Objective: Exposure to environmental chemicals during embryonic development increases the risk of autism in offspring by disrupting intercellular communication in the Cornu Ammon3 (CA3) region of the hippocampus, which has many synaptic pathways. Most research has focused on the effect of neurons and microglial prenatal inflammation in autism, but potential modifications of astrocytes and neuron-astrocyte communication have been less studied. In this context, the aim of the study is to investigate the effect of maternal exposure of triphenylphosphite (TPP), an environmental neurotoxic substance, on astrocyte junction channels in the hippocampal CA3 region of adolescent and adult rats with the expression of Connexin43. Methods: The study has 6 groups: Three group of juvenile rats: Control, VPA (500 mg/kg) and TPP (100 mg/kg) (Postnatal day=35) and the group of adult rats control, VPA (500 mg/kg) and TPP (Postnatal day=60). There are 3 pregnant rats in each group. Maternal SF, VPA, TPP ip was administered 12.5 days of pregnancy. Rats were perfused on P35 (n=10 for each group) and P60 (n=10 for each group) for connexin43 immunohistochemically staining. The immunohisto-logical staining, the sections were incubated with anti-connexin 43 antibody and the reaction was observed under a light microscope. The immunoreactivity data was obtained by using Image J and cellSens software. Results: The Comu Ammon 3 (CA3) area was considered. The results showed that connexin43 expression increased on CA3 region in VPA and TPP group (both juvenile and adult rats). Conclusion: The increase of connexin 43 in the TPP group both in adolescence and adulthood proved impaired intercellular communication and increased neuroinflammation. Consequently, TPP exposure during embryonic development increases the risk of autism by disrupting synaptic transmission in the long term. However behavioral, biochemical and molecular analyzes are required to investigate the effect of maternal TPP exposure in multiple perspective. [ABSTRACT FROM AUTHOR]