Changes in the firing rates of hippocampal units in pilocarpine-treated rats.

<p><b>A</b>. Relative discharge rates 30 min before and after pilocarpine treatment in SE (red) and nonSE (blue) rats. <b>B</b>. Rate-by-rate comparison of firing rate change before [-10∶0 minute] and after [5∶15 minute] pilocarpine injection (see gray zones in panel A) of individual neurons from SE (red dots) and nonSE (blue dots) rats. Filled circles indicate significant difference of firing rate after pilocarpine injection. Open circles indicate no change in firing rate.</p

Recording and analysis profiles of neuronal ensembles.

<p><b>A</b>. Histological locations (asterisks) of recording electrode tips in the hippocampus. Scale bar indicates 500 μm. <b>B</b>. Waveforms of hippocampal spikes (yellow) and noise signals (whitish-gray) separated by morphology (calibration: 0.2 ms, 100 μV). <b>C</b>. Clusters of single units and noise signals separated according to the first two principal components (PC1 on x-axis; PC2 on y-axis). <b>D</b>. Autocorrelogram of a single unit with an absolute refractory period of a minimum of 2 ms.</p

Cross-correlation histograms show coincident firing of a sample pair of neurons from one SE rat between the baseline period and early preictal period.

<p>Black line indicates the raw correlation smoothed with a 7 ms boxcar window (CCH_raw). The jitter-predicted correlation (Jitter₅₀, blue) indicates the correlation driven by common input, as determined by jitter shuffling of the spike train with a 50 ms window. The cross-correlogram (‘CCG’, or COIN₅₀, red) corresponds to pair-specific coincident activity, defined as the difference between raw coincidences and jitter coincidences.</p

Table_1_Characterization of Hippocampal-Thalamic-Cortical Morphometric Reorganization in Temporal Lobe Epilepsy.docx

IntroductionBrain cortico-subcortical connectivity has been investigated in epilepsy using the functional MRI (MRI). Although structural images cannot demonstrate dynamic changes, they provide higher spatial resolution, which allows exploration of the organization of brain in greater detail.MethodsWe used high-resolution brain MRI to study the hippocampal-thalamic-cortical networks in temporal lobe epilepsy (TLE) using a volume-based morphometric method. We enrolled 22 right-TLE, 33 left-TLE, and 28 age/gender-matched controls retrospectively. FreeSurfer software was used for the thalamus segmentation.ResultsAmong the 50 subfields, ipsilateral anterior, lateral, and parts of the intralaminar and medial nuclei, as well as the contralateral parts of lateral nuclei had significant volume loss in both TLE. The anteroventral nucleus was most vulnerable. Most thalamic subfields were susceptible to seizure burden, especially the left-TLE. SPM12 was used to conduct an analysis of the gray matter density (GMD) maps. Decreased extratemporal GMD occurred bilaterally. Both TLE demonstrated significant GMD loss over the ipsilateral inferior frontal gyrus, precentral gyrus, and medial orbital cortices.SignificanceThalamic subfield atrophy was related to the ipsilateral inferior frontal GMD changes, which presented positively in left-TLE and negatively in right-TLE. These findings suggest prefrontal-thalamo-hippocampal network disruption in TLE.</p

Local field potentials in 10-sec time windows of representative SE and nonSE rats at baseline period (upper panel) and at 5 min (middle panel) and 85 min (lower panel) after pilocarpine treatment.

<p>Local field potentials in 10-sec time windows of representative SE and nonSE rats at baseline period (upper panel) and at 5 min (middle panel) and 85 min (lower panel) after pilocarpine treatment.</p

Changes in functional connectivity across all neuronal pairs from cross-correlation analysis.

<p>Upper panel shows the raw correlation (CCH_raw), correlation driven by common input (Jitter₅₀), and correlation of neuronal pairs (COIN₅₀) based on peak values at baseline and early preictal periods. Lower panel shows log ratios of the coincident peak of early preictal period to that of baseline period. The vertical scatter plots integrate the distributions of all ratio results in CCH_raw, Jitter₅₀, and COIN₅₀. Each data point represents a result from one neuronal pair. The mean peak ratio is indicated by black horizontal line, and the median peak ratio is shown in green. The correlation value of neuronal pairs was significantly larger in nonSE rats than SE rats.</p

Outline of the experimental procedure.

<p><b>A</b>. Experimental steps for induction of status epilepticus (SE). <b>B</b>. Temporal profiles of SE in 9 rats after injection of pilocarpine. No SE was identified in 12 rats. The black bar indicates the occurrence of SE. The early post-pilocarpine period was defined as the time period of 5–15 min after injection of pilocarpine, as delimited between the two vertical dashed lines.</p

Mean onset time (± SEM) of status epilepticus (SE) relative to behavioral and local field potential (LFP) patterns after i.p. pilocarpine injection in nonSE and SE groups.

<p>Mean onset time (± SEM) of status epilepticus (SE) relative to behavioral and local field potential (LFP) patterns after i.p. pilocarpine injection in nonSE and SE groups.</p

Resting state networks from EEG data.

<p>(a) Distributions of averaged cortical activation during an eyes-closed resting-state condition in 21 AD and 21 MCI patients, respectively. (b) 5 activated maps on the sagittal, coronal and axial MR images are shown. The sources values were smoothed after being re-interpolated (the size of the smoothing kernel = 5). The current strength of cortical sources is color coded; large values are represented in red, and small values are in blue.</p

The estimated normalized and averaged power spectrum of 12 ROIs at 1–40 Hz across AD and MCI, respectively.

<p>The bar plots represent the normalized power values in each frequency band in AD and MCI. δ, delta; θ, theta; α1, alpha1; α2, alpha2; β1, beta1; β2, beta2; γ, gamma. *, p<0.05; **, p<0.01; ***, p<0.001.</p