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. 2021 Mar 31;15:652721. doi: 10.3389/fncel.2021.652721

Figure 1.

Figure 1

Single or repeated traumatic brain injury (TBI) results in persistent hyperexcitability at CA3-CA1 synapses. Rats subjected to a single TBI (sTBI), or repeated TBI (rTBI), exhibited persistent upregulation at CA3-CA1 synapses, as revealed using extracellular field recordings (fEPSPs). (A1) fEPSP Input-output curves obtained from CA1 hippocampal field recordings using Schaffer collateral stimulation, 30 days after sham surgery, sTBI or rTBI, demonstrating increasing field potential (fEPSP) slopes resulting from increasing stimulus intensity ranging from 100 μA to 1,000 μA. fEPSPs from both the sTBI and rTBI groups showed a steeper slope at most stimulus intensities compared to the sham treatment group, with no significant difference between the sTBI and rTBI groups. (A2) Representative input-output fEPSP traces taken from sham, sTBI, and rTBI rats. (B1) sTBI and rTBI did not affect the paired-pulse ratio of fEPSPs, compared to sham, indicating that there was no significant difference in the presynaptic release probability of glutamate between groups. (B2) Representative traces showing paired fEPSPs evoked at a 50 ms interstimulus interval. All recordings were on the hippocampal side ipsilateral to the TBI impact site (over the right sensorimotor cortex). #p < 0.05 for sham vs. sTBI. *p < 0.05.for sham vs. rTBI. Error bars represent the standard error of the mean.