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. 2016 Dec 20;5:e21616. doi: 10.7554/eLife.21616

Figure 3. The impaired autonomous activity of STN neurons in BACHD mice is rescued by antagonism of NMDARs.

Figure 3.

(A) Examples of loose-seal cell-attached recordings of 6-month-old BACHD STN neurons from an untreated slice (left) and a slice that was treated with 50 µM D-AP5 for 3–5 hr prior to recording. (B) Population data showing elevated autonomous firing in STN neurons from D-AP5 pre-treated slices from 2-month-old and 6-month-old BACHD mice but not in WT mice. (C) Population data showing increased firing regularity in STN neurons from D-AP5 pre-treated slices from 6-month-old BACHD mice but not 2-month-old BACHD mice or WT mice. (D) Population data showing a higher proportion of active neurons in STN neurons from D-AP5 pre-treated slices from 2-month-old and 6-month-old BACHD mice but not in WT mice. *p < 0.05. ns, not significant. Data for panels B–C provided in Figure 3—source data 1.

DOI: http://dx.doi.org/10.7554/eLife.21616.008

Figure 3—source data 1. Autonomous firing frequency and CV for BACHD control and D-AP5 pretreated STN neurons in Figure 3B–C.
DOI: http://dx.doi.org/10.7554/eLife.21616.009
elife-21616-fig3-data1.xlsx (34.2KB, xlsx)
DOI: 10.7554/eLife.21616.009