Miyazawa T, Nishiye H, Sato K, Kobayashi R, Hattori S, Shirai T, Obata K
Department of Neurosurgery, Juntendo University School of Medicine, Tokyo, Japan.
Brain Dev. 1992 Mar;14(2):75-9. doi: 10.1016/s0387-7604(12)80089-1.
We attempted to develop a method for investigating impairment of synaptogenesis quantitatively involving measurement of the fluorescence intensity emitted by immunohistochemically stained rat brain using a monoclonal antibody (Mab 171B5) against a synaptic vesicle protein (SVP-38). We applied this method to congenitally hydrocephalic and non-hydrocephalic brains of HTX-rats, and compared the postnatal changes in the fluorescence intensity in the molecular layer of the cerebral cortex. In non-hydrocephalic HTX-rats, the fluorescence intensity remained nearly unchanged from the 1st to 7th postnatal day and then increased at an almost linear rate until the 21st postnatal day, when it reached 4.5 times the value on the 7th postnatal day. The increase thereafter was gradual until the 28th postnatal day. In hydrocephalic HTX-rats, the fluorescence intensity increased nearly in parallel with that in non-hydrocephalic HTX-rats up to the 21st postnatal day. On the 28th postnatal day, the fluorescence intensity showed a marked reduction (P less than 0.01). This finding indicates that despite the presence of continuous pressure due to progressive ventricular dilatation after birth, synaptogenesis in the cerebral cortex may be relatively resilient.
