Kostiantyn Cherkas1, G. H. Im1, and S.G. Kim2
1Cener for Neuroscience Imaging Research (CNIR), Institute for Basic Science (IBS), Suwon 16419, Republic of Korea, Suwon, Korea, Republic of, 2Cener for Neuroscience Imaging Research (CNIR), Institute for Basic Science (IBS), Suwon 16419, Republic of Korea, Department of Biomedical Engineering, Sungkyunkwan University, Suwon, Korea, Suwon, Korea, Republic of
Synopsis
To investigate neural source of positive and
negative BOLD signals, we modulated a balance of excitatory and inhibitory
activity (EI) within the same somatosensory area to determine whether the polarity
of evoked BOLD response is reversed. We measured BOLD fMRI at 15.2T and calcium
photometry of ketamine/xylazine-anesthetized mice in response to frequency
dependent whisker pad stimulation. At 4
Hz, positive BOLD and increased calcium activity were observed in the barrel
cortex, whereas at 20 Hz stimulation, negative BOLD and decreased calcium
activity were detected. This indicates
that the BOLD polarity closely links to the EI balance.
Introduction
Being extensively studied, positive BOLD1 response (PBR) is known to originate through functional
hyperaemia, which is due to an increased neural activity2,3. In contrast to this, negative BOLD response (NBR)
has a diverse set of explanations and possible mechanisms, mainly depending on
the way of manifestation. NBR
may come as a result of: increased
metabolism with insufficient vascular response4,5, reduction of
neural activity that leads to decrease in CBF accompanied by decrease or
increase in CBV6,7, blood flow redistribution with a decrease in CBV
- ‘blood-steal8, in subcortical areas concurrent with increases in
neuronal activity and decreases in CBV9, due to volume change in
CSF10,11. To further investigate neural source of PBR
and NBR, we propose to modulate a balance of excitatory and inhibitory activity
(EI) within the same cortical area to determine whether the polarity of evoked BOLD response is reversed.
We hypothesize that these properties, as well as polarity of response, can be
controlled by frequency-dependent somatosensory paradigm.Methods
Naïve C57BL/6 mice were used to determine BOLD fMRI (N=3) and intracellular
calcium changes (N=6) to somatosensory stimulation with an approved IACUC protocol.
Mice were anesthetized by continuous infusion of ketamine-xylazine
13 through
IV administration. Mouse unilateral whisker electrical stimulation was delivered through electrodes
placed on top of the skin, current intensity fixed to 0.5 mA with pulse width
of 0.5 ms, and a number of different frequencies were applied by a pulse generator.
- 15.2T (Bruker BioSpec, Billerica,
MA, USA) MR scanner was used to obtain BOLD fMRI in response to whisker stimulation frequencies of 4 Hz and 20Hz[KSG3] . Parameters of fMRI studies[KSG4] 14
were: GE EPI, TR/TE = 1000/11.5 ms, matrix = 96 × 64, in-plane
resolution = 188 × 188 μm2, slice thickness = 500 μm, 9 coronal
slices without gap. Each fMRI trial consisted of a 40-s pre-stimulus, 20-s
stimulus, and 60-s post-stimulus period.
- To obtain dependency of net local neuronal activity to stimulation frequency
change, a custom-made spectrally resolved fiber-photometer was used in
combination with bulk loading of OGB BAPTA – 1 as calcium indicator. Calcium
indicator was loaded into the left mouse barrel cortex using pump (calcium
indicator dissolved in the 20% Pluronic F-127/DMSO to a concentration of 10 mM
and injected with speed - 100 nl/min for 10 minutes, resulting in 1 μl total
volume). Photometer utilizes 2 wavelengths (488 nm and 561 nm) for calcium
reading and hemodynamic correction15.
Stimulation was performed as a train of 7 equidistant 3 seconds blocks of
stimulations with frequencies (1, 2, 4, 8, 10, 16, 20) Hz.
Results
We have obtained high-quality single-shot GE EPI
images of mouse brain at an ultrahigh field of 15.2T (see background images of
Fig. 1). During 4 Hz right-forepaw stimulation,
positive BOLD responses (hot colour in Fig. 1, A) were observed in many
somatosensory networked areas including the left (contralateral) barrel field
(SSp-bfd), right barrel field, secondary somatosensory cortex, and thalamus. When
a stimulation frequency increased to 20 Hz, PBR was changed to NPR in bilateral
barrel fields (cold colour in Fig. 1, B).
This frequency-dependent BOLD polarity change was consistently observed
in all three animals. To quantify these
changes, we determined Z-score values in the left (contralateral) and right (ipsilateral)
barrel field. Eight data points from 3
animals (5 time points per animal) were plotted in Fig. 2. Mean magnitude of NBR
is slightly less than that of PBR.
To determine a potential source of NPR, we measured calcium response with correction of hemodynamic inference15. Average of 6 mice, 49 runs with 7 frequency stimulation is shown as insets in Fig. 3. During each 3-s stimulation period, evoked responses
were observed (main plots). At a low frequency stimulation, calcium response to
each contralateral (and ipsilateral) whisker stimulation pulse was clearly
detected. that is not a case at a higher frequency due to calcium’s
intrinsic property. Evoked calcium signals
increase with respect to a frequency increase (Fig. 3, A-B), reaching its local
maximum at 4 Hz. Further frequency increase results in an initial increase
followed by a decrease below the pre-stimulus baseline (Fig. 3, C-D), which is
likely due to neuronal inhibition. During 20 s stimulation used for fMRI
studies, prolonged inhibition after the initial excitation will be dominant for
20 Hz stimulation, whereas prolonged excitation will be maintained during the
entire stimulation period.Discussion
We have successfully observed BOLD signals polarity change by modulating stimulation frequency. Calcium measurements support idea that neuronal origin of BOLD polarity closely
links to EI balance and are in coherence with current understanding of
NVC. At low frequency stimulation, excitation is dominant, while at high frequency
stimulation, inhibition is dominant as seen in Fig. 3. An important question
is how to induce inhibi-tion by high frequency stimulation. We do speculate
that excitatory neuronal activity by whisker stimulation has much longer
recovery time than fast spiking inhibitory activity. Consequently,
excitatory activity is sustained for prolonged low frequency stimulation.
However, at high frequency, the excitatory activity is adapted, whereas
inhibitory neuronal activity is sustained. Consequently, the excitatory
activity is suppressed below the pre-stimulus baseline at a later time. This
hypothesis should be investigated by measuring cell-type specific calcium
activity in the future.Acknowledgements
This
work was supported by the Institute of Basic Science (IBS-R015-D1)References
- Ogawa S, Menon RS, Tank DW, et al.
Functional brain mapping by blood oxygenation level-dependent contrast magnetic
resonance imaging. A comparison of signal characteristics with a biophysical
model. Biophys J. 1993;64(3):803-812
-
Iadecola C. The neurovascular unit
coming of age: a journey through neurovascular coupling in health and
disease. Neuron 2017;96:17–42
-
Hillman E.M.C. Coupling mechanism
and significance of the BOLD signal: a status report. Annu. Rev. Neurosci. 2014;37:161–181
-
Nagaoka, T., Zhao, F., Wang, P.,
Harel, N., Kennan, R. P., Ogawa, S., et al., Increases in oxygen consumption without cerebral blood volume
change during visual stimulation under hypotension condition. J. Cereb. Blood Flow Metab. 2006;26:1043–1051
-
Schridde, U., Khubchandani, M.,
Motelow, J. E., Sanganahalli, B. G., Hyder, F., and Blumenfeld, H. Negative
BOLD with large increases in neuronal activity. Cereb. Cortex 2008;18:1814–1827
-
Shmuel, A., Augath, M.,
Oeltermann, A., and Logothetis, N.K. Negative functional MRI response
correlates with decreases in neuronal activity in monkey visual area V1. Nat.
Neurosci. 2006;9: 569–577
-
Devor, A., Hillman, E. M., Tian,
P., Waeber, C., Teng, I. C., et al. Stimulus-induced changes in blood flow and 2-deoxyglucose
uptake dissociate in ipsilateral somatosensory cortex. J. Neurosci. 2008;28:14347–14357
-
Harel, N., Lee, S. P., Nagaoka,
T., Kim, D.S., and Kim, S.G. Origin of negative blood oxygenation
level-dependent fMRI signals. J. Cereb. Blood Flow Metab. 2002;22:908–917
-
Shih, Y. Y., Chen, C. C., Shyu, B.
C., Lin, Z. J., Chiang, Y. C., Jaw, F. S., et al. A new scenario for negative functional magnetic resonance
imaging signals: endogenous neurotransmission. J. Neurosci. 2009;29:3036–3044
-
Bianciardi, M., Fukunaga, M., van
Gelderen, P., de Zwart, J. A., and Duyn, J. H. Negative BOLD-fMRI signals in
large cerebral veins. J. Cereb. Blood Flow Metab. 2011;31:401–412
-
Thomas, B. P., Liu, P., Aslan,S.,
King, K. S., van Osch, M. J., and Lu, H. Physiologic underpinnings of negative BOLD
cerebrovascular reactivity in brain ventricles. Neuroimage 2013;83:505–512
-
Ross W, et al. Spatially congruent
negative BOLD responses to different stimuli do not summate in visual cortex, NeuroImage
2020;218
-
H.J. Shim, et al. Mouse fMRI under
ketamine and xylazine anesthesia: robust contralateral somatosensory cortex
activation in response to forepaw stimulation. Neuroimage, 177; 2018:30-44
-
W. B. Jung, H. J. Shim, S. G. Kim,
Mouse BOLD fMRI at ultrahigh field detects somatosensory networks including
thalamic nuclei. NeuroImage, 2019;195:203-214
-
Hillman EM, Devor A, Bouchard MB,
Dunn AK, Krauss GW, Skoch J, Bacskai BJ, Dale AM, Boas DA. Depth-resolved
optical imaging and microscopy of vascular compartment dynamics during
somatosensory stimulation. Neuroimage 2007;35:89–104