Cerebellar climbing fibers impact experience-dependent plasticity in the mouse primary somatosensory cortex
- Department of Neurology, University of Chicago, United States
- Department of Neurobiology and Neuroscience Institute, University of Chicago, United States
Figures
Figure 1 with 4 supplements
Optogenetic climbing fiber (CF) co-activation prevents adaptive L2/3 pyramidal cell potentiation in S1 cortex.
(A) Experimental schematic for D–L. (B and C) ChR2 expression in the inferior olive (IO) and optogenetic CF activation evokes calcium transients in Purkinje cells (PCs). (B) Calbindin staining of PCs marks the cerebellum (shown here in the same plane as the IO, where ChR2 is injected; white arrowhead). Scale bar: 1 mm. (C) Two-photon field of view of PC dendrites with calcium responses evoked by 470 nm, 50 ms LED pulses. Scale bar: 100 µm. Right: Distribution of response amplitudes (box: 25th and 75th percentiles; line: median; points: mean across trials). Trace scale bar: 0.2 ∆F/F; 0.5s; line represents mean; shaded region represents SEM across neurons. (D) GCaMP6f expression in S1 cortex. Scale bar: 1 mm. (E) Sagittal view of ChR2-expressing CF terminals in the contralateral cerebellar cortex that are activated in optogenetic experiments. Scale bar: 100 µm. (F) Left: example of the morphological identification of L2/3 pyramidal cells by apical dendrites (green arrowheads) and INs (white arrowheads) in a two-photon field of view. Scale bar: 100 µm. Right: two-photon field of view of Pyramidal cell at higher magnification. Scale bar: 15 µm. (G) Pyramidal cell plasticity after RWS (N=12 mice, n=287 neurons) and after pairing with CF activation (RWS+CF; N=11 mice, n=534 neurons). Trace scale bars: 0.1 ∆F/F; 0.5 s; line represents mean; shaded region represents SEM across neurons. Right: quantification of the evoked responses across neurons. Box: 25th and 75th percentiles; line: median; whiskers: range. (H) Data in G binned across time. Blue shading: RWS or RWS+CF. Points: mean; error bars: SEM across neurons. (I) Quantification across mice, normalized to the pre-plasticity response. Blue line: mean across animals. (J–L) Analyses for INs in the same mice; data visualization as in G-I. All summary data, statistical methods, and significance levels are available in Figure 1—source data 1.
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Figure 1—source data 1
Summary data, statistical methods, and significance levels for data in Figure 1.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig1-data1-v1.xlsx
Figure 1—figure supplement 1
Optogenetic climbing fiber (CF) activation causes GCaMP6f-encoded calcium transients in Purkinje cells.
(A) Schematic of inferior olive (IO) injection. Top left: cerebellum (calbindin-staining of PCs) and IO; white arrowhead (as in Figure 1B). Scale bar: 1 mm. Bottom: ChR2 expression in the principal IO (IOPr) and dorsal IO (IOD) in the same animal at higher magnification. Scale bar: 100 µm bottom. (B) Overlap of VGluT2-stained excitatory terminals with ChR2 expression and calbindin-staining of PCs in the contralateral cerebellar cortex. Scale bars: 40 µm. (C) Post-hoc verification of ChR2 expression in CF terminals in crus I and II. Scale bars: 50 µm. (D) Measure of distance from the pial surface to the cerebellar nuclei (CBN). While the IO innervates both the cerebellar cortex and CBN directly, it is unlikely that CF terminals other than the superficial ones innervating PCs are optogenetically activated as the intensity of blue light decreases exponentially in brain tissue. Scale bar: 300 µm. Dashed line: 2 mm. (E) Experimental schematic for F-I. (F) Test of various stimulus protocols: 3×15 ms, 2×20 ms, 1×50 ms (interval 50 ms) and (3×15 ms)*2 (interval 50 ms). Traces show response averages (n=102 cells from one mouse). Trace scale bars: 0.1 ∆F/F; shaded region: SEM across cells. (G) Bar graphs showing response peaks (left) and integrals (right) from the corresponding data in F. Data: mean ± SEM. (H) Right: calcium transients evoked by 470 nm, 50 ms LED light pulses in PCs in crus I/II (n=131 cells; N=2 mice) in comparison to spontaneous events (left). Trace scale bars: 0.1 ∆F/F; 0.5 s; shaded region: SEM across cells. (I) Amplitude (top) and latency to peak (bottom) measures from the corresponding data in H. Data: mean ± SEM. All summary data, statistical methods, and significance levels are available in Figure 1—figure supplement 1—source data 1.
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Figure 1—figure supplement 1—source data 1
Summary data, statistical methods, and significance levels for data in Figure 1—figure supplement 1.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig1-figsupp1-data1-v1.xlsx
Figure 1—figure supplement 2
Plasticity in different neuron types.
(A) Experimental schematic. (B) Event (spike) probability around stimulus onset with the window for detection of stimulus-evoked events (orange; three standard deviations above the mean event probability, calculated across all frames collected during the 20 s trial periods). (C) Pie chart indicating the percentage of L2/3 pyramidal cells recruited or suppressed by repeated whisker stimulation (RWS)/RWS+CF activity (only responsive to whisker stimulation in post- or pre-periods, respectively) and how many remained entirely unresponsive. (D) Left: RWS-evoked response changes in L2/3 pyramidal neurons (n=329 cells; N=12 mice) and RWS+CF-evoked response changes in L2/3 pyramidal neurons (n=597 cells; N=11 mice). Trace scale bars: 0.05 ∆F/F; 0.5 s; shaded region: SEM across neurons. Right: box plots quantify calcium responses across all cells and trials (i.e. including unresponsive neurons and trials without whisker-evoked responses). Box: 25th and 75th percentiles; line: median; whiskers: range. (E) The same as D in interneurons (INs) in the same mice (n=616 cells for RWS; n=590 cells for RWS+CF). (F, G) Same as D, E in tdTomato-tagged somatostatin (SST) interneurons (F; n=41 cells and N=3 mice for RWS; n=31 cells and N=3 mice for RWS+CF) and parvalbumin (PV) interneurons (G; n=83 cells; N=5 mice for RWS; n=113 cells; N=5 mice for RWS+CF). All summary data, statistical methods, and significance levels are available in Figure 1—figure supplement 2—source data 1.
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Figure 1—figure supplement 2—source data 1
Summary data, statistical methods, and significance levels for data in Figure 1—figure supplement 2.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig1-figsupp2-data1-v1.xlsx
Figure 1—figure supplement 3
Impact of repeated whisker stimulation (RWS)- and RWS + climbing fiber (RWS+CF)-stimulation on animal motion.
(A) Experimental schematic. Mice are awake and head-fixed but can walk/run on the treadmill. (B) Average cross-correlation coefficient between neural calcium signals and movement activity data, segregated by neuron type. The numbers below the box charts indicate the number of recorded cells. Box: 25th and 75th percentiles; line: median; whiskers: range. (C) Left: probability distribution of animal movement in Rest trials, demonstrating the absence of movement both before and after stimulus onset. Right: probability distribution of animal movement in Active trials. (D) Pie charts indicating the percentage of Rest, Active, and Stop trials pre-vs post-RWS (left) or RWS+CF (right). (E) Average probability of animal movement in Rest trials pre- and post-RWS (left) or RWS+CF (right) over the same time scale as the neural traces shown below. Line: mean; shaded region: SEM. Y-axis represents arbitrary P(Movement) units. (F) and (H) RWS-evoked potentiation in L2/3 pyramidal neurons (n=124; N=12) and RWS+CF-mediated suppression of potentiation (n=388; N=11) in the absence of animal movement (i.e. in Rest trials). Trace scale bars: 0.2 ∆F/F; 0.5 s; line: mean; shaded region: SEM across neurons. Box: 25th and 75th percentiles; line: median; whiskers: range. (G) and (I) Analysis for INs in the same mice (n=212 cells for RWS; n=296 cells for RWS+CF); data visualization as in F and H. Note motion activity traces capture both whisking and running activity. All summary data, statistical methods, and significance levels are available in Figure 1—figure supplement 3—source data 1.
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Figure 1—figure supplement 3—source data 1
Summary data, statistical methods, and significance levels for data in Figure 1—figure supplement 3.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig1-figsupp3-data1-v1.xlsx
Figure 1—figure supplement 4
Intrinsic optical imaging confirms climbing fiber (CF)-mediated suppression of S1 plasticity.
(A) Experimental schematic. Intrinsic optical imaging is performed using a high-speed camera. The field of view is illuminated with red light (625 nm). A decrease in ∆R/R (dark area) indicates increased oxygen consumption by neurons activated by single whisker stimulation (blue arrow). (B) Top: example of S1 plasticity evoked by stimulation of the C2 whisker at 8 Hz. Bottom: example of suppression of response potentiation when 8 Hz whisker stimulation is paired with optogenetic CF co-activation at 1 Hz. (C) Quantification of RWS-evoked potentiation of the single whisker response area (blue; N=4 mice) and repeated whisker stimulation (RWS) + CF-mediated suppression of response potentiation (red; N=4 mice). No response potentiation is observed in the absence of repeated whisker stimulation or CF activation (gray; N=4 mice). Data are normalized to the pre-plasticity response area. Light blue line indicates mean across animals. All summary data, statistical methods, and significance levels are available in Figure 1—figure supplement 4—source data 1.
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Figure 1—figure supplement 4—source data 1
Summary data, statistical methods, and significance levels for data in Figure 1—figure supplement 4.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig1-figsupp4-data1-v1.xlsx
Figure 2
Optogenetic climbing fiber (CF) co-activation differentially modulates basic responses to whisker stimulation in different types of neocortical neurons.
(A) Schematic of the recording configuration (left) and S1 cortex microcircuit (right). (B) CF co-activation with whisker stimulation significantly alters evoked responses of morphologically identified L2/3 pyramidal neurons. Left: averaged traces. Trace scale bars: 0.1 ∆F/F; 0.5 s; shaded region: SEM across neurons. Middle: analysis by neuron (AUC from 0 to 700 ms). Box: 25th and 75th percentiles; line: median; whiskers: range. Violin plot: kernel density. Right: analysis by mouse, normalized to whisker-only response. Blue line indicates mean across animals. (C) CF co-activation significantly enhances responses in putative interneurons (interneurons INs; n=2014 cells; N=53 mice) in the same mice. (D–F) Sample two-photon field of view (left) and post-hoc verification of expression in S1 using confocal microscopy (right). Arrowheads indicate neurons co-expressing GCaMP6f and tdTomato in vasoactive intestinal polypeptide (VIP) interneurons (D), somatostatin (SST) interneurons (E), or parvalbumin (PV) interneurons (F). Scale bars: 100 µm (left); 500 µm (right). (G) CF co-activation with whisker stimulation significantly reduces VIP population responses (n=129 cells, N=7 mice), but enhances responses in SST interneurons (n=102 cells; N=12 mice; H) and PV interneurons (n=177 cells; N=18 mice; I). Note VIP responses are reduced in a late analysis window (650–850 ms), while SST and PV responses are enhanced in the default 0–700 ms analysis window. Middle plots show analysis by neuron, right plots analysis by mouse (blue line indicates mean). Data visualization for C and G-I as in B. All summary data, statistical methods, and significance levels are available in Figure 2—source data 1.
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Figure 2—source data 1
Summary data, statistical methods, and significance levels for data in Figure 2.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig2-data1-v1.xlsx
Figure 3
Somatostatin (SST) interneurons are recruited to prevent L2/3 pyramidal cell plasticity.
(A) Circuit diagram highlighting the chemogenetic activation of SST interneurons and recording configuration. (B) Expression of activating hM3D(Gq) receptors is localized to neocortical SST interneurons. Scale bar: 100 µm (top) and 500 µm (bottom). (C) Deschloroclozapine (DCZ) application enhances responses in SST interneurons (n=12 cells; N=7 mice). Box: 25th and 75th percentiles; line: median; whiskers: range. (D) In the presence of DCZ, repeated whisker stimulation (RWS) stimulation suppresses L2/3 pyramidal cell potentiation, and even causes depression, even when the climbing fiber (CF) is not co-activated (n=255 cells; N=4 mice). Left: average traces; middle: AUC analysis by cell; right: maximum response amplitude by cell. Trace scale bars: 0.2 ∆F/F; 0.5 s; shaded region: SEM across neurons. Box: 25th and 75th percentiles; line: median; whiskers: range. (E) Circuit diagram highlighting the chemogenetic inhibition of SST interneurons and recording configuration. (F) Expression of inhibiting hM4D(Gi) receptors is localized to neocortical SST interneurons. Scale bars as in B. (G) DCZ application reduces responses in SST interneurons (n=53 cells; N=6 mice). (H) In the presence of DCZ, pyramidal cell potentiation is observed, despite CF-co-activation (n=183 cells; N=3 mice). Data visualization for G-H is the same as C-D. All summary data, statistical methods, and significance levels are available in Figure 3—source data 1.
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Figure 3—source data 1
Summary data, statistical methods, and significance levels for data in Figure 3.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig3-data1-v1.xlsx
Figure 4 with 1 supplement
Vasoactive intestinal polypeptide (VIP) interneurons mediate the effects of optogenetic climbing fiber (CF) activation.
(A) Circuit diagram highlighting the chemogenetic inhibition of VIP interneurons and recording configuration. (B) Expression of inhibiting hM4D(Gi) receptors is localized to neocortical VIP interneurons. Scale bars: 100 µm (top) and 500 µm (bottom). (C) Deschloroclozapine (DCZ) application reduces responses in VIP interneurons (n=10 cells; N=3 mice). Box: 25th and 75th percentiles; line: median; whiskers: range. (D) In the presence of DCZ, repeated whisker stimulation (RWS) stimulation suppresses L2/3 pyramidal cell potentiation, and even causes depression, even when the CF is not co-activated (n=189 cells; N=3 mice). Left: averaged traces; middle: AUC analysis by cell; right: maximum response amplitude by cell. Trace scale bars: 0.1 ∆F/F; 0.5 s; shaded region: SEM across neurons. Box: 25th and 75th percentiles; line: median; whiskers: range. (E) Circuit diagram highlighting the chemogenetic activation of VIP interneurons and recording configuration. (F) Expression of activating hM3D(Gq) receptors is localized to neocortical VIP interneurons. Scale bars as in B. (G) DCZ application enhances responses in VIP interneurons (n=14 cells; N=3 mice). (H) In the presence of DCZ, pyramidal cell potentiation is observed, despite CF co-activation (n=202 cells; N=4 mice). Data visualization for G-H is the same as C-D. All summary data, statistical methods, and significance levels are available in Figure 4—source data 1.
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Figure 4—source data 1
Summary data, statistical methods, and significance levels for data in Figure 4.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig4-data1-v1.xlsx
Figure 4—figure supplement 1
Plasticity effects in L2/3 pyramidal neurons (PNs) vs controls in chemogenetic manipulation experiments.
(A) Chemogenetic activation of somatostatin-positive interneurons (SSTs). Left: experimental schematic. Middle: circuit diagram. Right: deschloroclozapine (DCZ) injection activates SSTs (yellow). Top: control protocol. ‘Post’ marks the period equivalent in time to the period for the measurement of plasticity effects after repeated whisker stimulation (RWS, bottom). (B) Responses in L2/3 PNs during Pre, DCZ wash-in, and Post periods in control experiments. (C) The difference in response (∆AUC) of L2/3 pyramidal cells to whisker stimulation between the DCZ wash-in and Post periods; (control: n=218 cells; N=3 mice; plasticity: n=253 cells; N=4 mice); negative ∆AUC values indicate AUC values in the Post period are lower than in the DCZ wash-in period. The ∆AUC in control and plasticity experiments are normalized to the absolute ∆AUC in control experiments to demonstrate changes in the plasticity experiments relative to controls. Note the absence of PN potentiation in the plasticity experiment. (D–F) Equivalent measures during chemogenetic vasoactive intestinal polypeptide (VIP) inhibition (red; control: n=173 cells; N=3 mice; plasticity: n=164 cells; N=3 mice). Note the absence of PN potentiation in the plasticity experiment. (G-I) Equivalent measures during chemogenetic SST inhibition (control: n=175 cells; N=3 mice; plasticity: n=181 cells; N=3 mice). (J-L) Equivalent measures during chemogenetic PV inhibition (control: n=368 cells; N=4 mice; plasticity: n=258 cells; N=3 mice). PNs are significantly potentiated after plasticity experiments beyond changes in controls. (M-O) Equivalent measures during chemogenetic VIP activation (control: 145 cells; N=3 mice; plasticity: n=197 cells; N=4 mice). PNs are significantly potentiated after plasticity experiments beyond changes in controls. Optogenetic CF co-activation is applied during RWS in the experiments shown in G-O. Data: mean ± SEM. All summary data, statistical methods, and significance levels are available in Figure 4—figure supplement 1—source data 1.
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Figure 4—figure supplement 1—source data 1
Summary data, statistical methods, and significance levels for data in Figure 4—figure supplement 1.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig4-figsupp1-data1-v1.xlsx
Figure 5
Vasoactive intestinal polypeptide (VIP) interneurons orchestrate the inhibitory network in S1.
(A) Circuit diagram highlighting the chemogenetic inhibition of VIP interneurons and recording configuration. (B) Inhibiting hM4D(Gi) receptors are expressed in neocortical VIP interneurons. Note A-B are identical to Figure 4A–B. (C) In the presence of deschloroclozapine (DCZ), repeated whisker stimulation (RWS) stimulation activates L2/3 interneurons, even when the climbing fiber (CF) is not co-activated (n=27 cells; N=3 mice). Left: averaged traces; middle: AUC analysis by cell; right: maximum response amplitude by cell. Trace scale bars: 0.2 ∆F/F; 0.5 s; shaded region: SEM across neurons. Box: 25th and 75th percentiles; line: median; whiskers: range. (D) Circuit diagram highlighting the chemogenetic activation of VIP interneurons and recording configuration. (E) Activating hM3D(Gq) receptors are expressed in neocortical VIP interneurons. Note D-E are identical to Figure 4E–F. (F) In the presence of DCZ, IN depression is observed, despite CF co-activation (n=105 cells; N=4 mice). Data visualization is the same as in C. All summary data, statistical methods, and significance levels are available in Figure 5—source data 1.
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Figure 5—source data 1
Summary data, statistical methods, and significance levels for data in Figure 5.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig5-data1-v1.xlsx
Figure 6 with 3 supplements
A pathway from the cerebellar nuclei via the zona incerta and thalamic nucleus posterior medial nucleus (POm) to S1 cortex.
(A) Schematic of dual-injection strategy to label outputs of zona incerta (ZI) neurons receiving input from contralateral cerebellar nuclei (CBN). (B) EYFP expression in the left hemisphere (left; scale bar: 1 mm) with higher magnification images taken in the same slice. Center: EYFP expression in the ZI (scale bar: 20 µm). Right: labeled axons in the posterior medial nucleus (POm; bottom; scale bar: 20 µm) and S1 cortex (top; scale bar: 10 µm). (C) Quantification of cerebellar nuclei projections to the ZI. Curves show terminal density distribution from dorsal ZI (dZI) to ventral ZI (vZI). Color of curves correspond to images taken along the rostro-caudal axis: green: top (rostral) image; navy: center image; light blue: bottom (caudal) image. Scale bars: 500 µm. (D) Labeling strategy for electrophysiological recordings shown in E–F. Scale bar: 1 mm. (E) Whole-cell patch-clamp recordings from POm-projecting ZI neurons receiving input from cerebellar nuclei. Top: responses to depolarizing current pulses in the absence (left) and presence (right) of TTX (1 µM). Bottom: responses in ZI cells to photostimulation of ChR2-expressing terminals from cerebellar nuclei neurons in the absence (left) and presence (right) of TTX. (F) Amplitude (left) and latency (right) of photostimulation-evoked EPSPs before (n=5) and after (n=3) wash-in of TTX. (G) Experimental configuration for recordings from mice expressing inhibiting hM4D(Gi) receptors in PV-expressing ZI interneurons. (H) In the presence of deschloroclozapine (DCZ), the suppressive effect of climbing fiber (CF) co-activation on acute whisker responses of L2/3 pyramidal neurons is blocked (n=80 cells; N=3 mice). Trace scale bars: 0.1 ∆F/F; 0.5 s; shaded region: SEM across neurons. (I) Analysis by neuron. Box: 25th and 75th percentiles; line: median; whiskers: range. Violin plot: kernel density. All summary data, statistical methods, and significance levels are available in Figure 6—source data 1.
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Figure 6—source data 1
Summary data, statistical methods, and significance levels for data in Figure 6.
- https://cdn.elifesciences.org/articles/109183/elife-109183-fig6-data1-v1.xlsx
Figure 6—figure supplement 1
Cerebellar nuclei do not strongly project to thalamic reticular nucleus.
(A) Schematic of labeling approach (top) and injection site of retrograde tracer (bottom). Scale bar: 1 mm. (B) Image of retrograde label from the somatosensory thalamus (POm and VPM; cyan) and orthograde label from the contralateral cerebellar nuclei (red) taken approximately –1.0 mm posterior from bregma, demonstrating lack of overlap between neurons in the thalamic reticular nucleus (TRN) and cerebellar nuclei terminals in the adjacent thalamic nuclei. Representative images are shown from two separate mice. Scale bars: 1 mm (left images) and 250 µm (right images). (C) Projection diagram. DCN: deep cerebellar nuclei; ZI: zona incerta; POm: posterior medial thalamic nucleus; TRN: thalamic reticular nucleus; VPM: ventral posterior medial nucleus; VPL: ventral posterior lateral nucleus; VA: ventral anterior nucleus; VL: ventral lateral nucleus.
Figure 6—figure supplement 2
Transsynaptic labeling identifies projections from the cerebellar nuclei to posterior medial nucleus (POm).
(A) Schematic of dual-injection approach to label outputs of zona incerta (ZI) neurons receiving input from the contralateral cerebellar nuclei (CBN). (B) Top left: EYFP-expressing terminals and cell bodies within ZI (dashed lines) and axonal projections out of the ZI (arrowheads). Scale bar: 100 µm. Bottom left: projections from the ZI terminate in POm (arrowheads). Scale bar: 50 µm. Right: zoomed-out view showing projections from ZI to POm in the same plane. Scale bar: 200 µm. (C) ZI neurons receiving cerebellar input project to S1. Synaptic terminals are observed in L1 and L5a. Scale bar: 100 µm. (D) Series of coronal sections showing details of the projections from the contralateral CBN to ZI and POm. Scale bars: 1 mm. The first image in D is the same as the left image shown in Figure 6B. (E) The same as D in a second mouse, showing robust EYFP expression across the rostro-caudal extent of ZI. Scale bars: 1 mm. (F) Higher-magnification images of corresponding images in E, showing EYFP expression in POm. Scale bars: 100 µm. Colored dots mark images taken from the same sections. POm: posterior medial thalamic nuclei; POt: posterior thalamic nucleus (triangular part); S1BF: primary somatosensory cortex, barrel field; ZI: zona incerta.
Figure 6—figure supplement 3
Whole-cell patch-clamp recordings are performed from neurons in the zona incerta (ZI) that project to posterior medial nucleus (POm) and receive input from cerebellar nuclei.
(A) Left: differential interference contrast (DIC) image showing the ZI (white dashed circle) at low magnification (top; scale bar: 500 µm), and a neuron selected for patching at higher magnification (bottom; scale bar: 100 µm). Middle left: same images showing ChR2-expression. Middle right: same images showing retrograde fluoro-Ruby label originating in the POm. Right: merged images (boxed area with yellow dashed line marks the recording area shown in the images below). (B) Post-hoc confocal image of an acute slice used for recordings demonstrating the details of cerebellar innervation of the ZI, separated by dorsal ZI (dZI) and ventral ZI (vZI; image corresponds to Figure 6D, separated by channel). Scale bar: 500 µm. (C) Quantification of the terminal fluorescence segregated by dZI and vZI. Data: mean ± SEM.
Tables
Key resources table
| Reagent type (species) or resource | Designation | Source or reference | Identifiers | Additional information |
|---|---|---|---|---|
| Strain, strain background (Mus musculus) | C57BL/6J | The Jackson Laboratory | Strain #: 000664; RRID:IMSR_JAX:000664 | Common name: B6 |
| Strain, strain background (Mus musculus) | B6.129P2-Pvalbtm1(cre)Arbr/J | The Jackson Laboratory | Strain #: 017320; RRID:IMSR_JAX:017320 | Common name: B6 PVcre |
| Strain, strain background (Mus musculus) | STOCK Ssttm2.1(cre)Zjh/J | The Jackson Laboratory | Strain #: 013044; RRID:IMSR_JAX:013044 | Common name: Sst-IRES-Cre |
| Strain, strain background (Mus musculus) | B6J.Cg-Viptm1(cre)Zjh/AreckJ | The Jackson Laboratory | Strain #: 031628; RRID:IMSR_JAX:031628 | Common name: Vip-IRES-cre (C57BL/6J) |
| Strain, strain background (Mus musculus) | B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J | The Jackson Laboratory | Strain #: 007909; RRID:IMSR_JAX:007909 | Common name: Ai9 |
| Recombinant DNA reagent | AAV9-CaMKIIa-hChR2(H134R)-mCherry (viral prep) | Addgene | Addgene #: 26975-AAV9; RRID:Addgene_26975 | Titer (GC/ml): 2.4×1013 |
| Recombinant DNA reagent | AAV9-CaMKIIa-hChR2(H134R)-EYFP (viral prep) | Addgene | Addgene #: 26969-AAV9; RRID:Addgene_26969 | Titer (GC/ml): 3.1×1013 |
| Recombinant DNA reagent | AAV1.CAG.Flex.GCaMP6f.WPRE.SV40 (viral prep) | Addgene | Addgene #: 100835-AAV1; RRID:Addgene_100835 | Titer (GC/ml): 8.9×1012 |
| Recombinant DNA reagent | AAV1.Syn.GCaMP6f.WPRE.SV40 (viral prep) | Addgene | Addgene #: 100837-AAV1; RRID:Addgene_100837 | Titer (GC/ml): 7.4×1012 |
| Recombinant DNA reagent | AAV9-FLEX-tdTomato (viral prep) | Addgene | Addgene #: 28306-AAV9; RRID:Addgene_28306 | Titer (GC/ml): 3.1×1013 |
| Recombinant DNA reagent | AAV5-hSyn-DIO-hM3D(Gq)-mCherry (viral prep) | Addgene | Addgene #: 44361-AAV5; RRID:Addgene_44361 | Titer (GC/ml): 2.2×1013 |
| Recombinant DNA reagent | AAV5-hSyn-DIO-hM4D(Gi)-mCherry (viral prep) | Addgene | Addgene #: 44362-AAV5; RRID:Addgene_44362 | Titer (GC/ml): 2.3×1013 |
| Recombinant DNA reagent | AAV1-EF1a-Flpo (viral prep) | Addgene | Addgene #: 55637-AAV1; RRID:Addgene_55637 | Titer (GC/ml): 8.9×1012 |
| Recombinant DNA reagent | hSyn-Coff/Fon hChR2(H134R)-EYFP (plasmid) | Addgene | Plasmid #: 55648; RRID:Addgene_55648 | Packaged as AAV1 by UNC Vector Core. Titer (GC/ml): 2.4×1013 |
| Recombinant DNA reagent | AAV5-hSyn-hChR2(H134R)-EYFP (viral prep) | Addgene | Addgene #: 26973-AAV5; RRID:Addgene_26973 | Packaged as AAV5 by UNC Vector Core. Titer (GC/ml): 5.3×1012 |
| Recombinant DNA reagent | pAAV-sL7-Cre-HA-WPRE (plasmid) | Addgene | Plasmid #: 204488; RRID:Addgene_204488 | Packaged as AAV1 by Princeton Neuroscience Institute Viral Core Facility. Titer (GC/ml): 3.0×1013 |
| Chemical compound, drug | Fluoro-Ruby | Invitrogen | Thermo Fisher Scientific catalog #: D1817 | |
| Chemical compound, drug | Fluoro-Gold | Fluorochrome | Fluorochrome cat # Fluoro-Gold; US Patent No. 4, 716,905 | |
| Antibody | anti-Calbindin (Guinea pig polyclonal) | Synaptic Systems GmBH | Synaptic Systems GmBH Catalog #: 214 004; RRID:AB_10550535 | IHC: 1:500 |
| Antibody | anti-Guinea Pig IgG (Donkey polyclonal) | Jackson ImmunoResearch Labs | Jackson ImmunoResearch Labs Catalog #: 706-165-148; RRID:AB_2340460 | IHC: 1:200 Conjugate: Cyanine Cy3 |
| Antibody | anti-VGLUT2 (Rabbit polyclonal) | Thermo Fisher Scientific | Thermo Fisher Scientific Cat# 42–7800, RRID:AB_2533537 | IHC: 1:500 |
| Antibody | anti-Rabbit IgG (Donkey polyclonal) | Jackson ImmunoResearch Labs | Jackson ImmunoResearch Labs Cat# 711-605-152, RRID:AB_2492288 | IHC: 1:500 Conjugate: Alexa Fluor 647 |
| Software, algorithm | Fiji | PMID:22743772 | RRID:SCR_002285 | Version: 2.9.0/1.53t |
| Software, algorithm | MATLAB | PMID:30609523, PMID:21934110 | RRID:SCR_001622 | Version R2017b (data collection and preprocessing) and version R2022a (data analysis) |
| Software, algorithm | GraphPad Prism | GraphPad | RRID:SCR_002798 | Version: 7.0 |
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Cerebellar climbing fibers impact experience-dependent plasticity in the mouse primary somatosensory cortex
eLife 14:RP109183.
https://doi.org/10.7554/eLife.109183.3
