT-PCR method, ELISA method and immunohistochemical analysis. Results: DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior and increased repetitive behavior compared with the control rats. The mRNA expression levels of serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) were down-regulated whereas interleukin 1 b　(IL-b), and heme oxygenase 1 (HO-1) were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA compared to the control rats. In addition, the expression of mast cells and microglia marker ionized calcium-binding adapter molecule (Iba)1 were increased in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was increased significantly in the prefrontal cortex of both male and female rats exposed to DE-SOA. Conclusion: Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior in rats by modulating neurological and immunological markers in the prefrontal cortex.

scholarly journals Perinatal Exposure to Diesel Exhaust-Origin Secondary Organic Aerosol Induces Autism-Like Behavior in Rats

2021 ◽  
Vol 22 (2) ◽  
pp. 538
Author(s):  
Tin-Tin Win-Shwe ◽  
Chaw Kyi-Tha-Thu ◽  
Yuji Fujitani ◽  
Shinji Tsukahara ◽  
Seishiro Hirano
Keyword(s):  
Prefrontal Cortex ◽  
Diesel Exhaust ◽  
Secondary Organic Aerosol ◽  
Organic Aerosol ◽  
Female Rats ◽  
Perinatal Exposure ◽  
Male And Female ◽  
Glutamate Concentration ◽  
Immunological Markers ◽  
Male And Female Rats

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication, poor social interactions, and repetitive behaviors. We aimed to examine autism-like behaviors and related gene expressions in rats exposed to diesel exhaust (DE)-origin secondary organic aerosol (DE-SOA) perinatally. Sprague–Dawley pregnant rats were exposed to clean air (control), DE, and DE-SOA in the exposure chamber from gestational day 14 to postnatal day 21. Behavioral phenotypes of ASD were investigated in 10~13-week-old offspring using a three-chambered social behavior test, social dominance tube test, and marble burying test. Prefrontal cortex was collected to examine molecular analyses including neurological and immunological markers and glutamate concentration, using RT-PCR and ELISA methods. DE-SOA-exposed male and female rats showed poor sociability and social novelty preference, socially dominant behavior, and increased repetitive behavior. Serotonin receptor (5-HT(5B)) and brain-derived neurotrophic factor (BDNF) mRNAs were downregulated whereas interleukin 1 β (IL-β) and heme oxygenase 1 (HO-1) mRNAs were upregulated in the prefrontal cortex of male and female rats exposed to DE-SOA. Glutamate concentration was also increased significantly in DE-SOA-exposed male and female rats. Our results indicate that perinatal exposure to DE-SOA may induce autism-like behavior by modulating molecules such as neurological and immunological markers in rats.

scholarly journals Maternal cannabinoid exposure during lactation alters the developmental trajectory of prefrontal cortex GABA-currents in offspring

2018 ◽  
Author(s):  
Andrew F. Scheyer ◽  
Jim Wager-Miller ◽  
Anne-Laure Pelissier-Alicot ◽  
Michelle N. Murphy ◽  
Ken Mackie ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Critical Period ◽  
Illicit Drug ◽  
Perinatal Period ◽  
Developmental Trajectory ◽  
Female Rats ◽  
Perinatal Exposure ◽  
Inhibitory Neurotransmitter ◽  
Male And Female Rats ◽  
Dependent Mechanism

AbstractCannabis is the most widely used illicit drug in the world, and its usage is increasing with its widespread legalization. Use of the drug by mothers during lactation may transfer active cannabinoids to the developing offspring, altering postnatal neurodevelopment during this critical period. During early life, GABA undergoes a functional switch from an excitatory to an inhibitory neurotransmitter due to reciprocal changes in expression of the K+/Cl- co-transporters KCC2 and NKCC1. Here, we characterize the functional GABA switch in the prefrontal cortex of both male and female rats. We show that treating rat dams with Δ9-THC or a synthetic cannabinoid during early lactation (PND01-10) retards KCC2 expression and delays the GABA switch in pups of both sexes via a CB1R-dependent mechanism. Our results indicate that the developmental trajectory of GABA in PFC neurons is significantly altered by perinatal exposure to cannabinoids through lactation during the early perinatal period.

scholarly journals SEX DIFFERENCES IN μ-OPIOID REGULATION OF COERULEAR-CORTICAL TRANSMISSION

2020 ◽  
Author(s):  
Herminio M Guajardo ◽  
Rita J Valentino
Keyword(s):  
Sex Differences ◽  
Prefrontal Cortex ◽  
Cognitive Flexibility ◽  
Field Potential ◽  
Endogenous Opioids ◽  
Female Rats ◽  
Cognitive Responses ◽  
Female Rat ◽  
Male And Female ◽  
Male And Female Rats

ABSTRACTStress-induced activation of locus coeruleus (LC)-norepinephrine (NE) projections to the prefrontal cortex is thought to promote cognitive responses to stressors. LC activation by stressors is modulated by endogenous opioids that serve to restrain LC activation and to facilitate a return to baseline activity upon stress termination. Sex differences in this opioid influence could be a basis for sex differences in stress vulnerability. Consistent with this, we recently demonstrated that μ-opioid receptor (MOR) expression is decreased in the female rat LC compared to the male LC and this was associated with sexually distinct consequences of activating MOR in the LC on cognitive flexibility. Given that the LC-NE system affects cognitive flexibility through its projections to the medial prefrontal cortex (mPFC), the present study quantified and compared the effects of LC-MOR activation on mPFC neural activity in male and female rats. Local field potential (LFPs) were recorded from the mPFC of freely behaving male and female rats before and following local LC microinjection of the MOR agonist, DAMGO or vehicle. Intra-LC DAMGO altered the LFP power spectrum selectively in male, but not female rats, resulting in a time-dependent increase in the power in delta and alpha frequency bands. LC microinfusion of ACSF had no effect in either sex. Together, the results are consistent with previous evidence for decreased MOR function in the female rat LC and demonstrate that this translates to a diminished effect on cortical activity that can account for sex differences in cognitive consequences. Decreased LC-MOR function in females could contribute to greater stress-induced activation of the LC, and increased vulnerability of females to hyperarousal symptoms of stress-related neuropsychiatric pathologies.

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