METHODS: Thirty-eight participants were divided into control (n = 19) and MBI (n = 19) groups. Control participants were normal, healthy people, and participants with MBI were assigned into two groups: MBI 1st Test (7 days after a road traffic accident (RTA)) and MBI 2nd Test (2-6 months after RTA with the same participants of the 1st Test group). The 128-ERP nets were used on the heads of the participants during the experiments. Under the auditory oddball paradigm, all participants silently counted the target tones, while ignoring the standard tones. This study used the sLORETA tool in the Net Station software for the source localization of the P300 ERP component. The Mann-Whitney U test was used to compare intensities between groups, while the Wilcoxon Signed-Rank test was applied for paired observations within groups.
RESULTS: Standard stimuli evoked P300 sources in the superior frontal gyrus (BA11) of the right frontal lobe in the control group, the superior temporal gyrus (BA38) of the right temporal lobe in the MBI 1st Test group, and the inferior frontal gyrus (BA47) of the left frontal lobe in the MBI 2nd Test group. Meanwhile, target stimuli evoked P300 sources at BA11 for all groups but in different gyrus: the superior frontal gyrus, orbital gyrus, and rectal gyrus in the control, MBI 1st Test, and MBI 2nd Test groups, respectively. In addition, there were significant differences in dipole intensities between and within groups among control and MBI patients in both standard and target stimuli.
CONCLUSION: P300 source localization was shifted presumably due to the auditory cognitive impairment, and the dipole intensities were significantly higher in the MBI group than in the control group, indicating that the MBI group compensated for both standard and target tone stimuli, reflected in the sLORETA investigation.
Methods: Using a pilocarpine-induced epileptic mouse model, sensory-motor and visual cortical slices were prepared, and the whole-cell patch clamp technique was used to record spontaneous inhibitory post-synaptic currents (sIPSCs).
Results: The primary finding was that the mean amplitude of sIPSC from the sensory-motor cortex increased significantly in epileptic mice when the recording pipette contained MK-801 compared to control mice, whereas the mean sIPSC frequency was not significantly different, indicating that post-synaptic mechanisms are involved. However, there was no significant pre-synaptic inhibition through preNMDARs in the acute brain slices from pilocarpine-induced epileptic mice.
Conclusion: In the acute case of epilepsy, a compensatory mechanism of post-synaptic inhibition, possibly from ambient GABA, was observed through changes in the amplitude without significant changes in the frequency of sIPSC compared to control mice. The role of preNMDAR-mediated inhibition in epileptogenesis during the chronic condition or in the juvenile stage warrants further investigation.
Methods: We used a 128-child ERP net for the ERP experiment. Two types of stimuli were presented as either congruent or incongruent stimuli. Congruent stimuli included a matching auditory sound with an animal image, whereas incongruent stimuli included unmatched animal sounds. A total of 24 age-matched children were recruited in the control (n = 12) and dyslexia (n = 12) groups. Children pressed button '1' or '2' when presented with congruent or incongruent stimuli, respectively. The P300 amplitudes and latencies with topographic voltage distribution were analysed for both groups.
Results: The dyslexia group evoked significantly higher P300 amplitudes at the T4 area than the control group. No significant differences were found in cases of P300 latency. Moreover, the dyslexia group demonstrated a higher intensity of P300 voltage distribution in the right parietal and left occipital areas than the control group.
Conclusion: Post-attentive integration for children with dyslexia is higher and that this integration process implicated the parietal and occipital areas.
METHODS: Embryonic day 18 (E-18) rat hippocampus neurons were cultured with poly-L-lysine coated glass coverslips. Following optimisation, KA (0.5 μM), a chemoconvulsant agent, was administered at three different time-points (30, 60 and 90 min) to induce seizure in rat hippocampal neuronal cell culture. We examined cell viability, neurite outgrowth density and immunoreactivity of the hippocampus neuron culture by measuring brain derived neurotrophic factor (BDNF), γ-amino butyric acid A (GABAA) subunit α-1 (GABRA1), tyrosine receptor kinase B (TrkB), and inositol trisphosphate receptor (IP3R/IP3) levels.
RESULTS: The results revealed significantly decreased and increased immunoreactivity changes in TrkB (a BDNF receptor) and IP3R, respectively, at 60 min time point.
CONCLUSION: The current findings suggest that TrkB and IP3 could have a neuroprotective role which could be a potential pharmacological target for anti-epilepsy drugs.