RT Journal Article
SR Electronic
T1 Prenatal Exposure to MAM Impairs mPFC and Hippocampal Inhibitory Function in Mice during Adolescence and Adulthood
JF eneuro
JO eNeuro
FD Society for Neuroscience
SP ENEURO.0362-24.2024
DO 10.1523/ENEURO.0362-24.2024
VO 11
IS 11
A1 He, Zhiyin
A1 He, Qian
A1 Tang, Xiaorong
A1 Huang, Keni
A1 Lin, Yiwen
A1 Xu, Jianrui
A1 Chen, Qiliang
A1 Xu, Nenggui
A1 Yao, Lulu
YR 2024
UL http://www.eneuro.org/content/11/11/ENEURO.0362-24.2024.abstract
AB Neurodevelopmental abnormalities are considered to be one of the important causes of schizophrenia. The offspring of methylazoxymethanol acetate (MAM)–exposed mice are recognized for the dysregulation of neurodevelopment and are well-characterized with schizophrenia-like phenotypes. However, the inhibition-related properties of the medial prefrontal cortex (mPFC) and hippocampus throughout adolescence and adulthood have not been systematically elucidated. In this study, both 10 and 15 mg/kg MAM-exposed mice exhibited schizophrenia-related phenotypes in both adolescence and adulthood, including spontaneous locomotion hyperactivity and deficits in prepulse inhibition. We observed that there was an obvious parvalbumin (PV) loss in the mPFC and hippocampus of MAM-exposed mice, extending from adolescence to adulthood. Moreover, the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) in pyramidal neurons at mPFC and hippocampus was significantly dampened in the 10 and 15 mg/kg MAM-exposed mice. Furthermore, the firing rate of putative pyramidal neurons in mPFC and hippocampus was increased, while that of putative inhibitory neurons was decreased during both adolescence and adulthood. In conclusion, PV loss in mPFC and hippocampus of MAM-exposed mice may contribute to the impaired inhibitory function leading to the attenuation of inhibition in the brain both in vitro and in vivo.