Rapid signalling in distinct dopaminergic axons during locomotion and reward

Abstract

Dopaminergic projection axons from the midbrain to the striatum are crucial for motor control, as their degeneration in Parkinson disease results in profound movement deficits. Paradoxically, most recording methods report rapid phasic dopamine signalling (~100-ms bursts) in response to unpredicted rewards, with little evidence for movement-related signalling. The leading model posits that phasic signalling in striatum-targeting dopamine neurons drives reward-based learning, whereas slow variations in firing (tens of seconds to minutes) in these same neurons bias animals towards or away from movement. However, current methods have provided little evidence to support or refute this model. Here, using new optical recording methods, we report the discovery of rapid phasic signalling in striatum-targeting dopaminergic axons that is associated with, and capable of triggering, locomotion in mice. Axons expressing these signals were largely distinct from those that responded to unexpected rewards. These results suggest that dopaminergic neuromodulation can differentially impact motor control and reward learning with sub-second precision, and indicate that both precise signal timing and neuronal subtype are important parameters to consider in the treatment of dopamine-related disorders.

Extended Data Fig 1. Synchronized dopamine projection axon dynamics across a single field in dorsal striatum

a, Representative mean fluorescence image in dorsal striatum of a dense field of dopamine axons (compare to the sparse fields from sparse labeling, i.e. Fig 4c, i) from one mouse (out of 6) labeled with GCaMP6f. b, Coronal schematic showing approximate location and scale of region imaged at top. Arrow indicates the approximate range of medial/lateral positions used for two-photon imaging (see Methods). c, DF/F traces for the rectangular ROIs indicated in a. d, Correlation matrix for the ROIs indicated in a. Note high degree of transient co-activation across ROIs. e, Mean image of fluorescence during the transient indicated by the arrow in c minus mean image of fluorescence during non-transient periods for the field shown in a. Note that the morphology of active regions closely resembles the morphology of GCaMP6f expressing axons in the whole field in a, indicating synchronous activation of large, dense regions of axons, likely belonging to several different parent neurons.

Extended Data Fig 2. Further characterization of two-photon imaging and analysis methods

a and b, Top, Example mean fluorescence images of a putative single SNc axon imaged over 2 consecutive days in one mouse. c and d, Mean images of fluorescence during locomotion periods minus mean image of fluorescence during reward periods for fields in a and b. White axonal regions indicate regions of elevated signaling during locomotion. Note the similar morphology and behavior signaling of the identified axon (red arrow) over days. e, Acceleration (black) and DF/F (green) for the identified axon in a–d across the two imaging days. Note the similar transient amplitudes and the elevated transient signaling during locomotion acceleration periods. f, Mean transient DF/F (mean of significant transients, excluding baseline periods) during locomotion and rest on days 1 and 2 for the axon shown in a–d. g, Histograms of calcium transient duration times across all putative single axons imaged in dorsal striatum from SNc (n = 3556 transients, 5 mice top) and VTA (n = 5140 transients, 5 mice bottom). Note the similar duration profile across the two populations (medians not significantly different, P > 0.05 Wilcoxon sign rank test). h, Histograms of maximum calcium transient amplitudes across all putative single axons imaged in dorsal striatum from SNc (top) and VTA (bottom) (medians not significantly different, P > 0.05 Wilcoxon sign rank test). i, Post-mortem image of a coronal section from a representative mouse showing the striatum imaging cannula window cortical lesion site. j, Post-mortem image from a different mouse than i that was used for fiber photometry recording (fiber track indicated by arrow). k, Similarity of raw (no baseline normalization) whole-field GCaMP6f DF/F trace (top) with baseline normalized DF/F trace (bottom) for the example whole-field imaging session shown in Fig 1e. In the top trace, note the lack of baseline change over the recording session and particularly the stability of the baseline level during locomotion periods. Bottom trace is duplicate of trace in Fig. 1e.

Extended Data Fig 3. Interpretation of mechanisms underlying calcium transients and characterization of putative single dopamine axon calcium transients

a, Left, Mock trace representing expected GCaMP6f calcium transient from a short millisecond timescale influx of calcium (arrows; e.g. short burst of action potentials over tens of milliseconds; local modulation may also contribute to calcium influx). Right, Three representative low-amplitude, short duration calcium transients (from putative single dopamine axons in dorsal striatum) (see Methods, Fig 4) that display onset and decay kinetics consistent with mock transient (left). b, Left, Mock trace representing expected GCaMP6f calcium transient from multiple calcium influx events separated by less than the indicator decay time (arrows; e.g. longer burst of action potential firing over ~100’s of milliseconds). Right, representative larger amplitude calcium transients (from putative single dopamine axons in dorsal striatum) with rapid rise times consistent with mock transient (left). c, Left, Mock trace representing expected GCaMP6f calcium transient from a sustained increase in the rate of influx events separated by less than the decay time (e.g. sustained increase in action potential firing). Right, representative trace of one of the longest duration calcium transients observed (from putative single dopamine axons in dorsal striatum). Note that no sustained increases (baseline shifts) similar to the mock trace (left) were observed in single axon recordings or whole-field DF/F measurements; however, the long duration transient shown (right) indicates that if such sustained increases had occurred, they would have been detected using our methods. Also, note that the mock traces shown in a–c are for descriptive purposes and are not based on new data. These traces are based on two main assumptions: 1. DF/F is a monotonically increasing function of intracellular calcium concentration, which itself is a monotonically increasing function of the number of underlying action potentials (i.e. a greater number of action potentials leads to a larger DF/F, but the relationship is not necessarily linear), and 2. DF/F transients summate (not necessarily linearly) when they overlap in time. d, Duration vs. peak DF/F for all identified significant calcium transients in putative single SNc originating axons (see Methods, Fig 4, n = 3556 transients from 73 axons in 5 mice; Spearman’s Rho = 0.3 P<10⁻¹⁰). e, Histogram of sustained locomotion period durations (from SNc injected mice, n = 5, top) and calcium transient durations for all putative single SNc axons (n = 5 mice, mid) and all whole fields (n = 5 mice, bottom). Note that the median calcium transient duration (for either single axon or whole-field) is far less than the median locomotion duration, indicating that the increase in dopamine axon GCaMP6f DF/F observed during locomotion is due to an increase in relatively short duration calcium transients, rather than long-duration (sustained) increases in DF/F.

Extended Data Fig 4. Further characterization of acceleration-associated dopamine signaling

a, Representative whole-field D/DF fluorescence trace (one field from one out of 6 mice, green) aligned to treadmill acceleration (black) during a locomotion onset (dashed line: onset). b, Video frames of mouse for time points shown in a. c, d same as a, b but for a period of continuous locomotion. e, Top, Normalized spectral power of treadmill acceleration trace during continuous locomotion periods for each two-photon imaging session (each row represents a session, n = 6 mice). Bottom, Normalized mean power from all sessions shown in e, top. f, Top, Mean whole-field DF/F trace triggered on reward delivery time for all fields; each row is mean for each field/session (n = 22 fields, 6 mice). Bottom, mean treadmill velocity (black), mean whole-field DF/F (green), and spout licking (light blue) all triggered on reward time (mean across all 22 fields/sessions in 6 mice). g, Mean whole-field DF/F (top), velocity (mid), and acceleration (bottom) for trials in which reward was delivered mid-locomotion (n = 13 sessions, 4 mice, red) or when animals were at rest (n = 12 sessions, 4 mice, blue). Note the sharp decrease in D/DF relative to baseline when animals decelerated from locomotion to consume the reward and the relative absence of phasic reward signaling when animals were given reward from rest. Reward responses were also not observed in single SNc axons when animals received reward from rest (see Extended Data Fig. 6). h, Comparison of mean whole-field fluorescence change from significant calcium transients (excluding baseline periods) between locomotion and resting periods; each point represents mean DF/F for running or resting over one session for each field (lines connect same field/session). All fields included here were imaged prior to mice ever receiving any rewards on the treadmill (n = 14 fields, 4 mice). *, p <10⁻⁵ (Wilcoxon Rank Sum Test). i, top, Mean acceleration (black) and whole-field DF/F (green) triggered on acceleration onsets (mean across all fields) during continuous locomotion. Bottom, Mean acceleration (black) triggered on all short duration calcium transients (green, mean of transients) during continuous locomotion across all fields. All fields included here were imaged prior to mice ever receiving any rewards on the treadmill (n = 14 fields, 4 mice). j, Top, Whole-field DF/F from all locomotion initiations in a representative single session (single imaging field, single session, one out of 6 mice); each row represents a single locomotion initiation time period (sorted by peak DF/F time). Mid, treadmill accelerations corresponding to locomotion initiations shown in j, top. Bottom, average of acceleration (black) and DF/F (green) across all locomotion onset traces displayed in Top and Mid panels. k, same as j, but for continuous locomotion periods. l, Reproduction of Figure 2e with zoomed-in time axes to show the timing of the mean DF/F in relation to the first acceleration at locomotion initiations from rest. Shaded red region indicates bins that were significantly (* p < 0.01 Wilcoxon, n = 15 fields in 6 mice) elevated relative to rest baseline. Shaded region covers ~107ms prior to acceleration onset. m, Reproduction of Figure 2f with zoomed-in time axes to show the timing of the mean dopamine transient in relation to the accelerations during continuous locomotion (n = 18 fields, 6 mice). n, ROC curves for each two-photon whole-field DF/F trace (n = 22 fields from 6 mice, grey; mean, black line) assessed for ability to discriminate locomotion versus resting periods (21/22 exhibited significant discriminability, p <0.01). Mean area under the curve (AUC) = 0.76+/−0.02 S.E.M. o, ROC curves for each two-photon whole-field DF/F trace (n = 17 fields in 6 mice, grey; mean, black line) assessed for ability to discriminate pre-locomotion onset rest periods (250ms before onset) from other rest periods (10/17 exhibited significant discriminability, p <0.01, 2 sessions included did not meet onset criteria for Fig 2e, Methods). Mean AUC = 0.58+/−0.02 S.E.M. Dashed red lines indicate the line of no discrimination. Shaded regions in f, g, i, l, m mean +/−s.e.m.

Extended Data Fig. 5. Dopamine axon calcium transients are temporally associated with preceding acceleration bursts and their amplitude is correlated with both preceding and subsequent acceleration bursts

a and b, Distribution of latencies from each significant calcium transient onset (mean whole-field fluorescence; 6 mice) to the first acceleration burst onset within 1s preceding (n = 1087, 6 mice a) or following (n = 990, 6 mice b) during continuous locomotion. Latencies are less variable (F-test for difference between variance of latencies, P = 7.1e-5) and shorter (Wilcoxon test for difference between latency means, P = 1.2e-5) to the preceding acceleration onsets, indicating more precise relative timing between the GCamp6f transients and the preceding acceleration burst versus the following acceleration burst. c and d, Mean acceleration traces from the first acceleration (within 1s) preceding (c) or following (d) all short duration (<0.5s) large amplitude (>75^th percentile, n = 149 transients, grey) and small amplitude (<25^th percentile, n = 149 transients, bronze) calcium transients occurring during continuous locomotion; aligned on acceleration onsets. Insets are schematics of the GCaMP6f transients. A significant correlation is present between the transient amplitudes and the immediately preceding acceleration amplitudes (Spearman’s Rho = 0.16, P = 1.2e-4, from all transient-acceleration pairs; binned data from this plot shown in c). A significant correlation is also present between the transient amplitudes and the immediately following acceleration amplitudes (Spearman’s Rho = 0.13, P = 0.006, from all transient-acceleration pairs; binned data from this plot shown in d). e, Schematic summarizing relationship between the timing and amplitude of dopamine axon calcium transients and acceleration bursts during continuous locomotion. f, Mean acceleration (black) and whole-field DF/F (green) all triggered on all accelerations during continuous locomotion that were less than 1.7m/s² in amplitude (n = 596 accelerations, n = 6 mice); this demonstrates that dopamine axon GCaMP6f signaling displays a timing preference with respect to small amplitude accelerations, with similar timing and amplitude to that shown in Fig 2f (which includes both large and small amplitude accelerations).

Extended Data Fig 6. Pulsed optogenetic stimulation of dorsal striatum projecting dopamine axons can entrain accelerations during locomotion (a–d); Pulsed optogenetic stimulation of ventral striatum projecting dopamine axons leads to little effect on locomotion (e–h)

a and b, Representative acceleration traces from continuous locomotion periods during (and initiated by) 6Hz (a) and 3Hz (b) laser stimulation trains in the same mouse. (Blue, laser stimulation train, one mouse out of 7). c, d, Mean accelerations triggered on individual laser burst onsets during continuous locomotion periods for 6Hz (c) and 3Hz (d) across all laser bursts in all mice and sessions (n = 7 mice). e, Mean absolute value of mouse accelerations aligned on onset of laser stimulation train applied to mice at rest (mean across all stimulation onsets, n = 55 and 91 for ventral and dorsal respectively, in all sessions and mice, 3 and 6Hz stimulation included). Dorsal and ventral striatum stimulations are from same ChR2 expressing mice (n=4). Three mice were not stimulated in ventral striatum and thus not included in this figure. Mean acceleration elicited by ventral stimulation was significantly (P < 0.01, Wilcoxon Rank Sum Test) less than that elicited by dorsal axon stimulation. However, acceleration from ventral stimulation was significantly greater than chance (P < 0.01 shuffle test). This small effect in the ventral striatum could be due to activation of fibers which also project to dorsal striatum or to an increase in arousal. Though note that acceleration frequency during locomotion was not altered for stimulation in ventral striatum (see f–d). f, g Center of mass of acceleration power spectra for each mouse for locomotion periods initiated during 3 or 6Hz stimulations (n = 4 mice). Horizontal bars indicate means, lines connect same mouse. h, Mean difference between the center of mass of the acceleration power spectra computed for locomotion periods initiated during 3Hz or 6Hz axon stimulations in ventral (f) or dorsal (g) striatum. Positive values indicate a shift towards higher frequency accelerations for 6Hz stimulations (COM, center of mass of acceleration power spectrum). * P < 0.05 Wilcoxon Rank Sum Test.

Extended Data Fig. 7. Histology and response distributions from each sparsely injected mouse

a, GCaMP6f expression (green) and TH immunofluorescence (red) from all VTA targeted mice (n = 5). b, Reward response vs locomotion index (as in Fig 4m) for each axon recorded from the corresponding mice in a. Green, significant locomotion; red, significant reward; blue both significant; neither significant not shown. c and d, Same as a, b, except from all SNc injected mice (n = 5). 6/10 mice were not stained for TH. Scalebars=500 μm.

Extended Data Fig 8. Distribution of reward and locomotion indexes and fraction of reward and locomotion signaling axons from VTA and SNc are highly similar using different correlation thresholds for clustering axon segments

a, Reward response vs. locomotion index for putative single axons from SNc (n = 5 mice, top row) and VTA (n = 5 mice, bottom row) using different correlation thresholds (No clustering, 0.5, and 0.2) for hierarchical clustering of activity patterns (see Methods). Axons are color-coded by significant responses to locomotion (green), reward (red), or both (blue). Note that despite the total number of putative axons decreasing with correlation threshold, the inverse relationship between locomotion and reward signaling across the population remains the same. b, Table showing the total numbers and fractions of responsive axons across the VTA and SNc populations for different clustering thresholds. Note that despite the total number of putative axons decreasing with correlation threshold, the fraction of axons signaling either reward, locomotion, both or neither is highly similar. c, Correlations (Pearson’s) between acceleration and selected putative single SNc axon DF/F traces at different relative time-lags (i.e. cross-correlations) during locomotion initiation periods; each row is mean for each axon for a single session (axons from n = 3/5 mice). d, Same as c, but during continuous locomotion periods; same axons during same sessions as in c. e, Peak cross-correlation times for data shown in c, d (lines connect same axons during same sessions).

Extended Data Fig 9. Further characterization of putative single dopamine axons in relation to reward and licking

a, Mean DF/F trace for VTA reward responsive axons (Methods, n = 23 axons, n = 4 mice with variable reward sessions) (top), velocity (mid), and licking (bottom) triggered on large volume (red), small volume (blue) and omission (black, solenoid click was present, but no reward delivered; Methods, n = 17 axons, 3 mice with omission sessions) reward deliveries. b, Same as a except for SNc locomotion responsive axons (n = 62 and 18 axons for reward and omission traces respectively). c, Mean VTA reward axon DF/F trace (top) and velocity (bottom) triggered on reward deliveries during continuous locomotion (red, n = 25 axons) or rest periods (blue, n = 37 axons). d, Same as c except for SNc locomotion responsive axons (n = 25 and 62 axons for locomotion and rest respectively). e, Mean VTA reward axon DF/F (top) and mouse licking (bottom) triggered on spontaneous, non-reward licking onsets (n = 15 axons, 3 mice). f, Same as e except for SNc locomotion responsive axons (n = 15 axons, 3 mice). Mice that did not outside reward periods were excluded. Shaded regions in a–f, mean +/− s.e.m.

Extended Data Fig 10. Dopamine axon locomotion signaling measured by fiber photometry from different striatal sub regions

a, Top, Comparison of mean photometry fluorescence DF/F (mean of significant transients, excluding baseline periods) recorded from dorsal striatum between locomotion and resting periods; each point represents mean DF/F for running or resting over one session for recording from a single dorsal striatum location (lines connect same recording location/session; n = 5 mice). Bottom, Comparison of mean baseline (periods with no significant calcium transients) photometry DF/F recorded from dorsal striatum between locomotion and resting periods; each point represents mean baseline DF/F for running or resting over one session for recording from a single dorsal striatum location (lines connect same recording location/session, n = 5 mice). b and c, same as a, except for recordings from central and ventral striatum, respectively. d, Mean photometry DF/F recorded from dorsal striatum triggered on locomotion initiations (mean across all initiations, n = 5 mice). e and f, same as d, except for recordings from central and ventral striatum, respectively. g, Locomotion index (top) and reward response (bottom) vs. striatum recording depth (from data presented in Fig 5). h, Schematic of prominent current model for dopamine signaling dynamics in striatum. i, Schematic of our new model for dopamine signaling dynamics based on data presented here. j and k, Saggital schematics illustrating current homogenous dopamine signaling model (j) and our new model incorporating functional heterogeneity (h). a–c, **, p < 0.01 (Wilcoxon Rank Sum Test); n.s., not significant. Shaded regions in d–f, mean +/− s.e.m across initiations (n = 20, 28, and 56 from dorsal, central, and ventral respectively in 5 mice).

Fig 1. Locomotion related signaling in dorsal striatal projecting dopamine axons

a, Schematic of methods. b, Mouse running on treadmill under microscope. c, Representative field of GCaMP6f labeled dopamine axons in dorsal striatum. d, GCamp6f expression in dopamine neurons (green) overlaid with TH immunofluorescence (red). Right insets are high-zoom. e, Average whole field DF/F fluorescence from a representative field in one mouse (bottom, n = 6 mice total) and corresponding treadmill velocity (top) and acceleration (middle) during locomotion. f, Comparison of mean baseline (periods with no significant calcium transients) whole-field DF/F between locomotion and resting periods. g, Comparison of mean whole-field fluorescence change (mean of significant calcium transients, excluded baseline periods) between locomotion and resting periods. f, g, each point represents mean baseline DF/F for running or resting over one session for each field (n = 17 sessions from 6 mice, lines connect same field/session, short lines: mean over sessions); **, p <10⁻⁵, Wilcoxon Rank Sum Test.

Fig 2. Phasic dopamine signaling displays a sub-second timing preference with respect to acceleration bursts

a, Top, Mean of whole-field DF/F triggered on accelerations at locomotion initiations; each row is mean for each field/session (DF/F normalized for each row and sorted by peak time). Bottom, Mean acceleration (black) and whole-field DF/F (green) all triggered on locomotion initiations (mean across all fields). b, Same as a, except triggered on accelerations during continuous locomotion periods. c, Same as a, except triggered on locomotion terminations; note lack of DF/F transient peak (arrow) following final acceleration. d, Correlations between acceleration and whole-field fluorescence at different relative time-lags (i.e. cross-correlations) during locomotion initiation periods (sorted by peak correlation time); each row is mean for each field/session. e, Same as d, but during continuous locomotion periods. f, Mean cross-correlations between acceleration and whole-field fluorescence for initiation (blue) and continuous (red) locomotion periods. g, Mean acceleration (black) triggered on all short duration calcium transients (green, mean of transients) during continuous locomotion across all fields. Shaded regions in a, b, c, f, g mean +/− s.e.m. a–f include all n=6 mice.

Fig 3. Pulsed optogenetic stimulation of dorsal striatum projecting dopamine axons can rapidly initiate locomotion and control acceleration frequency

a, Schematic of methods. b, Pulsed laser delivery protocol for dopamine axon ChR2 stimulation (used for all data presented in this paper). c, Representative acceleration from a single stimulation session (blue regions, laser train stimulation to dorsal striatum). d, Absolute value of mouse acceleration aligned on onset of all laser stimulation trains (red line) during a representative single session from one mouse (n = 7 mice total, each row represents a single trial stimulation from rest). e, All mean accelerations aligned on laser stimulation trains applied to mice at rest (each row represents mean over one session; rows corresponding to sessions for each mouse grouped together; sessions from different mice separated by dashed lines). f, Mean absolute value of mouse accelerations aligned on the onsets of laser stimulation trains applied to mice at rest (mean across all stimulation onsets, n = 161 and 267 onsets for ChR2 and control respectively, in all sessions and mice, 3 and 6Hz stimulation included). g, Same data as f, but stimulations separated into 3 or 6 Hz groups and zoomed-in time (blue, laser stimulation). Dashed lines, time when acceleration becomes significantly (P<0.01) greater than random shuffle (thin grey line, mean random shuffle). h, Power spectra of acceleration for two representative mice during locomotion periods initiated during 3 and 6Hz stimulations. i and j, Center of mass of acceleration power spectra for each ChR2 (i) or control (j) mouse for locomotion periods initiated during 3 and 6Hz stimulations. Horizontal bars indicate means, lines connect same mouse. k, Mean difference between center of mass of acceleration power spectra during 3Hz and 6Hz stimulations (differences calculated for each mouse) averaged across control or ChR2 mice (COM, center of mass of acceleration power spectrum). l, Mean velocity across mice during 6Hz and 3Hz stimulations included in k. Shaded regions in f,g mean +/− s.e.m. k,** P < 0.01 (compared to 0),* P < 0.05; l, n.s. P>0.05 Wilcoxon Rank Sum test.

Fig 4. Functional heterogeneity and anatomical origin of dorsal striatum projecting dopamine axons

a, Mean image during locomotion periods minus mean image during reward periods for two representative dopamine axon fields (arrows, axon segments signaling more during reward). b, Coronal sections showing restricted GCamp6f expression (green) in VTA (top) and SNc (bottom) overlaid with TH immunofluorescence (red). c, Representative maximum fluorescence projection image from one field in a mouse with GCaMP6f expression localized to VTA (n = 5 total VTA targeted mice). Gold and purple regions are identified ROIs from putative single axons (grey, background). d, DF/F from ROIs in c aligned with treadmill velocity and reward time. e, Reward triggered DF/F from the purple (top) and gold (bottom) ROIs from c; each row represents a single reward delivery. f, Mean reward-triggered DF/F (gold, purple, top), velocity (black, bottom) and licking (grey, bottom) for the two axons in c over the recording session. g, h, Same as e, f, except triggered on locomotion onsets. i, same as a, but for field shown in c. j, Mean DF/F triggered on acceleration onsets for all putative single axons from all SNc injected (n = 5 mice, 73 axons, green) and VTA injected (n = 5 mice, 98 axons, red) mice. Bottom, mean acceleration. k, Mean DF/F triggered on reward for all putative single axons in (j) from SNc (green) and VTA (red). Bottom, mean mouse licking triggered on reward delivery. l, Reward triggered DF/F for all putative VTA (left) and SNc (right) axons (same axons in j–k, sorted by reward response magnitude); each row represents mean DF/F for each axon. m, Mean DF/F triggered on acceleration onsets (top) and rewards (bottom) for all significant (P < 0.01) VTA reward responsive (n = 43 axons from 5 mice, red) and SNc locomotion responsive (n = 63 axons from 5 mice, green) axons. n, Reward response vs locomotion index for all VTA (n = 5 mice, top) and SNc (n = 5 mice, bottom) putative axons. Green, significant locomotion; red, significant reward; blue both significant; neither significant not shown. o, Mean DF/F during locomotion (top) and rest (bottom, non-reward periods during rest) periods for all locomotion (n = 19 axons, 4 mice green) and reward (n = 43 axons, 5 mice red) responsive VTA axons. o, *, p < 10⁻⁵. Shaded regions in j,k,m, mean +/− s.e.m.

Fig 5. Functional topography of reward and locomotion dopamine signaling across striatum dorsal-ventral axis

a, Schematic of photometry methods. b, Representative photometry DF/F (green) and treadmill accelerations (black) during locomotion and reward delivery (dashed lines) periods from dorsal (top) and ventral (bottom) striatum from same mouse (same session, n = 5 mice total). c, Representative photometry DF/F from individual locomotion initiations (left column) and reward deliveries (right column) measured at indicated depths (not averaged). d, Mean DF/F across all photometry recording sessions (n = 5 mice) triggered on acceleration onsets (left) and reward deliveries (right) at depths indicated in c (black, mean acceleration).