scholarly journals Neurovascular coupling during optogenetic functional activation: Local and remote stimulus-response characteristics, and uncoupling by spreading depression

2019 ◽  
Vol 40 (4) ◽  
pp. 808-822 ◽  
Author(s):  
Maximilian Böhm ◽  
David Y Chung ◽  
Carlos A Gómez ◽  
Tao Qin ◽  
Tsubasa Takizawa ◽  
...  
Keyword(s):  
Minimally Invasive ◽  
Spreading Depression ◽  
Barrel Cortex ◽  
Disease Process ◽  
Neurovascular Coupling ◽  
Laser Speckle ◽  
Cortical Activation ◽  
Somatosensory Stimulation ◽  
Response Characteristics ◽  
Electrophysiological Activity

Neurovascular coupling is a fundamental response that links activity to perfusion. Traditional paradigms of neurovascular coupling utilize somatosensory stimulation to activate the primary sensory cortex through subcortical relays. Therefore, examination of neurovascular coupling in disease models can be confounded if the disease process affects these multisynaptic pathways. Optogenetic stimulation is an alternative to directly activate neurons, bypassing the subcortical relays. We employed minimally invasive optogenetic cortical activation through intact skull in Thy1-channelrhodopsin-2 transgenic mice, examined the blood flow changes using laser speckle imaging, and related these to evoked electrophysiological activity. Our data show that optogenetic activation of barrel cortex triggers intensity- and frequency-dependent hyperemia both locally within the barrel cortex (>50% CBF increase), and remotely within the ipsilateral motor cortex (>30% CBF increase). Intriguingly, activation of the barrel cortex causes a small (∼10%) but reproducible hypoperfusion within the contralateral barrel cortex, electrophysiologically linked to transhemispheric inhibition. Cortical spreading depression, known to cause neurovascular uncoupling, diminishes optogenetic hyperemia by more than 50% for up to an hour despite rapid recovery of evoked electrophysiological activity, recapitulating a unique feature of physiological neurovascular coupling. Altogether, these data establish a minimally invasive paradigm to investigate neurovascular coupling for longitudinal characterization of cerebrovascular pathologies.

scholarly journals Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

2005 ◽  
Vol 10 (1) ◽  
pp. 011004 ◽  
Author(s):  
Michael Guiou ◽  
Sameer Sheth ◽  
Masahito Nemoto ◽  
Melissa Walker ◽  
Nader Pouratian ◽  
...  
Keyword(s):  
Blood Volume ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
Neurovascular Coupling

scholarly journals Difficult Decisions in Minimally Invasive Surgery of the Thymus

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 5887
Author(s):  
Ankit Dhamija ◽  
Jahnavi Kakuturu ◽  
J. W. Awori Hayanga ◽  
Alper Toker
Keyword(s):  
Minimally Invasive Surgery ◽  
Minimally Invasive ◽  
Myasthenia Gravis ◽  
Invasive Surgery ◽  
Early Stage ◽  
Disease Process ◽  
Standard Of Care ◽  
Prognostic Importance

A minimally invasive resection of thymomas has been accepted as standard of care in the last decade for early stage thymomas. This is somewhat controversial in terms of higher-staged thymomas and myasthenia gravis patients due to the prognostic importance of complete resections and the indolent characteristics of the disease process. Despite concerted efforts to standardize minimally invasive approaches, there is still controversy as to the extent of excision, approach of surgery, and the platform utilized. In this article, we aim to provide our surgical perspective of thymic resection and a review of the existing literature.

Microfabricated Electrode Array Compatible With Optical Imaging of Intrinsic Signals During Somatosensory Stimulation and Cortical Spreading Depression

2006 ◽  
Author(s):  
Jeremy J. Theriot ◽  
Neal Prakash ◽  
Arthur W. Toga ◽  
Y. Sungtaek Ju
Keyword(s):  
Optical Imaging ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
Electrode Array ◽  
Transparent Electrode ◽  
Electrophysiological Recording ◽  
Pathological State ◽  
Somatosensory Stimulation ◽  
Intrinsic Signals

Accurate interpretation of functional brain images requires knowledge of the relationship between neurons and their supporting cells and vasculature. Our understanding of this complex and dynamic system would improve if we measure multiple aspects of brain function simultaneously. We have developed a semi-transparent electrode array which allows for concurrent multi-site electrophysiological recording and high-resolution optical imaging of intrinsic signals. The 8-channel electrode array is fabricated on a transparent glass substrate with platinum recording surfaces. We map stimulus-induced field potentials (evoked potentials) and changes in cerebral blood volume in rat somatosensory cortex. We also examine the evolution of these responses during the neuro-pathological state of cortical spreading depression. We have developed a planar multi-electrode array that is fully compatible with Optical imaging of Intrinsic Signals. It provides a sensitive and reliable tool to use in the study of neurovascular coupling in brain activation.

CHIVA, ASVAL and related techniques – Concepts and evidence

2015 ◽  
Vol 30 (2_suppl) ◽  
pp. 42-45 ◽  
Author(s):  
Sarah Onida ◽  
Alun H Davies
Keyword(s):  
Minimally Invasive ◽  
Varicose Veins ◽  
Disease Process ◽  
Chronic Venous Disease ◽  
Treatment Modalities ◽  
Venous Disease ◽  
Invasive Treatment ◽  
Venous Circulation ◽  
Underlying Pathophysiology

Chronic venous disease (CVD) is a highly prevalent condition with significant effects on patients’ quality of life. Despite this, the underlying pathophysiology of venous disease still remains unclear. Two schools of thought exist, explaining the development and propagation of venous disease as an “ascending” and “descending” process, respectively. The descending theory, stating that CVD is secondary to proximal disease (e.g. saphenofemoral/saphenous incompetence), is the most widely accepted when planning treatment aiming to remove or destroy the junction or truncal veins. The ascending theory, describing the disease process as developing in the lower most part of the leg and propagating cranially, aims to re-route the venous circulation via minimally invasive interventions. Classically, superficial venous insufficiency has been treated with the removal of the incompetent trunk, via open surgery or, increasingly, with endovenous interventions. Minimally invasive treatment modalities aiming to preserve the saphenous trunk, such as CHIVA and ASVAL, may also play an important role in the treatment of the patient with varicose veins.

scholarly journals Developmental Switch in Neurovascular Coupling in the Immature Rodent Barrel Cortex

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80749 ◽  
Author(s):  
Christoph M. Zehendner ◽  
Simeon Tsohataridis ◽  
Heiko J. Luhmann ◽  
Jenq-Wei Yang
Keyword(s):  
Barrel Cortex ◽  
Neurovascular Coupling ◽  
Developmental Switch

scholarly journals Cyclosporine A, FK506, and NIM811 ameliorate prolonged CBF reduction and impaired neurovascular coupling after cortical spreading depression

2011 ◽  
Vol 31 (7) ◽  
pp. 1588-1598 ◽  
Author(s):  
Henning Piilgaard ◽  
Brent M Witgen ◽  
Peter Rasmussen ◽  
Martin Lauritzen
Keyword(s):  
Cyclosporine A ◽  
Cortical Spreading Depression ◽  
Vascular Reactivity ◽  
Spreading Depression ◽  
Mitochondrial Permeability Transition ◽  
Neurovascular Coupling ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Doppler Flowmetry ◽  
Electrocortical Activity

Cortical spreading depression (CSD) is associated with mitochondrial depolarization, increasing intracellular Ca2+, and the release of free fatty acids, which favor opening of the mitochondrial permeability transition pore (mPTP) and activation of calcineurin (CaN). Here, we test the hypothesis that cyclosporine A (CsA), which blocks both mPTP and CaN, ameliorates the persistent reduction of cerebral blood flow (CBF), impaired vascular reactivity, and a persistent rise in the cerebral metabolic rate of oxygen (CMRO2) following CSD. In addition to CsA, we used the specific mPTP blocker NIM811 and the specific CaN blocker FK506. Cortical spreading depression was induced in rat frontal cortex. Electrocortical activity was recorded by glass microelectrodes, CBF by laser Doppler flowmetry, and tissue oxygen tension with polarographic microelectrodes. Electrocortical activity, basal CBF, CMRO2, and neurovascular and neurometabolic coupling were unaffected by all three drugs under control conditions. NIM811 augmented the rise in CBF observed during CSD. Cyclosporine A and FK506 ameliorated the persistent decrease in CBF after CSD. All three drugs prevented disruption of neurovascular coupling after CSD; the rise in CMRO2 was unchanged. Our data suggest that blockade of mPTP formation and CaN activation may prevent persistent CBF reduction and vascular dysfunction after CSD.

scholarly journals Persistent Increase in Oxygen Consumption and Impaired Neurovascular Coupling after Spreading Depression in Rat Neocortex

2009 ◽  
Vol 29 (9) ◽  
pp. 1517-1527 ◽  
Author(s):  
Henning Piilgaard ◽  
Martin Lauritzen
Keyword(s):  
Cortical Spreading Depression ◽  
Vascular Reactivity ◽  
Spreading Depression ◽  
Acute Hypoxia ◽  
Ion Homeostasis ◽  
Neurovascular Coupling ◽  
Doppler Flowmetry ◽  
Neurometabolic Coupling ◽  
Rat Neocortex ◽  
Cortical Electrical Activity

Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is the mechanism of migraine, and involved in progressive neuronal injury in stroke and head trauma. Here we tested the hypothesis that single episodes of CSD induced acute hypoxia, and prolonged impairment of neurovascular and neurometabolic coupling. Cortical spreading depression was induced in rat frontal cortex, whereas cortical electrical activity and local field potentials (LFPs) were recorded by glass microelectrodes, cerebral blood flow (CBF) by laser—Doppler flowmetry, and tissue oxygen tension (tpO2) with Polarographic microelectrodes. Cortical spreading depression increased cerebral metabolic rate of oxygen (CMRO2) by 71% ± 6.7% and CBF by 238% ± 48.1% for 1 to 2 mins. For the following 2 h, basal tpO2 and CBF were reduced whereas basal CMRO2 was persistently elevated by 8.1% ± 2.9%. In addition, within first hour after CSD we found impaired neurovascular coupling (LFP versus CBF), whereas neurometabolic coupling (LFP versus CMRO2) remained unaffected. Impaired neurovascular coupling was explained by both reduced vascular reactivity and suppressed function of cortical inhibitory interneurons. The protracted effects of CSD on basal CMRO2 and neurovascular coupling may contribute to cellular dysfunction in patients with migraine and acutely injured cerebral cortex.

scholarly journals Modulation of artificial whisking related signals in barrel cortex

2015 ◽  
Vol 113 (5) ◽  
pp. 1287-1301 ◽  
Author(s):  
Manuel A. Castro-Alamancos ◽  
Tatiana Bezdudnaya
Keyword(s):  
Superior Colliculus ◽  
Sensory Processing ◽  
Barrel Cortex ◽  
Motor Nerve ◽  
Low Frequency ◽  
Cortical Activation ◽  
Neural Responses ◽  
Population Responses ◽  
Processing Abilities ◽  
Network States

Rats use rhythmic whisker movements, called active whisking, to sense the environment, which include whisker protractions followed by retractions at various frequencies. Using a proxy of active whisking in anesthetized rats, called artificial whisking, which is induced by electrically stimulating the facial motor nerve, we characterized the neural responses evoked in the barrel cortex by whisking in air (without contact) and on a surface (with contact). Neural responses were compared between distinct network states consisting of cortical deactivation (synchronized slow oscillations) and activation (desynchronized state) produced by neuromodulation (cholinergic or noradrenergic stimulation in neocortex or thalamus). Here we show that population responses in the barrel cortex consist of a robust signal driven by the onset of the whisker protraction followed by a whisking retraction signal that emerges during low frequency whisking on a surface. The whisking movement onset signal is suppressed by increasing whisking frequency, is controlled by cortical synaptic inhibition, is suppressed during cortical activation states, is little affected by whisking on a surface, and is ubiquitous in ventroposterior medial (VPM) thalamus, barrel cortex, and superior colliculus. The whisking retraction signal codes the duration of the preceding whisker protraction, is present in thalamocortical networks but not in superior colliculus, and is robust during cortical activation; a state associated with natural exploratory whisking. The expression of different whisking signals in forebrain and midbrain may define the sensory processing abilities of those sensorimotor circuits. Whisking related signals in the barrel cortex are controlled by network states that are set by neuromodulators.

scholarly journals Assessment of neurovascular coupling and cortical spreading depression in mixed mouse models of atherosclerosis and Alzheimer’s disease

eLife ◽  
2022 ◽  
Vol 11 ◽  
Author(s):  
Osman Shabir ◽  
Ben Pendry ◽  
Llywelyn Lee ◽  
Beth Eyre ◽  
Paul S Sharp ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Spreading Depression ◽  
Mixed Model ◽  
Spreading Depression ◽  
Neurovascular Coupling ◽  
Cardiovascular Comorbidities ◽  
Neurological Conditions ◽  
Electrode Insertion ◽  
The Brain

Neurovascular coupling is a critical brain mechanism whereby changes to blood flow accompany localised neural activity. The breakdown of neurovascular coupling is linked to the development and progression of several neurological conditions including dementia. In this study, we examined cortical haemodynamics in mouse preparations that modelled Alzheimer’s disease (J20-AD) and atherosclerosis (PCSK9-ATH) between 9 and 12 m of age. We report novel findings with atherosclerosis where neurovascular decline is characterised by significantly reduced blood volume, altered levels of oxyhaemoglobin and deoxyhaemoglobin, in addition to global neuroinflammation. In the comorbid mixed model (J20-PCSK9-MIX), we report a 3 x increase in hippocampal amyloid-beta plaques. A key finding was that cortical spreading depression (CSD) due to electrode insertion into the brain was worse in the diseased animals and led to a prolonged period of hypoxia. These findings suggest that systemic atherosclerosis can be detrimental to neurovascular health and that having cardiovascular comorbidities can exacerbate pre-existing Alzheimer’s-related amyloid-plaques.

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