25th Biennial Meeting of the International-Society-for-Neurochemistry Jointly with the 13th Meeting of the Asian-Pacific-Society-for-Neurochemistry in Conjunction with the 35th Meeting of the Australasian-Neuroscience-Society location:Cairns, Australia date:August 23-27, 2015
Mild traumatic brain injury (TBI) results in impairments of hippocampal synaptic plasticity and acute cognitive deficits in mice.
L. Marschner1,2, T. Ahmed2, J. Johannsen1, D. Balschun2
1 Unit for Cognitive Neuroscience, Øster Farimagsgade 2A, 1353 Copenhagen K, Denmark
2 Laboratory of Biological Psychology, KU Leuven, Tiensestraat 102, B-3000 Leuven, Belgium
Traumatic brain injury (TBI) has been recognized as a major health issue and receives therefore increasing attention. TBI has devastating acute effects and seems to initiate long-term neurodegeneration. Concussion is a mild form of TBI which results in transient cognitive impairments in humans. Although not directly injured by the impact, the hippocampus has been found to be highly vulnerable to TBI. In the days, weeks and months following TBI, the hippocampus undergoes atrophy and severe changes in synaptic plasticity.
Here we subjected adult mice to a single mild impact on the intact skull, just above the midline suture. Three days after trauma, we measured long-term potentiation (LTP) and long-term depression (LTD), the two most established cellular correlates of learning & memory and best investigated types of synaptic plasticity. Using ex vivo long-term field recordings in hippocampal CA1-region, we found that TBI mice show an impaired LTP and slight changes in LTD as compared with sham-treated mice. In agreement with these deficits in synaptic plasticity, TBI mice exhibited transient deficits in spatial memory as measured in the Morris water maze. These findings support a substantial impairment of hippocampal synaptic plasticity and cognition in response to even mild TBI despite the lack of gross pathological changes in the hippocampus. Our data advocate LTP and LTD as sensitive tools for the development of new lead compounds and therapeutic targets for TBI.