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 Parenchymal Spin-Lock fMRI Signals Associated with Cortical Spreading Depression

2014 ◽  
Vol 34 (5) ◽  
pp. 768-775 ◽  
Author(s):  
Joonas A Autio ◽  
Artem Shatillo ◽  
Rashid Giniatullin ◽  
Olli H Gröhn
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebral Blood Volume ◽  
High Energy ◽  
Blood Oxygenation ◽  
Acute Ischemia ◽  
High Energy Phosphates ◽  
Ph Change ◽  
Spin Lock ◽  
Fmri Signal

We found novel types of parenchymal functional magnetic resonance imaging (fMRI) signals in the rat brain during large increases in metabolism. Cortical spreading depression (CSD), a self-propagating wave of cellular activation, is associated with several pathologic conditions such as migraine and stroke. It was used as a paradigm to evoke transient neuronal depolarization leading to enhanced energy consumption. Activation of CSD was investigated using spin-lock (SL), diffusion, blood oxygenation level-dependent and cerebral blood volume fMRI techniques. Our results show that the SL-fMRI signal is generated by endogenous parenchymal mechanisms during CSD propagation, and these mechanisms are not associated with hemodynamic changes or cellular swelling. Protein phantoms suggest that pH change alone does not explain the observed SL-fMRI signal changes. However, increased amounts of inorganic phosphates released from high-energy phosphates combined with pH changes may produce SL- power-dependent longitudinal relaxation in the rotating frame ( R1ρ) changes in protein phantoms that are similar to those observed during CSD, as seen before in acute ischemia under our experimental conditions. This links SL-fMRI changes intimately to energy metabolism and supports the use of the SL technique as a new, promising functional approach for noninvasive imaging of metabolic transitions in the active or pathologic brain.

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.

Spreading Depression Enhances Human Neocortical Excitability in vitro

Cephalalgia ◽  
2008 ◽  
Vol 28 (5) ◽  
pp. 558-562 ◽  
Author(s):  
M Berger ◽  
E-J Speckmann ◽  
HC Pape ◽  
A Gorji
Keyword(s):  
Migraine With Aura ◽  
Epilepsy Surgery ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Long Term Potentiation ◽  
Human Cortex ◽  
The Third ◽  
Term Potentiation

Cortical spreading depression (CSD) plays a role in migraine with aura. However, studies of the neuronal effects of CSD in human cortex are scarce. Therefore, in the present study, the effects of CSD on the field excitatory postsynaptic potentials (fEPSP) and the induction of long-term potentiation (LTP) were investigated in human neocortical slices obtained during epilepsy surgery. CSD significantly enhanced the amplitude of fEPSP following a transient suppressive period and increased the induction of LTP in the third layer of neocortical tissues. These results indicate that CSD facilitates synaptic excitability and efficacy in human neocortical tissues, which can be assumed to contribute to hyperexcitability of neocortical tissues in patients suffering from migraine.

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.

Blood volume and optical intrinsic signal imaging of cortical spreading depression

NeuroImage ◽  
2000 ◽  
Vol 11 (5) ◽  
pp. S770
Author(s):  
A.M. O'Farrell ◽  
D.E. Rex ◽  
A. Muthialu ◽  
G.K. Wong ◽  
N. Pouratian ◽  
...  
Keyword(s):  
Blood Volume ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Intrinsic Signal ◽  
Optical Intrinsic Signal

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.

Sign in / Sign up

Export Citation Format

Share Document