A recent study published in Neuroscience Bulletin demonstrated that astrocytic gap junctions facilitate the abnormal neuronal synchrony in young autistic model MeCP2 overexpressing mice, revealing the potential role of the astrocyte network in the pathogenesis of autism. This work was performed by researchers in Dr. XU Hua-tai’s lab at the Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology of the Chinese Academy of Sciences, State Key Laboratory of Neuroscience.  

　　Abnormality in synchronous neuronal activity has been widely detected by brain imaging of autistic patients, but its underlying neural mechanism remains unclear. Combining in vivo two-photon calcium imaging with multichannel electrophysiological whole-cell patch-clamp recordings, they found gap junctions among astrocytes significantly contribute to the aberrant neuronal synchronization in Tg1 mice over-expressing human autism risk gene MeCP2 (A widely used mouse model of Autism Spectrum Disorder). Using in vivo two-photon calcium imaging on the somatosensory cortex of Tg1 mice, the authors carried out a longitudinal study from early postanal development stage to adulthood. They found, compared with wild-type control mice, Tg1 mice exhibited higher neural synchrony at the early postnatal stage but lower at adulthood. Whole-cell recording on neuronal pairs from acute brain slices further revealed that higher neuronal synchrony in the young postnatal Tg1 mice could be attributed mainly to the more prevalent giant slow inward currents (SICs). In addition, both in vivo and acute brain slice calcium imaging demonstrated the hyperactive astrocytes in Tg1 mice at early postnatal stage. Blocking the astrocytic gap junctions in vivo markedly decreased the generation of SIC on neurons, and also reduced the neural synchrony level in young Tg1 brain. Thus, astrocytic gap junction propagated the effects for hyperactive astrocyte on neuronal network, triggering synchronized SICs on neurons within larger distance, further promoted the abnormally high neural synchrony for neocortical network in Tg1 brain at early postnatal stage. Their results demonstrated the critical role of astrocytic-neuronal network communication in the pathogenesis of autism disorder.