Lindsay Walton1,2,3, Matthew Verber4, Tzu-Hao Chao1,2,3, R. Mark Wightman4, and Yen-Yu Ian Shih1,2,3
1Center for Animal MRI, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States, 2Biomedical Research Imaging Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States, 3Department of Neurology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States, 4Department of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States
Synopsis
fMRI
interpretations based on traditional neurovascular coupling ignore the possible
impact of vasoactive neurotransmitters released during brain activity. The
striatum has atypical neurovascular coupling, and the highest concentrations of
vasoactive dopamine. We evoked dopamine release in ventral striatum, and used simultaneous
BOLD-fMRI and fast-scan cyclic voltammetry (FSCV) to observe global hemodynamics
and quantify local dopamine and oxygen changes, respectively. Voltammetric
oxygen correlated highly with BOLD, and increased linearly with local dopamine
release, such that dopamine hemodynamic response functions could be derived. This
multimodality explores hemodynamics at multiple spatiotemporal scales with the
additional context of neurotransmission, which will improve fMRI
interpretation.
Introduction
BOLD
fMRI interpretation assumes vascular responses couple predictably with neuronal
activity across the brain, despite the diversity of cell types and chemical
messengers between brain regions. Studies show that neurovascular coupling is
not always conserved1-3, suggesting that concurrent neurotransmitter
release may also play a role. The striatum is a dopamine-rich brain area with atypical
neurovascular coupling4-6, and though dopamine is known to be vasomodulatory7-8,
its role in local hemodynamic changes is unclear. To study dopamine neurotransmission
effects on striatal hemodynamics, we optimized multimodal BOLD fMRI and
fast-scan cyclic voltammetry (FSCV) to simultaneously detect evoked dopamine
release and oxygen changes at multiple spatiotemporal scales.Methods
FSCV
was selected over other neurotransmitter-detecting techniques for its high
spatiotemporal resolution, affordability, and chemical selectivity (Fig.1A).
A modifiable voltage waveform applied to a carbon-fiber microelectrode oxidizes
and/or reduces analytes, detected as changes in current (Fig.1B,C). Simultaneous
FSCV/fMRI required optimizing both modalities to become cross-compatible. fMRI
studies were performed using a Bruker 9.4T/30cm scanner and homemade RF-coil.
FSCV data were obtained and analyzed with High-Definition Cyclic Voltammetry
software and instrumentation9. FSCV microelectrodes were hand-fabricated
using fused-silica/polyimide capillaries (Fig.2A)10, and
scanned in 1.5% agarose gel phantoms to confirm MR compatibility (Fig.2B).
In vivo dental acrylic headcaps were modified to accommodate fragile, MR-compatible,
silver wire electrode connections (Fig.2C,D).
Low-pass filters removed high-frequency gradient amplifier noise, and in vitro
flow-through analysis of dopamine HCl in phosphate-buffered saline (pH=7.40) verified
that filters did not deform signals (Fig.3A). The effect of each
gradient on baseline noise was characterized at a 10MΩ resistor inside the bore
(Fig.3B). To avoid EPI encoding artifacts (Fig.3D), TTL pulses
were used to trigger per-slice MR data acquisitions after each FSCV waveform, interleaving
FSCV and fMRI data (Fig.3E). For in vivo experiments, a twisted tungsten
stimulating electrode was implanted in the ventral tegmental area (VTA) to
evoke oxygen changes in the nucleus accumbens (NAc). An FSCV microelectrode and
Ag/AgCl reference were implanted in the ipsilateral NAc and contralateral
cerebellum, respectively (Fig.4A). Subjects were scanned within 1 week
of electrode implantation, requiring endotracheal intubation under 0.5%
isoflurane and intraperitoneal dexmedetomidine (0.05mg/kg/hr) and pancuronium (0.5mg/kg/hr)
sedation. Stimulations (300-900µA, 2s at 60Hz, pulse width=1ms) were repeated
using both oxygen- and dopamine-sensitive waveforms at the microelectrode (0 to
+0.8V, to –1.4V, then back to 0V at 400V/s, then ‑0.4 to +1.3V, and back to
-0.4V, Fig.1C)11. BOLD fMRI was acquired simultaneously
(TR/TE=1000/15ms, matrix=80x80, FOV=2.56cm2, slices=5x1mm).
Oxygen challenges were performed in triplicate by ventilating the subject with
100% medical air for 60s, then changing to 100% oxygen for 60s. Principal
component analysis extracted FSCV analyte currents. Correlation plots were derived
from FSCV oxygen time-courses, using significantly correlated fMRI time-courses
from voxels nearest the microelectrode location (15-27 voxel averages).
Significance was determined using a p<0.001 threshold.Results and Discussion
Electrical
VTA stimulations evoked oxygen increases in NAc, detected with simultaneous FSCV/fMRI
at different spatiotemporal scales (Fig.4A,B). FSCV had higher signal-to-noise
than a single voxel BOLD (p<0.001, unpaired t-test, Fig.4B,C). FSCV
data collected at 10Hz was decimated for 1Hz fMRI time-course comparisons (Fig.4D).
The simultaneously-acquired time-courses per stimulation were averaged and
found to highly correlate between modalities (Fig.4D). Significant
correlations to FSCV time-courses were found in the ipsilateral NAc,
contralateral cortex, and forebrain (Fig.4E). These data show that BOLD
fMRI and FSCV are complementary methods of detecting local and whole-brain
hemodynamic responses.
We also examined whether evoked FSCV oxygen correlates with BOLD fMRI using
the same stimulation parameters, but under separate sessions (Fig.4D;
Stim#2). Time-shift analyses revealed that fMRI responses correlated
most highly with FSCV when the latter shifted +1s (Fig.4D), reflecting slight
differences in evoked oxygen dynamics that are likely due to a spatial
sampling mismatch (Fig. 4B). The reliable correlations between FSCV oxygen and BOLD fMRI means
that stimulations can be repeated with other FSCV waveforms in the same
experiment; fMRI still collects highly-correlative hemodynamic information during
cases where FSCV waveforms may be insensitive to it (e.g., dopamine-sensitive
waveform, Fig.1C). To
investigate the relationship between BOLD and FSCV oxygen without using
electrical stimulations, an oxygen-breathing challenge was performed. 100%
oxygen evoked large oxygen increases throughout the brain, correlating highly
with simultaneously-acquired FSCV oxygen (Fig. 4F,G). Interestingly, these
data correlated highest when the FSCV time-course shifted 4s forwards,
indicating a lag in the BOLD response (Fig.4H).
Electrical VTA stimulation
evoked dopamine release in the NAc, allowing us to detect dopamine and
simultaneous BOLD. Dopamine release preceded the hemodynamic response and
returned to baseline (Fig.5A). Increasing stimulation parameters
increased amplitudes of both evoked dopamine release and oxygen responses (Fig.5B).
We used graded stimulation to examine the relationship between maximal evoked
dopamine and oxygen increases, which were linear within subjects in agreement with existing literature (Fig.5C)12.
Using the highly linear data as training sets, we derived dopamine hemodynamic
response functions (DA-HRF), which serve as transfer functions between dopamine
and oxygen responses under physiological conditions and provide information
about neurotransmitter-related neurovascular coupling (Fig.5D).Conclusion
Hemodynamic
changes measured by FSCV/fMRI highly correlate across disparate
spatiotemporal resolutions. FSCV measures high-resolution oxygen
changes and dopamine release, which linearly relate and can be used to derive DA-HRFs. This multimodal platform can be used uniquely to identify
the contribution of neurotransmitter release to BOLD signals.Acknowledgements
We thank UNC CAMRI members for their helpful discussions and critiques. This
project is funded by F32 MH115439-01 as part of the BRAIN Initiative, and supported in part by NIH grants RF1MH117053, R01MH111429, R01NS091236, P60AA011605, and U54HD079124.References
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