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Results: 5

1.
Figure 2

Figure 2. Interneuron markers in the PFC of NVHL rats. From: A neonatal ventral hippocampal lesion causes functional deficits in adult prefrontal cortical interneurons.

A: Representative autoradiograms illustrating the expression of GAD67 (top) and PV (bottom) mRNAs in a control rat. The densities of hybridization signals are presented in a pseudocolor manner according to the calibration scales. The densities were quantified in the area indicated by the broken lines. B: Graphs summarizing the mean ± SD for GAD67 (left) and PV (right) mRNA levels in right and left PFC of control (gray bars) and NVHL (black bars) rats.

Kuei Y. Tseng, et al. J Neurosci. ;28(48):12691-12699.
2.
Figure 1

Figure 1. Neonatal ventral hippocampal lesion. From: A neonatal ventral hippocampal lesion causes functional deficits in adult prefrontal cortical interneurons.

A: Drawings showing the extension of the ventral hippocampal damage induced by neonatal ibotenic acid observed in adulthood. Gray and dark areas indicate maximal and minimal extents of damage, respectively. B: Coronal Nissl stained sections showing the ventral hippocampus of a sham rat (top, Sham) and a typical neonatal ventral hippocampal lesion (bottom, NVHL), characterized by cell loss (thick arrows), and enlarged ventricles (asterisks).

Kuei Y. Tseng, et al. J Neurosci. ;28(48):12691-12699.
3.
Figure 3

Figure 3. Basic membrane properties of PFC interneurons in NVHL and sham rats. From: A neonatal ventral hippocampal lesion causes functional deficits in adult prefrontal cortical interneurons.

A: Traces illustrating the firing pattern of fast-spiking interneurons (FSI) in PFC slices from developmentally mature (PD>60) sham and NVHL rats. FSI exhibited a pronounced fast AHP (center panel inset) and responded with a constant instantaneous firing rate throughout the current pulse (center panel: no spike-frequency adaptation). Right: Neurobiotin staining of the FSI from which the traces were obtained. B: Traces form a NFS interneuron, which instead show increasingly longer interspike intervals when activated with current injection (left and center panels). Right: Neurobiotin staining of the interneuron recorded. C: Plots of afterhyperpolarization (AHP) amplitude, half width, and action potential amplitudes and duration for both cell types.

Kuei Y. Tseng, et al. J Neurosci. ;28(48):12691-12699.
4.
Figure 4

Figure 4. Abnormal mat uration of PFC interneurons in NVHL rats. From: A neonatal ventral hippocampal lesion causes functional deficits in adult prefrontal cortical interneurons.

A: Plot showing the effect of quinpirole (1 µM) on PFC interneuron excitability in slices from developmentally mature (PD>60) sham (A) and NVHL (B) rats. The excitatory action of quinpirole was observed only in the PFC of adult sham rats. In the lesioned animals, quinpirole failed to increase PFC interneuron excitability. Instead, some neurons were inhibited with quinpirole. C: Representative traces illustrating the increase in excitability in a neuron from a sham rat (top) and a neuron from a NVHL rat (bottom). D,E: Plot showing the lack of effect of quinpirole (1 µM) in pre-pubertal (PD<35) sham (D) and NVHL (E) rats. F: Plot of normalized responses in cell excitability changes by quinpirole in all groups. An excitatory action of quinpirole was observed only in the PFC of adult sham rats. In contrast, the majority of adult NVHL interneurons (70 %) recorded remained unchanged after quinpirole, resembling the response observed in the PFC of pre-pubertal rats, while others showed a decrease in excitability.

Kuei Y. Tseng, et al. J Neurosci. ;28(48):12691-12699.
5.
Figure 5

Figure 5. Loss of a D2-dependent GABA modulation of synaptic responses of pyramidal neurons in NVHL rats. From: A neonatal ventral hippocampal lesion causes functional deficits in adult prefrontal cortical interneurons.

A: Electrical stimulation of layers I–II in the medial PFC of NVHL elicited a primarily AMPA-dependent excitatory postsynaptic potential (EPSP) in deep layer pyramidal neurons. Diagram illustrating the arrangement of stimulating electrode (upper right; layers I–II) and recording sites (lower left; layers V–VI), along with an overlay of EPSPs recorded in the pyramidal neuron. Inset shows EPSPs at higher magnification. B: Diagram illustrating the decrease in EPSP amplitude by quinpirole (2 µM) in slices from sham rats. C: Plot illustrating the effects of quinpirole in slices from NVHL rats. D: Plot summarizing the time course of these effects. The D2-dependent synaptic attenuation in pyramidal neurons was persistent in the PFC of sham rats (open squares), but not in NVHL rats (filled squares). The GABA-A antagonist picrotoxin blocked the persistent component of this D2 effect in slices from sham rats (open circles), but did not affect the response when given alone (open triangles). Thus, the D2 modulation of cortico-cortical synaptic responses in adult NVHL rats lacks the recruitment of interneurons. ***P<0.0005, **P<0.005, *P<0.05; quinpirole vs. quinpirole + picrotoxin.

Kuei Y. Tseng, et al. J Neurosci. ;28(48):12691-12699.

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