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. Author manuscript; available in PMC: 2019 Feb 8.
Published in final edited form as: Cell. 2018 Feb 8;172(4):683–695.e15. doi: 10.1016/j.cell.2018.01.005

Figure 2. Striatal FSIs control MSN calcium transient rates.

Figure 2

(A) Recording configuration and (B) schematic of light path for head-mounted microscope enabling imaging with simultaneous optogenetic suppression of FSIs in vivo. (C) Calcium signals recorded in an open field. Sweeps represent successive light pulses from one exemplar MSN. (D) Raster and PSTH of calcium transients detected in the MSN recording depicted in Panel C. (E) Cell fields for control (left) and PV-eNpHR3.0 (right) mice, color-coded to reveal optogenetically driven change in calcium transient rates. (F) Electrophysiological spikes and calcium transients are both disinhibited by PV-eNpHR3.0 silencing of FSIs. (N=5 PV-eNpHR3.0 mice, n=34 MSNs for electrophysiology, sign rank test P<10−4 Pre-Light, P<10−6 Post-Light; N=4 PV-eNpHR3.0 mice, n=235 neurons for calcium transients, sign rank test P<10−33 Pre-Light, P<10−36 Post-light). Comparison of spiking and calcium transients reveals greater disinhibition of calcium, consistent with a preferential role for FSIs in controlling MSN calcium signaling (rank sum test, P<0.01). (G) Modulation index (Light On)/(Light On + Light Off) for all neurons shows disinhibition of calcium transients during eNpHR3.0 suppression of FSIs, but not in control animals. (N=4 control mice, n=400 neurons, sign rank test against 0.5, P>0.1; N=4 test mice, n=235 neurons, sign rank test against 0.5, P<10−32). (H) Calcium transient peak amplitudes are increased during FSI silencing (N=4 control mice, n=120 neurons, P>0.2 N=4 PV-eNpHR3.0 mice, n=212 neurons, P<10−9). Average transient from exemplar neuron inset with Light Off (black) and Light On (Amber). All error bars are s.e.m. and center values are group means.