Infrared thermal imaging of rat somatosensory cortex with whisker stimulation

2012 ◽  
Vol 112 (7) ◽  
pp. 1215-1222 ◽  
Author(s):  
Takashi Suzuki ◽  
Yasuhiro Ooi ◽  
Junji Seki

The present study aims to validate the applicability of infrared (IR) thermal imaging for the study of brain function through experiments on the rat barrel cortex. Regional changes in neural activity within the brain produce alterations in local thermal equilibrium via increases in metabolic activity and blood flow. We studied the relationship between temperature change and neural activity in anesthetized rats using IR imaging to visualize stimulus-induced changes in the somatosensory cortex of the brain. Sensory stimulation of the vibrissae (whiskers) was given for 10 s using an oscillating whisker vibrator (5-mm deflection at 10, 5, and 1 Hz). The brain temperature in the observational region continued to increase significantly with whisker stimulation. The mean peak recorded temperature changes were 0.048 ± 0.028, 0.054 ± 0.036, and 0.097 ± 0.015°C at 10, 5, and 1 Hz, respectively. We also observed that the temperature increase occurred in a focal spot, radiating to encompass a larger region within the contralateral barrel cortex region during single-whisker stimulation. Whisker stimulation also produced ipsilateral cortex temperature increases, which were localized in the same region as the pial arterioles. Temperature increase in the barrel cortex was also observed in rats treated with a calcium channel blocker (nimodipine), which acts to suppress the hemodynamic response to neural activity. Thus the location and area of temperature increase were found to change in accordance with the region of neural activation. These results indicate that IR thermal imaging is viable as a functional quantitative neuroimaging technique.

2003 ◽  
Vol 285 (5) ◽  
pp. H1890-H1899 ◽  
Author(s):  
Ken Kazama ◽  
Gang Wang ◽  
Kelly Frys ◽  
Josef Anrather ◽  
Costantino Iadecola

We investigated whether angiotensin II (ANG II), a peptide that plays a central role in the genesis of hypertension, alters the coupling between synaptic activity and cerebral blood flow (CBF), a critical homeostatic mechanism that assures adequate cerebral perfusion to active brain regions. The somatosensory cortex was activated by stroking the facial whiskers in anesthetized C57BL/6J mice while local CBF was recorded by laser-Doppler flowmetry. Intravenous ANG II infusion (0.25 μg·kg–1·min–1) increased mean arterial pressure (MAP) from 82 ± 2 to 102 ± 3 mmHg ( P < 0.05) without affecting resting CBF ( P > 0.05). ANG II attenuated the CBF increase produced by whisker stimulation by 65% ( P < 0.05) but did not affect the response to hypercapnia or to neocortical application of the nitric oxide donor S-nitroso- N-acetyl penicillamine ( P > 0.05). The effect of ANG II on functional hyperemia persisted if the elevation in MAP was offset by controlled hemorrhage or prevented by topical application of the peptide to the activated cortex. ANG II did not reduce the amplitude of the P1 wave of the field potentials evoked by whisker stimulation ( P > 0.05). Infusion of phenylephrine increased MAP ( P > 0.05 from ANG II) but did not alter the functional hyperemic response ( P > 0.05). The data suggest that ANG II alters the coupling between CBF and neural activity. The mechanisms of the effect are not related to the elevation in MAP and/or to inhibition of the synaptic activity evoked by whisker stimulation. The imbalance between CBF and neural activity induced by ANG II may alter the homeostasis of the neuronal microenvironment and contribute to brain dysfunction during ANG II-induced hypertension.


2007 ◽  
Vol 28 (4) ◽  
pp. 772-785 ◽  
Author(s):  
Sridhar S Kannurpatti ◽  
Bharat B Biswal

Effects of mitochondrial calcium signaling blockade on neural activation-induced CBF response were studied in urethane-anesthetized rats. Ruthenium red (RuR), a nonspecific inhibitor of the mitochondrial calcium uniporter (MCU), and Ru360, a highly specific inhibitor of the MCU, were delivered intravenously (i.v.) or intracerebroventricularly (i.c.v.). Baseline cerebral blood flow (CBF) and cerebral hyperemic response to whisker stimulation were measured through a thinned skull over the somatosensory cortex using laser Doppler imaging (LDI). Ruthenium red or Ru360 did not alter the baseline CBF at all doses used. However, the hyperemic response, defined as the activation area and amplitude of CBF increase in response to mechanical whisker stimulation, was significantly reduced in the presence of either RuR or Ru360 delivered i.c.v. The hyperemic response reduced significantly with a dose of 14.5 nmol RuR (i.c.v.), showing a further decrease with 29 nmol RuR (i.c.v.). A comparable decrease in the hyperemic response was observed during treatment with a relatively lower dose of 4.5 and 9 nmol Ru360 (i.c.v.). Delivered intravenously, Ru360 significantly diminished the cerebral hyperemic response at doses greater than 80 μg/kg i.v., up to a dose of 320 μg/kg i.v. However, RuR (i.v.) had an opposite effect with an enhancement in the cerebral hyperemic response at all doses studied. Ruthenium red or Ru360 had no significant effect on the cerebral reactivity to hypercapnia, indicating that altered cerebral hyperemic response to whisker stimulation was predominantly neural. We conclude that mitochondrial calcium signaling through the MCU mediates neural activation-induced CBF response in vivo.


2019 ◽  
Author(s):  
Yi Chen ◽  
Filip Sobczak ◽  
Patricia Pais-Roldán ◽  
Cornelius Schwarz ◽  
Alan P. Koretsky ◽  
...  

ABSTRACTThe optogenetically driven manipulation of circuit-specific activity enabled functional causality studies in animals, but its global effect on the brain is rarely reported. Here, we applied simultaneous fMRI with calcium recording to map brain-wide activity by optogenetic activation of fibers running in one orientation along the corpus callosum(CC) connecting the barrel cortex(BC). Robust positive BOLD signals were detected in the ipsilateral BC due to antidromic activity, which spread to ipsilateral motor cortex(MC) and posterior thalamus(PO). In the orthodromic target (contralateral barrel cortex), positive BOLD signals were reliably evoked by 2Hz light pulses, whereas 40Hz light pulses led to a reversed sign of BOLD - indicative of CC-mediated inhibition. This presumed optogenetic CC-mediated inhibition was further elucidated by pairing light with peripheral whisker stimulation at varied inter-stimulus intervals. Whisker induced positive BOLD, and calcium signals were reduced at inter-stimulus intervals of 50/100ms. The calcium-amplitude modulation (AM)-based correlation with whole-brain fMRI signal revealed that the inhibitory effects spread to contralateral BC as well as ipsilateral MC and PO. This work raises the need of fMRI to elucidate the brain-wide network activation in response to projection-specific optogenetic stimulation.


2021 ◽  
Author(s):  
Ramon Nogueira ◽  
Chris C. Rodgers ◽  
Randy M. Bruno ◽  
Stefano Fusi

Adaptive behavior in humans, rodents, and other animals often requires the integration over time of multiple sensory inputs. Here we studied the behavior and the neural activity of mice trained to actively integrate information from different whiskers to report the curvature of an object. The analysis of high speed videos of the whiskers revealed that the task could be solved by integrating linearly the whisker contacts on the object. However, recordings from the mouse barrel cortex revealed that the neural representations are high dimensional as the inputs from multiple whiskers are mixed non-linearly to produce the observed neural activity. The observed representation enables the animal to perform a broad class of significantly more complex tasks, with minimal disruption of the ability to generalize to novel situations in simpler tasks. Simulated recurrent neural networks trained to perform similar tasks reproduced both the behavioral and neuronal experimental observations. Our work suggests that the somatosensory cortex operates in a regime that represents an efficient compromise between generalization, which typically requires pure and linear mixed selectivity representations, and the ability to perform complex discrimination tasks, which is granted by non-linear mixed representations.


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
William Zeiger ◽  
Mate Marosi ◽  
Satvir Saggi ◽  
Natalie Noble ◽  
Isa Samad ◽  
...  

Following ischemic stroke, many patients exhibit partial spontaneous recovery, suggesting that the brain has endogenous mechanisms to recover lost functions. Evidence supports a role for peri-infarct cortex in recovery as this area undergoes structural, physiologic, and transcriptomic changes following stroke. It has been hypothesized that these changes promote circuit rewiring, leading spared neurons in the peri-infarct cortex to “remap” and subsume the function previously performed by neurons in the ischemic core. However, direct evidence for remapping at the single neuron level is lacking. To test this, we targeted photothrombotic (PT) strokes to an individual barrel (C1) in the barrel field of mouse primary somatosensory cortex (S1BF). We then performed longitudinal in vivo two-photon (2P) calcium imaging in Thy1 -GCaMP6s transgenic mice and recorded whisker-evoked responses of individual layer 2/3 neurons in the adjacent D3 barrel. Before stroke, ~30% of active neurons in the D3 barrel respond to stimulation of the D3 whisker and ~8% of neurons respond to the C1 whisker. Based on the remapping hypothesis, we predicted that the percentage of C1 whisker-responsive neurons in the spared D3 barrel would increase after stroke; however, we found that only ~2% of neurons in the D3 barrel responded to C1 whisker stimulation one month after stroke. We also tested the effect of forced-use therapy on recovery by plucking all whiskers, except the C1 whisker corresponding to the infarcted barrel, following stroke. Still, we found that forced-use therapy did not lead to an increased percentage of C1 whisker-responsive neurons, but it did enhance the responses to C1 whisker stimulation in surviving C1-responsive neurons in the peri-infarct cortex. These results suggest that at the circuit level recovery may occur through potentiation of spared homotopic neurons rather than remapping of neurons to perform new functions.


2004 ◽  
Vol 24 (9) ◽  
pp. 1057-1068 ◽  
Author(s):  
Hrachya Nersesyan ◽  
Peter Herman ◽  
Ersan Erdogan ◽  
Fahmeed Hyder ◽  
Hal Blumenfeld

There is broad agreement that generalized tonic–clonic seizures (GTCS) and normal somatosensory stimulation are associated with increases in regional CBF. However, the data regarding CBF changes during absence seizures are controversial. Electrophysiologic studies in WAG/Rij rats, an established animal model of absence seizures, have shown spike-wave discharges (SWD) that are largest in the perioral somatosensory cortex while sparing the visual cortex. Recent functional magnetic resonance imaging (fMRI) studies in the same model have also shown localized increases in fMRI signals in the perioral somatosensory cortex during SWD. Because fMRI signals are only indirectly related to neuronal activity, the authors directly measured CBF and neuronal activity from specific microdomains of the WAG/Rij cortex using a specially designed probe combining laser-Doppler flowmetry and extracellular microelectrode recordings under fentanyl/haloperidol anesthesia. Using this approach, parallel increases in neuronal activity and CBF were observed during SWD in the whisker somatosensory (barrel) cortex, whereas the visual cortex showed no significant changes. For comparison, these measurements were repeated during somatosensory (whisker) stimulation, and bicuculline-induced GTCS in the same animals. Interestingly, whisker stimulation increased neuronal activity and CBF in the barrel cortex more than during SWD. During GTCS, much larger increases that included both the somatosensory and visual cortex were observed. Thus, SWD in this model produce parallel localized increases in neuronal activity and CBF with similar distribution to somatosensory stimulation, whereas GTCS produce larger and more widespread changes. The normal response to somatosensory stimulation appears to be poised between two abnormal responses produced by two physiologically different types of seizures.


2015 ◽  
Vol 3 (1-2) ◽  
pp. 172-188
Author(s):  
Brandon T. Paul ◽  
Per B. Sederberg ◽  
Lawrence L. Feth

Temporal patterns within complex sound signals, such as music, are not merely processed after they are heard. We also focus attention to upcoming points in time to aid perception, contingent upon regularities we perceive in the sounds’ inherent rhythms. Such organized predictions are endogenously maintained as meter — the patterning of sounds into hierarchical timing levels that manifest as strong and weak events. Models of neural oscillations provide potential means for how meter could arise in the brain, but little evidence of dynamic neural activity has been offered. To this end, we conducted a study instructing participants to imagine two-based or three-based metric patterns over identical, equally-spaced sounds while we recorded the electroencephalogram (EEG). In the three-based metric pattern, multivariate analysis of the EEG showed contrasting patterns of neural oscillations between strong and weak events in the delta (2–4 Hz) and alpha (9–14 Hz), frequency bands, while theta (4–9 Hz) and beta (16–24 Hz) bands contrasted two hierarchically weaker events. In two-based metric patterns, neural activity did not drastically differ between strong and weak events. We suggest the findings reflect patterns of neural activation and suppression responsible for shaping perception through time.


2019 ◽  
Vol 149 (5) ◽  
pp. 730-737
Author(s):  
Sungmin Kang ◽  
Yurie Hayashi ◽  
Michael Bruyns-Haylett ◽  
Daniel H Baker ◽  
Marcia Boura ◽  
...  

ABSTRACT Background Although vitamin B-12 (B-12) is known to contribute to the structural and functional development of the brain, it is unclear if B-12 supplementation has any beneficial effect in healthy populations in terms of enhanced neurologic status of the brain or improved cognitive function. Objectives We investigated the effect of dietary supplementation of B-12 on the cortical neural activity of well-nourished young adult rats and tested the hypothesis that B-12 supplementation in healthy rats may reduce sensory-evoked neural activity due to enhanced inhibition. Methods Female Lister Hooded rats weighing 190–265 g (2–4 mo old) were included in the study. The experimental group was fed with B-12 (cyanocobalamin)–enriched water at a concentration of 1 mg/L, and the control (CON) group with tap water for 3 wk. Animals were then anesthetized and cortical neural responses to whisker stimulation were recorded in vivo through the use of a multichannel microelectrode, from which local field potentials (LFPs) were extracted. Results Somatosensory-evoked LFP was 25% larger in the B-12 group (4.13 ± 0.24 mV) than in the CON group (3.30 ± 0.21 mV) (P = 0.02). Spontaneous neural activity did not differ between groups; frequency spectra at each frequency bin of interest did not pass the cluster-forming threshold at the 5% significance level. Conclusions These findings do not provide evidence supporting the hypothesis of decreased neural activity due to B-12 supplementation. As the spontaneous neural activity was unaffected, the increase in somatosensory-evoked LFP may be due to enhanced afferent signal reaching the barrel cortex from the whisker pad, indicating that B-12–supplemented rats may have enhanced sensitivity to sensory stimulation compared with the CON group. We suggest that this enhancement might be the result of lowered sensory threshold, although the underlying mechanism has yet to be elucidated.


2021 ◽  
Vol 1 ◽  
Author(s):  
Shan Xu ◽  
Xiangzhen Kong ◽  
Jia Liu

Navigation is a complex cognitive process. CRY2 gene has been proposed to play an important role in navigation behaviors in various non-human animal species. Utilizing a recently developed neuroimaging-transcriptomics approach, the present study reported a tentative link between the CRY2 gene and human navigation. Specifically, we showed a significant pattern similarity between CRY2 gene expression in the human brain and navigation-related neural activation in functional magnetic resonance imaging. To further illuminate the functionality of CRY2 in human navigation, we examined the correlation between CRY2 expression and various cognitive processes underlying navigation, and found high correlation of CRY2 expression with neural activity of multiple cognitive domains, particularly object and shape perception and spatial memory. Further analyses on the relation between the neural activity of human navigation and the expression maps of genes of two CRY2-related pathways, i.e., the magnetoreceptive and circadian-related functions, found a trend of correlation for the CLOCK gene, a core circadian regulator gene, suggesting that CRY2 may modulate human navigation through its role in circadian rhythm. This observation was further confirmed by a behavioral study where individuals with better circadian regularity in daily life showed better sense of direction. Taken together, our study presents the first neural evidence that links CRY2 with human navigation, possibly through the modulation of circadian rhythm.


2002 ◽  
Vol 283 (5) ◽  
pp. H2029-H2037 ◽  
Author(s):  
Xinqi Peng ◽  
Juan R. Carhuapoma ◽  
Anish Bhardwaj ◽  
Nabil J. Alkayed ◽  
John R. Falck ◽  
...  

Application of glutamate to glial cell cultures stimulates the formation and release of epoxyeicosatrienoic acids (EETs) from arachidonic acid by cytochome P-450 epoxygenases. Epoxygenase inhibitors reduce the cerebral vasodilator response to glutamate and N-methyl-d-aspartate. We tested the hypothesis that epoxygenase inhibitors reduce the somatosensory cortical blood flow response to whisker activation. In chloralose-anesthetized rats, percent changes in cortical perfusion over whisker barrel cortex were measured by laser-Doppler flowmetry during whisker stimulation. Two pharmacologically distinct inhibitors were superfused subdurally: 1) N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide (MS-PPOH), an epoxygenase substrate inhibitor; and 2) miconazole, a reversible cytochrome P-450 inhibitor acting on the heme moiety. Superfusion with 5 μmol/l MS-PPOH decreased the hyperemic response to whisker stimulation by 28% (from 25 ± 9 to 18 ± 7%, means ± SD, n = 8). With 20 μmol/l MS-PPOH superfusion, the response was decreased by 69% (from 28 ± 9% to 9 ± 4%, n = 8). Superfusion with 20 μmol/l miconazole decreased the flow response by 67% (from 31 ± 6% to 10 ± 3%, n = 8). Subsequent superfusion with vehicle restored the response to 26 ± 11%. Indomethacin did not prevent MS-PPOH inhibition of the flow response, suggesting that EET-related vasodilation was not dependent solely on cyclooxygenase metabolism of 5,6-EET. Neither MS-PPOH nor miconazole changed baseline flow, reduced the blood flow response to an adenosine A2 agonist, or decreased somatosensory evoked potentials. The marked reduction of the cortical flow response to whisker stimulation with two different types of epoxygenase inhibitors indicates that EETs play an important role in the physiological coupling of blood flow to neural activation.


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