Skip to main content
. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: Cerebellum. 2021 Feb;20(1):41–53. doi: 10.1007/s12311-020-01179-7

Figure 5. Purkinje neuron dysfunction persists in late symptomatic SCA3 mice.

Figure 5.

Patch-clamp recordings were performed in vehicle-treated WT, vehicle-treated SCA3, and ASO-5-treated SCA3 mice at 15 months of age. (A) Purkinje neuron firing frequency is increased in the posterior cerebellar lobules, but not anterior cerebellar lobules, of SCA3 mice. (B) The regularity of spiking is not significantly changed between SCA3 and WT neurons in either anterior or posterior cerebellum. (C) The increased spiking response to depolarizing current persists in SCA3 Purkinje neurons at 15 months of age in the anterior cerebellum, although this did not reach statistical significance in the posterior cerebellum (D). (E) The threshold of injected current to elicit depolarization block was significantly reduced in SCA3 Purkinje neurons compared to WT in both regions of the cerebellum. (F) Input resistance was not significantly altered in either anterior or posterior cerebellum at this age. * = p<0.05, ** = p<0.01, two-tailed Student’s t-test or two-way repeated measures ANOVA with Holm-Sidak correction for multiple comparisons in (C) and (D).