Figure 8.
Altered evoked excitatory synaptic response in nRT.
A
, Low-power videomicroscopic image of a horizontal slice obtained 7 d after the cortical infarct. The nRT is localized between the ventrobasal complex (VB), formed by somatosensory thalamic relay nuclei, and the internal capsule (ic), which is separated from the cortex by the striatum (Str.). Evoked responses in nRT were obtained with a concentric bipolar stimulating electrode (stim.) positioned in the adjacent ic activating glutamatergic fibers of passage from cortex or thalamus projecting to nRT. The asterisk indicates the tip of the recording electrode (e).
B1
, Top, Representative averaged threshold responses (n ≥ 10) from single nRT cells from control (black) and injured (red) rats. Bottom, Evoked excitatory synaptic current (EPSC) amplitudes were significantly decreased in the injured nRT cells (n = 17) versus the controls (n = 13) (****p < 0.0001).
B2
, Top, Normalized EPSCs depicted in
B1
. Bottom, Weighted decay time constant (τD,W) was significantly increased in the injured cells (n = 17) versus the controls (n = 13) (*p < 0.05).
C
, Altered evoked EPSC response to a train of five stimuli at 50 Hz.
C1
, Representative averaged responses (n ≥ 10) from single nRT cells from control (black) and injured (red) rats at 1.5× threshold.
C2
, Ratio of second response to first response (or PPR). Note the significant (*p < 0.05) decrease of the PPR in the injured cells (n = 10) versus the controls (n = 6).
C3
, Normalized EPSC amplitude plots from control (n = 6) and injured (n = 10) nRT cells during 50 Hz stimulation. The injured cells were less likely to potentiate than the control ones (
C1–C3
). The amplitude of the evoked EPSC was significantly decreased for each shock (*p < 0.05, injured vs control). Error bars indicate SEM.
D
, Representative evoked EPSPs at different potentials in nRT cells induced by a train of five stimuli at 200 Hz at 1.5× threshold in the ic. In the control cell, the synaptic stimulation induced action potential firing, which increased with membrane hyperpolarization (3 action potentials at −77 mV, 11 at −87 mV, and 13 at −95 mV), as a large LTS (arrow) crowned with high-frequency burst of action potentials was recruited. Note the less efficient summation of EPSPs in the injured cell and a decrease in the number of action potentials with hyperpolarization (2 action potentials at −76 mV, 1 at −86 mV, and 0 at −95 mV) associated with a lack of the LTS (compare
D
, bottom left, with bottom right traces). e, Recording electrode; EML, medullary lamina; ic, internal capsule; stim. stimulating electrode; Str., striatum; VB, ventral-basal thalamic complex.