Neural Imaging and Sensing are widely utilized in neuroscience research. The entire technical chain usually includes labeling, imaging, and image processing. Novel techniques are developed in rapid succession, and new applications follows.
This presentation will focus on a bibliometrics study related to the three directions of the emerging neural imaging and sensing techniques. Based on Web of Science and Scopus, the hot topics are easily selected. We will highlight several typical techniques emerged in recent years, and discuss their advantages and specialized applications.
Among those emerging techniques, a new crossdisciplinary field, brainsmatics, is growing up. Brainsmatics is the shorten term of Brain Spatial Informatics, which develops methods and tools for understanding brain based on brain spatial information. In neuroscience, scientific questions are focused and answered mainly in molecular, cellular, genetic, and electrophysiological levels, respectively. A full understanding of the brain calls for the integration of brain information in all levels. To combine all these different level data, the spatial information is the key reference. High resolution and precision positioning are two challenges in brainsmatics, while the image standard and brain-wide coordinate system definition are also important.
Cerebral blood flow (CBF) is critical for the maintenance of cerebral function by guaranteed constant oxygen and glucose supply to brain. Collateral channels (CCs) are recruited to provide alternatives to CBF to ischemic regions once the primary vessel is occluded during ischemic stroke. However, the knowledge of the relationship between dynamic evolution of collateral flow and the distribution of regional blood flow remains limited. In this study, laser speckle imaging was used to assess dynamic changes of CCs and regional blood flow in a rat cortex with permanent middle cerebral artery occlusion (MCAo). We found that CCs immediately provided blood flow to ischemic territories after MCAo. More importantly, there were three kinds of dynamic changes of CCs during acute stroke: persistent CC, impermanent CC, and transient CC, respectively, related to different distributions of regional blood flow. Although there was the possible occurrence of peri-infarct depolarization (PID) during ischemia, there was no obvious significance about the onset time and duration of CCs between rats with and without PID. These results suggest that the initial arising of CCs does not ensure their persistence, and that collateral flow could be varied with distribution of regional blood flow in acute ischemic stroke, which may facilitate the understanding of collateral recruitment and promote the development of collateral therapeutics in the future.
Stroke is a devastating disease. The changes in cerebral hemodynamics and oxygen metabolism associated with stroke play an important role in pathophysiology study. But the changes were difficult to describe with a single imaging modality. Here the changes in cerebral blood flow (CBF), cerebral blood volume (CBV), and oxygen saturation (SO2) were yielded with laser speckle imaging (LSI) and photoacoustic microscopy (PAM) during and after 3-h acute focal ischemic rats. These hemodynamic measures were further synthesized to deduce the changes in oxygen extraction fraction (OEF). The results indicate that all the hemodynamics except CBV had rapid declines within 40-min occlusion of middle cerebral artery (MCAO). CBV in arteries and veins first increased to the maximum value of 112.42±36.69% and 130.58±31.01% by 15 min MCAO; then all the hemodynamics had a persistent reduction with small fluctuations during the ischemic. When ischemia lasted for 3 h, CBF in arteries, veins decreased to 17±14.65%, 24.52±20.66%, respectively, CBV dropped to 62±18.56% and 59±18.48%. And the absolute SO2 decreased by 40.52±22.42% and 54.24±11.77%. After 180-min MCAO, the changes in hemodynamics and oxygen metabolism were also quantified. The study suggested that combining LSI and PAM provides an attractive approach for stroke detection in small animal studies.
Because cerebral hypoperfusion brings damage to the brain, prevention of cerebrovascular diseases correlative to hypoperfusion by studying animal models makes great sense. Since complicated cerebrovascular adaptive changes in hypoperfusion could not be revealed only by cerebral blood flow (CBF) velocity imaging, we performed multi-parameter imaging by combining laser speckle imaging and functional photoacoustic microscopy. The changes in CBF, hemoglobin oxygen saturation (SO2), and total hemoglobin concentration (HbT) in single blood vessels of ipsilateral cortex were observed during transient cerebral hypoperfusion by ligating the unilateral common carotid artery in rats. CBF, SO2, and HbT, respectively, decreased to 37±3%, 71±7.5%, and 92±1.3% of baseline in 6 s immediately after occlusion, and then recovered to 77±4.8%, 84±8%, and 96±2% of baseline in 60 s. These parameters presented the decrease with different degree and the following recovery over time after ligation, the recovery of SO2 lagged behind those of CBF and HbT, which had the similar response. The results demonstrated that complete monitoring of both cerebral hemodynamic response and oxygen metabolic changes occurred at the earliest period of cerebral hypoperfusion was possible by using the two image modalities with high temporal and spatial resolution.
Hyperglycemia and cortical spreading depression (CSD) are possible factors that worsen the outcome of ischemic stroke, and it is probable that there is a longterm cooperative effect of hyperglycemia and CSD on cerebral blood flow (CBF). Long-lasting and full-field observation of changes in CBF following CSD in vivo during acute hyperglycemia in rats might show whether this is the case. Here, we utilized laser speckle imaging to study influences of acute hyperglycemia on CBF at the level of individual vascular compartments for 3 h in normal rats and those with CSD. It is shown that there are extensive increases of CBF at the arteriole and parenchyma over the normal rat cortex during acute hyperglycemia, whereas there is no significant change in CBF at the venule. We also find that, at all vascular compartments, after the glucose administration there is a stepwise reduction of CBF following CSD, but after saline injection CBF following CSD is close to the baseline. Our results indicate that acute hyperglycemia could aggravate the severity of decrease in CBF following CSD, suggesting possible mechanisms by which hyperglycemia exacerbates cerebral damage after ischemic stroke.
Laser speckle temporal contrast analysis (LSTCA) was used to image the cerebral blood flow (CBF) of ischemic area in
reperfused mini-stroke model in rats. Focal cortical ischemia in male Sprague-Dawley rats (n=20) was induced by
deliberate ligation of multiple branches of the middle cerebral artery (MCA) together with a nylon ring and the dura.
LSTCA was used to monitor the spatio-temporal characteristics of cerebral blood flow dynamics in the rat
somatosensory cortex in the ischemic and reperfused stages. The infarction volume was measured by 2, 3, 5-
triphenyltetrazolium chloride (TTC) staining 24 hours after reperfusion. The distribution of changes in cerebral blood
flow which outlined by the laser speckle imaging represented the relative CBF gradient (21.98±1.96%, 67.2±1.67 %,
107.24±4.71 % of the baseline) from ischemic core, penumbra zone to normal tissue immediately after cortical
ischemia, in which a central ischemic core had little or no perfusion surrounded by a penumbral region with reduced
perfusion, in addition, we had shown the existence of a surrounding region of hyperemic tissue; Thereafter a postrecanalization
hyperperfusion occurred in the same infarct core since 24 hours after reperfusion (242.62±18.52% of the
baseline). Histology of the ischemic regions at 24 hours after reperfusion revealed small focal infarcts that were
typically 3~4 mm in diameter, approximately equal to the nylon ring in size and position and essentially accordant with
the spatial distribution of the ischemic cortex with below 30% residual CBF of the pre-ischemic baseline. It was
demonstrated that this technique of LSTCA was easy to implement and availably used to image the spatial and temporal
evolution of CBF changes with high resolution in rat reperfused mini-stroke model.
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