![]() ![]() Second, striatal unit–LFP coherence analysis confirmed the presence of high γ-oscillation in the striatum of R6/1 mice ( Fig. Contrary to R6/1 LFP, WT LFP showed only a single band of 15 to 25 Hz throughout the two training stages. The LFP of R6/1 mice also showed increased enrichment for 15 to 25 Hz at a late stage of training, suggesting that learning-related (i.e., behavioral) changes in trained R6/1 mice may contribute to the enrichment of this specific frequency. Averaged FFT for R6/1 mice showed a common enrichment of 40 to 80 Hz during both early and late stages of training, i.e., at the frequencies also seen in unit activity in these mice. To explore whether oscillatory single cells contribute to the striatal LFP oscillation (recorded from the same tetrodes) at γ frequency, we first examined power spectra by using fast Fourier transforms (FFTs Fig. Entrainment of Striatal INs to LFP High γ-Oscillation in R6/1 Mice. ( I and J) Coherence frequency distribution and phase relationship with high γ-cycle for coherent cells in R6/1 mice. ( H) Percentage of unit-to-LFP coherent INs and MSNs in both genotypes. Coherence value is display by the black line (left axis) and the phase by the red line (right axis). ( G) Typical example of a coherent IN at a frequency around 70 Hz. ( E and F) Power spectra of session-wide striatal LFP by FFT averaged for each genotype and training stage (early, E late, F). ( D) Relative frequency distribution of oscillatory frequencies among fast oscillatory pairs of cells in R6/1 mice. ( C) Proportions of pairs of neurons with slow (<10 Hz) and fast (50–80 Hz) oscillations in both genotypes. ( B) Relative frequency distribution of γ-oscillations frequencies for all fast oscillatory cells in R6/1 mice. ( A) Proportions of cells oscillating at low (<10 Hz, slow) and high (50-80 Hz, fast) frequencies in both genotypes. High γ-oscillation in the striatum in R6/1. Whereas the numbers of INs in the two groups were equivalent, the number of MSNs recorded from probes of R6/1 mice was significantly lower than in WT mice. 1 D) might have influenced these proportions, we compared the average numbers of MSN and IN recorded by tetrodes throughout the entire recording sessions ( Fig. To rule out the possibility that subtle differences in electrode locations between the two groups ( Fig. Previous studies have suggested heterogeneous density for IN along the dorsoventral axis of the striatum ( 15). These data provide crucial information on the in vivo cellular processes in the corticostriatal pathway through which the HD mutation exerts its effects on cognitive abilities in early HD. In addition, both the striatum and cortex in these mice showed a unique oscillation at high γ-frequency. Here, we report that a dramatically diminished recruitment of the vulnerable striatal projection cells, but not local interneurons, of R6/1 mice in coding for the task, compared with WT littermates, is associated with severe deficits in procedural learning. To test this hypothesis, we examined the firing properties of single cells and local field activity in the striatum and cortex of pre–motor-symptomatic R6/1 transgenic mice while they were engaged in a procedural learning task, the performance on which typically depends on the integrity of striatum and basal ganglia. In hereditary neurodegenerative Huntington disease (HD), early cognitive impairments before motor deficits have been hypothesized to result from dysfunction in the striatum and cortex before degeneration. ![]()
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