Perinatal complications, including low birth weight, have been proposed to be involved in the onset of psychiatric disorders such as schizophrenia. We have reported that expression levels of TrkB, a high affinity receptor for brain-derived neurotrophic factor (BDNF), was decreased although both ligand BDNF and p75 (low affinity receptor) levels were unchanged in cortical cultures prepared from low birth weight rats (postnatal 1-2 days) by intrauterine growth retardation (IUGR) (Neurosci lett, 2010, 476, 104-9). Here, we examined whether such a reduced TrkB affects phospholipase Cγ(PLCγ) signaling which is one of the TrkB downstream and has a role in the glutamatergic neurotransmission mediated by BDNF. We found that the BDNF-induced glutamate release and activation of PLCγ also were repressed in the IUGR cultures. Both impairments were completely restored after exogenous TrkB transfection. In vivo analysis, we observed that reduced levels of TrkB in the cerebral cortex continued until at least postnatal 7 days, although the weight of IUGR pups recovered. It is possible that reduced TrkB due to IUGR results in downregulation of BDNF-mediated neurotransmission (Neurochem Res., 2014, 39, 785-92). The study was supported by grants from the Grant-in-Aid for Challenging Exploratory Research (JSPS KAKENHI Grant Number 25640019) (T. N.) and for Scientific Research (B) (JSPS KAKENHI 24300139) (T. N.) in the Ministry of Education, Culture, Sports, Science, and Technology of Japan.