Mutations in THAP1/DYT6 reveal that diverse dystonia genes disrupt similar neuronal pathways and functions
Fig 5
Cortico-striatal synaptic plasticity is altered in Thap1+/- and Thap1C54Y/+ derived slices.
(A) Thap1+/- mice are deficient in synaptically-induced LTD in dorsolateral striatum compared to wildtype controls (A1; p < .05), while LTP in the dorsomedial region is intact (A2). Representative excitatory postsynaptic potential (EPSP) traces in this and panel B were averaged over the baseline period (thin line) and over the final 5 min of recording (thick line), color coded to the graph. Calibration for these and all other traces: 1 mV / 5 ms. (B) In Thap1C54Y/+ mice, LTD was not significantly reduced (B1), but LTP was deficient (B2; p < .05). Note that wildtype data are the same as for panel A, and that all genotypes were analyzed together. (C) Paired-pulse ratio was not altered in Thap1+/- and Thap1C54Y/+ mice. The traces show averaged EPSPs recorded at inter-stimulus interval = 50 ms (thin and thick lines show responses to first and second stimuli, respectively). All graphs show group means ± SEM, and the number of slices/mice for each group are shown in parentheses. Data were analyzed by ANOVAs performed over the final 5 minutes of recording (panels A and B) or on averaged paired-pulse data for each interval (panel C), followed where appropriate by Newman-Keuls post-hoc tests. *p<0.05 See also S9 Table.