We investigated the effects of traumatic brain injury (TBI) on the glutamatergic synaptic transmission in the hippocampal CA1 area. A moderate impact (3.8-4.8 atm) was applied onto the left parietal cerebral cortex by a fluid percussion injury (FPI) device. Conventional intracellular recordings were made from hippocampal CA1 pyramidal neurons in vitro. Electrophysiological properties of these neurons were compared between three groups (control, FPI-ipsilateral, and FPI-contralateral). The excitability of postsynaptic membrane of CA1 pyramidal neurons was not altered by the moderate FPI; however, the evoked glutamatergic excitatory synaptic transmission in the pyramidal neurons of post-FPI-CA1 was enhanced. Paired-pulse facilitation (PPF) was significantly suppressed in both the FPI-ipsilateral and FPI-contralateral groups and the frequencies of mEPSPs in neurons from the bilateral FPI groups were greater than the frequency in the control group. These results suggest that the glutamatergic synaptic transmission in the hipppocampal CA1 area is facilitated through presynaptic mechanisms after TBI.
Bibliographical noteFunding Information:
This work was supported by a Grant-in-Aid for Scientific Research (C) (17500279) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. This research was also supported from the Ministry of Education, Culture, Sports, Science and Technology as a part of a project for establishing open research centers in private universities.
- Glutamate release
- Hippocampal CA1
- Intracellular recording
- Synaptic transmission
- Traumatic brain injury