Archive for the 'BOLD' Category

SPM-Haemodynamic Response Function

Generally speaking, cognitive processing is associated with increases in neuronal firing rates. The increased neural activity lead to increased metabolic requirements for the neurons. The onset of neural activity leads to a systematic series of physiological changes in the local network of blood vessels that include changes in the cerebral blood volume per unit of brain tissue (CBV), changes in the rate of cerebral blood flow (CBF), and changes in the concentration of oxyhaemoglobin and deoxyhaemoglobin.

There are different fMRI techniques that can pick up a functional signal corresponding to changes in each of the previously mentioned components of the haemodynamic response. The most common functional imaging signal is the Blood Oxygenation Level Dependent signal (BOLD), which primarily corresponds to the concentration of deoxyhaemoglobin. In simple terms, the magnetic resonance signal comes from exciting hydrogen nuclei with a radiofrequency pulse, and detecting the radio waves emitted as the nuclei return to a lower-energy configuration. Deoxyhaemoglobin has different magnetic properties than oxyhaemoglobin– it is paramagnetic, which means that it will make the local magnetic field over a microscopic domain inhomogenous. This has the effect of dephasing the signal emitted by the nuclei in this domain, causing destructive interference in the observed MR signal. Over a macroscopic domain (i.e., one functional voxel) greater amounts of deoxyhaemoglobin lead to less signal. The functional BOLD signal is seen as an increase in the MR signal that corresponding to a decrease in the concentration of deoxyhaemoglobin. The decrease of deoxy-Hb is seen because the increase in CBF following neural activity more than accounts for the effect of increased uptake of oxygen.

Image:spm_hrf.png

For the purposes of estimating the BOLD signal in an experimental paradigm, SPM makes use of a canonical haemodynamic response function (HRF). This function is assumed to be the response of the system (as reflected by the MR signal) to a brief, intense period of neural stimulation. The SPM HRF is shown above, and exhibits a rise peaking around 6 sec, followed by an undershoot that persists for a considerable period. The code for this graph is below.

>> RT = 1; hrf = spm_hrf(RT); plot(0:RT:32, hrf);

In this graph, the y-axis is in arbitrary units. A common way to plot the impulse response is in units of percent signal change from a baseline condition. A very robust stimulus (such as a contrast taken between a flickering visual stimulus and no visual stimulus) may produce changes on the order of 2%-4% in the BOLD signal. The change observed in contrasts involving higher-level cognitive processes is typically much smaller.

Ref. http://en.wikibooks.org/wiki/SPM/Haemodynamic_Response_Function

Publicités

GIN, Neuro-imagerie Fonctionnelle et Métabolique (Animal, Humain)

http://neurosciences.ujf-grenoble.fr/equipes/equipe5/

Responsable d’équipe :
Christoph SEGEBARTH
Adresse postale :
  • Grenoble Institut de Neurosciences
  • BP 170
  • 38042 Grenoble Cedex 9
Adresse géographique :
  • Grenoble Institut de Neurosciences
  • Bâtiment Edmond J. Safra
  • Chemin Fortuné Ferrini
  • 38700 La Tronche
  • Tél : 04.56.52.06.00
  • Tél : 04.56.52.05.99 (secrétariat)
  • mailto : christoph.segebarth@ujf-grenoble.fr

Composition de l’équipe (2008) :

Les personnels rattachés à la Plate-forme IRM sont répertoriés sous le lien Plate-forme IRM de Grenoble.
Les chercheurs « associés » à l’équipe 5 – c’est à dire accueillis dans les locaux de l’équipe pour une fraction importante de leur temps de recherche – ont leur nom précédé d’un astérisque.

Asfour Aktham, Maître de Conférence Grand Sylvie, Maïtre de Conférence – Praticien Hospitalier Pannetier Nicolas, Doctorant
Barbier Emmanuel, Chargé de Recherche INSERM Grouiller Frédéric, Doctorant Payen Jean-François, Professeur-Praticien Hospitalier
Chipon Emilie, Doctorante Jessberger Philipp, Diplomarbeit – Praticien Hospitalier Polosan Mircea, Praticien Hospitalier-Doctorant
Christen Thomas, Doctorant Kabir Yacine, Doctorant Provent Peggy, Ingénieur de Recherche CDD
Coles Jonathan, Directeur de Recherche CNRS Krainik Alexandre, Praticien Hospitalo-Universitaire Rémy Chantal, Directeur de Recherche INSERM
David Olivier, Chargé de Recherche INSERM *Lafaye de Michaux Pierre, Maître de Conférence Reyt Sébastien, Doctorant
Delon-Martin Chantal, Chargée de Recherche INSERM Lahrech Hana, Chargée de Recherche INSERM Ricard Clément, Doctorant
Detante Olivier, Doctorant Lemasson Benjamin, Doctorant Scherrer Benoît, Doctorant
Dojat Michel, Ingénieur de Recherche INSERM Leviel Jean-Louis, Professeur Segebarth Christoph, Directeur de Recheche INSERM
Doyle Senan, Post-doctorant Mauconduit Franck, Etudiant Master 2 Stupar Vasilee, Ingénieur de Recherche INSERM
Fondraz Nadège, étudiante BTSA Mayan Virginie, Etudiante Master 2 Tachrount Mohamed, Doctorant
Francony Gilles, Doctorant Naegele Bernadette, Neuropsychologue Vasseur Flor, Doctorante
Girard Pascal, Ingénieur de Recherche CDD Noack Christoph, Diplomarbeit – Université de Würzburg Warnking Jan, Chargé de Recherche INSERM
Gottschalk Michael, Post-doctorant Pachot-Clouard Mathilde, Maître de Conférence Zanoni Marie Claude, Secrétaire – gestionnaire INSERM

equipe

Axes de Recherche :

recherche

Applications biomédicales in vivo de la Résonnace Magnétique Nucléaire (RMN). Travaux effectués tant chez l’Homme que chez le petit animal (rat, souris). Ils visent au développement, à l’évaluation et à l’exploitation du potentiel de l’ensemble des méthodes de neuroimagerie RMN en neurosciences cliniques, biologiques et cognitives. En savoir plus…

Techniques usuelles :

techniques

Publications récentes :

  • Vérant P, Serduc R, Van der Sanden B, Rémy C, Ricard C, Coles JA, Vial JC. A subtraction method for intravital two-photon microscopy: intraparenchymal imaging and quantificationof extravasation in mouse brain cortex. Journal of Biomedical Optics 2008;In Press.
  • Lahrech H, Perles-Barbacaru AT, Aous S, Farion R, Le Bas J-F, Debouzy JC, Gadelle A, Fries PH. Potential of a New Contrast Agent: Gadolinium Per (3,6) Anhydro Alpha Cyclodextrin for Magnetic Resonance Neuroimaging. Journal of Cerebral Blood Flow & Metabolism 2008;In Press.
  • Feddersen B, Vercueil L, S. N, David O, Depaulis A, Deransart C. Controling seizures is not controling epilepsy : a parametric study of deep brain stimulation for epilepsy. Neurobiology of Disease 2008;In Press.
  • Grouiller F, Vercueil L, Krainik A, Segebarth C, Kahane P. A comparative study of different artefact removal algorithms for EEG signals acquired during functional MRI. Neuroimage 2008;In Press.
  • Grillon E, Provent P, Montigon O, Segebarth C, Rémy C, Barbier EL. Blood-brain barrier permeability to manganese and to Gd-DOTA in a rat model of transient cerebral ischaemia. NMR Biomed 2008;In Press.
  • Kickler N, Krack P, Fraix V, Le Bas J-F, Lamalle L, Durif F, Krainik A, Remy C, Segebarth C, Pollak P. Glutamate measurement in Parkinson’s disease using magnetic resonance spectroscopy at 3 T field strength. NMR Biomed 2008;In Press.
  • Valable S, Barbier EL, Bernaudin M, Roussel S, Segebarth C, Petit E, Remy C. In vivo MRI tracking of exogenous monocytes/macrophages targeting brain tumours in a rat model of glioma. NeuroImage 2008;In Press.
  • van der Graaf M, Julia-Sape M, Howe FA, Ziegler A, Majos C, Moreno A, Rijpkema M, Acosta DM, Opstad K, van der Meulen YM, Arus C, Heerschap A. MRS quality assessment in a multicentre study on MRS-Based classification of brain tumours. NMR Biomed 2008;21:148-158.
  • Payen J-F, Chanques G, Mantz J, Hercule C, Auriant I, Lequillou JL, Binhas M, Genty C, Rolland C, Bosson J-L. Current practices in sedation and analgesia for mechanically ventilated critically ill patients: a prospective multicenter patient-based study. Anesthesiology 2007;106(4):687-695.
  • Provent P, Benito M, Hiba B, Farion R, Lopez-Larrubia P, Ballesteros P, Rémy C, Segebarth C, Cerdan S, Coles J, Garcia-Martin ML. Serial in vivo spectroscopic nuclear magnetic resonance imaging of lactate and extracellular pH in rat gliomas shows redistribution of protons away from sites of glycolysis. Cancer Res 2007;67(16):7638-7645.
  • Stephan K, Harrison L, Kiebel SJ, David O, Penny W, Friston KJ. Dynamic causal models of neural system dynamics: current state and future extensions. J Biosci 2007;32(1):129-144.
  • Perles-Barbacaru AT, Lahrech H. A new MRI method for mapping the cerebral blood volume fraction: the rapid steady-state T(1) method. J Cereb Blood Flow Metab 2007;27(3):318-631.
  • Provent P, Kickler N, Barbier EL, Bergerot A, Farion R, Goury S, Marcaggi P, Segebarth C, Coles JA. The ammonium-induced increase in rat brain lactate concentration is rapid and reversible and suggests a physiological role of ammonium in regulating energy metabolism. J Cereb Blood Flow Metab 2007;27:1830-1840.
  • Vérant P, Serduc R, Van der Sanden B, Rémy C, Vial JC. A direct method for measuring mouse capillary cortical blood volume using multiphoton laser scanning microscopy. J Cereb Blood Flow Metab 2007;27(5):1072-1081.
  • Verdonck O, Lahrech H, Francony G, Carle O, Farion R, van de Looij Y, Rémy C, Segebarth C, Payen J-F. Erythropoietin protects from posttraumatic edema in the rat brain. J Cereb Blood Flow Metab 2007;27(7):1369-1376.
  • Guyet T, Dojat M, Garbay C. Knowledge construction from time series data using a collaborative exploration system. Journal of Biomedical Informatics 2007;40:672-687.
  • Beaumont M, Lamalle L, Segebarth C, Barbier EL. Improved K-Space Trajectory Measurement with signal Shifting. Magnetic Resonance in Medicine 2007;58(1):200-205.
  • Barrillot C, Benali H, Dojat M, Gaignard A, Gibaud B, Kinkingnéhun S, Matsumoto JP, Pelegrini-Issac M, Simon E, Temal L. Federating Distributed and Heterogeneous Information Sources in Neuroimaging: The NeuroBase Project. Stud Health Technol Inform 2007;120:3-13.
  • Testylier G, Lahrech H, Montigon O, Foquin A, Delacour C, Bernabé D, Segebarth C, Dorandeu F, Carpentier P. Cerebral edema induced in mice by a convulsive dose of soman. Evaluation through diffusion-weighted magnetic resonance imaging and histology. Toxicology and Applied Pharmacology 2007;220(2):125-137.

initial dip

One page.

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Dynamics and nonlinearities of the BOLD response at very short stimulus durations.

Yeşilyurt B, Uğurbil K, Uludağ K.

Max-Planck-Institute for Biological Cybernetics, High-Field Magnetic Resonance Center, 72076 Tübingen, Germany.

In designing a functional imaging experiment or analyzing data, it is typically assumed that task duration and hemodynamic response are linearly related to each other. However, numerous human and animal studies have previously reported a deviation from linearity for short stimulus durations (<4 s). Here, we investigated nonlinearities of blood-oxygenation-level-dependent (BOLD) signals following visual stimulation of 5 to 1000 ms duration at two different luminance levels in human subjects. It was found that (a) a BOLD response to stimulus durations as short as 5 ms can be reliably detected; this stimulus duration is shorter than employed in any previous study investigating BOLD signal time courses; (b) the responses are more nonlinear than in any other previous study: the BOLD response to 1000 ms stimulation is only twice as large as the BOLD response to 5 ms stimulation although 200 times more photons were projected onto the retina; (c) the degree of nonlinearity depends on stimulus intensity; that is, nonlinearities have to be characterized not only by stimulus duration but also by stimulus features like luminance. These findings are especially of most practical importance in rapid event-related functional magnetic resonance imaging (fMRI) experimental designs. In addition, an ‘initial dip’ response – thought to be generated by a rapid increase in cerebral metabolic rate of oxygen metabolism (CMRO(2)) relative to cerebral blood flow – was observed and shown to colocalize well with the positive BOLD response. Highly intense stimulation, better tolerated by human subjects for short stimulus durations, causes early CMRO(2) increase, and thus, the experimental design utilized in this study is better for detecting the initial dip than standard fMRI designs. These results and those from other groups suggest that short stimulation combined with appropriate experimental designs allows neuronal events and interactions to be examined by BOLD signal analysis, despite its slow evolution.

PMID: 18479876 [PubMed – as supplied by publisher]


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Transient and sustained BOLD responses to sustained visual stimulation.

Uludağ K.

Max-Planck-Institute for Biological Cybernetics, High-Field Magnetic Resonance Center, 72076 Tübingen, Germany.

Examining the transients of the blood-oxygenation-level-dependent (BOLD) signal using functional magnetic resonance imaging is a tool to probe basic brain physiology. In addition to the so-called initial dip and poststimulus undershoot of the BOLD signal, occasionally, overshoot at the beginning and at the end of stimulation and stimulus onset and offset (‘phasic’) responses are observed. Hemifield visual stimulation was used in human subjects to study the latter transients. As expected, sustained (‘tonic’) stimulus-correlated contralateral activation in the visual cortex and LGN was observed. Interestingly, bilateral phasic responses were observed, which only partly overlapped with the tonic network and which would have been missed using a standard analysis. A biomechanical model of the BOLD signal (‘balloon model’) indicated that, in addition to phasic neuronal activity, vascular uncoupling can also give rise to phasic BOLD signals. Thus, additional physiological information (i.e., cerebral blood flow) and examination of spatial distribution of the activity might help to assess the BOLD signal transients correctly. In the current study, although vascular uncoupled responses cannot be ruled out as an explanation of the observed phasic BOLD network, the spatial distribution argues that sustained hemifield visual stimulation evokes both bilateral phasic and contralateral sustained neuronal responses. As a consequence, in rapid event-related experimental designs, both the phasic and tonic networks cannot be separated, possibly confounding the interpretation of BOLD signal data. Furthermore, a combination of phasic and tonic responses in the same region of interest might also mimic a BOLD response typically observed in adaptation experiments.

PMID: 18479869 [PubMed – as supplied by publisher]


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Independent components of the haemodynamic response in intrinsic optical imaging.

Schiessl I, Wang W, McLoughlin N.

Faculty of Life Sciences, University of Manchester, Manchester, M60 1QD, UK. i.schiessl@manchester.ac.uk

Functional brain imaging methods are prone to contamination from global vascular artefacts. A variety of methods have been proposed to help segment functional from non-specific changes. Here we quantify the improvement in the signal to noise ratio (SNR) of functional maps, derived from intrinsic optical imaging studies of macaque visual cortex, through the application of Extended Spatial Decorrelation (ESD). The resulting independent component maps and their corresponding time courses reveal for the first time a fast vascular component in the haemodynamic response. ESD is a blind source separation algorithm that utilises spatial statistical features in brain images to separate the recorded mixed sources into independent components. We have investigated differential and single condition experiments using a variety of visual stimuli. To calculate the improvement of the SNR in decibel (dB) we back project separated components onto the original single trial data and analyse the corresponding Fourier spectrum. The application of ESD improved SNR in the functional brain maps from 0.52 to 16.88 dB on differential imaging data and from 1.69 to 12.83 dB in the case of single condition experiments. Analysing the independent components further we found that they can separate different functional compartments of the cortical vasculature. Some of the components, classified as arterial through slit spectroscopy, revealed a strong fast response to the stimulus onset/offset starting approximately 0.2 s after the change of the stimulus and reaching a peak after approximately 0.4 s. This fast haemodynamic response raises new questions concerning the spatial specificity of the so-called « initial dip ».

Publication Types:

PMID: 17959391 [PubMed – indexed for MEDLINE]


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Temporal profiles and 2-dimensional oxy-, deoxy-, and total-hemoglobin somatosensory maps in rat versus mouse cortex.

Prakash N, Biag JD, Sheth SA, Mitsuyama S, Theriot J, Ramachandra C, Toga AW.

University of California, Los Angeles, David Geffen School of Medicine, Department of Neurology, Laboratory of Neuro Imaging, Los Angeles, CA 90095, USA. neal.prakash@gmail.com

BACKGROUND: Mechanisms of neurovascular coupling-the relationship between neuronal chemoelectrical activity and compensatory metabolic and hemodynamic changes-appear to be preserved across species from rats to humans despite differences in scale. However, previous work suggests that the highly cellular dense mouse somatosensory cortex has different functional hemodynamic changes compared to other species. METHODS: We developed novel hardware and software for 2-dimensional optical spectroscopy (2DOS). Optical changes at four simultaneously recorded wavelengths were measured in both rat and mouse primary somatosensory cortex (S1) evoked by forepaw stimulation to create four spectral maps. The spectral maps were converted to maps of deoxy-, oxy-, and total-hemoglobin (HbR, HbO, and HbT) concentration changes using the modified Beer-Lambert law and phantom HbR and HbO absorption spectra. RESULTS:: Functional hemodynamics were different in mouse versus rat neocortex. On average, hemodynamics were as expected in rat primary somatosensory cortex (S1): the fractional change in the log of HbT concentration increased monophasically 2 s after stimulus, whereas HbO changes mirrored HbR changes, with HbO showing a small initial dip at 0.5 s followed by a large increase 3.0 s post stimulus. In contrast, mouse S1 showed a novel type of stimulus-evoked hemodynamic response, with prolonged, concurrent, monophasic increases in HbR and HbT and a parallel decrease in HbO that all peaked 3.5-4.5 s post stimulus onset. For rats, at any given time point, the average size and shape of HbO and HbR forepaw maps were the same, whereas surface veins distorted the shape of the HbT map. For mice, HbO, HbR, and HbT forepaw maps were generally the same size and shape at any post-stimulus time point. CONCLUSIONS: 2DOS using image splitting optics is feasible across species for brain mapping and quantifying the map topography of cortical hemodynamics. These results suggest that during physiologic stimulation, different species and/or cortical architecture may give rise to different hemodynamic changes during neurovascular coupling.

Publication Types:

PMID: 17574868 [PubMed – indexed for MEDLINE]

PMCID: PMC2227950


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A coherent neurobiological framework for functional neuroimaging provided by a model integrating compartmentalized energy metabolism.

Aubert A, Pellerin L, Magistretti PJ, Costalat R.

Département de Physiologie, Université de Lausanne, 1005 Lausanne, Switzerland.

Functional neuroimaging has undergone spectacular developments in recent years. Paradoxically, its neurobiological bases have remained elusive, resulting in an intense debate around the cellular mechanisms taking place upon activation that could contribute to the signals measured. Taking advantage of a modeling approach, we propose here a coherent neurobiological framework that not only explains several in vitro and in vivo observations but also provides a physiological basis to interpret imaging signals. First, based on a model of compartmentalized energy metabolism, we show that complex kinetics of NADH changes observed in vitro can be accounted for by distinct metabolic responses in two cell populations reminiscent of neurons and astrocytes. Second, extended application of the model to an in vivo situation allowed us to reproduce the evolution of intraparenchymal oxygen levels upon activation as measured experimentally without substantially altering the initial parameter values. Finally, applying the same model to functional neuroimaging in humans, we were able to determine that the early negative component of the blood oxygenation level-dependent response recorded with functional MRI, known as the initial dip, critically depends on the oxidative response of neurons, whereas the late aspects of the signal correspond to a combination of responses from cell types with two distinct metabolic profiles that could be neurons and astrocytes. In summary, our results, obtained with such a modeling approach, support the concept that both neuronal and glial metabolic responses form essential components of neuroimaging signals.

Publication Types:

PMID: 17360498 [PubMed – indexed for MEDLINE]

PMCID: PMC1820730


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Intrinsic optical signal imaging of neocortical seizures: the ‘epileptic dip’.

Bahar S, Suh M, Zhao M, Schwartz TH.

Department of Neurological Surgery, Weill-Cornell Medical College, New York Presbyterian Hospital, New York, New York, USA. bahars@umsl.edu

Focal neocortical seizures, induced by injection of 4-aminopyridine, were imaged in the rat neocortex using the intrinsic optical signal, with incident light at various wavelengths. We observed focal, reproducible and prolonged reflectance drops following seizure onset, regardless of wavelength, in the ictal onset zone. A persistent drop in light reflectance with incident orange light, which corresponds to a decrease in oxygenated hemoglobin, was observed. We describe this phenomenon as an ‘epileptic dip’ as it is reminiscent of the ‘initial dip’ observed using the intrinsic optical signal, and also with blood oxygen level-dependent functional magnetic resonance imaging, after normal sensory processing, although with much longer duration. This persistent ictal ischemia was confirmed by direct measurement of tissue oxygenation using oxygen-sensitive electrodes.

Publication Types:

PMID: 16543814 [PubMed – indexed for MEDLINE]


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Brain lactate kinetics: Modeling evidence for neuronal lactate uptake upon activation.

Aubert A, Costalat R, Magistretti PJ, Pellerin L.

Département de Physiologie, Université de Lausanne, 1005 Lausanne, Switzerland.

A critical issue in brain energy metabolism is whether lactate produced within the brain by astrocytes is taken up and metabolized by neurons upon activation. Although there is ample evidence that neurons can efficiently use lactate as an energy substrate, at least in vitro, few experimental data exist to indicate that it is indeed the case in vivo. To address this question, we used a modeling approach to determine which mechanisms are necessary to explain typical brain lactate kinetics observed upon activation. On the basis of a previously validated model that takes into account the compartmentalization of energy metabolism, we developed a mathematical model of brain lactate kinetics, which was applied to published data describing the changes in extracellular lactate levels upon activation. Results show that the initial dip in the extracellular lactate concentration observed at the onset of stimulation can only be satisfactorily explained by a rapid uptake within an intraparenchymal cellular compartment. In contrast, neither blood flow increase, nor extracellular pH variation can be major causes of the lactate initial dip, whereas tissue lactate diffusion only tends to reduce its amplitude. The kinetic properties of monocarboxylate transporter isoforms strongly suggest that neurons represent the most likely compartment for activation-induced lactate uptake and that neuronal lactate utilization occurring early after activation onset is responsible for the initial dip in brain lactate levels observed in both animals and humans.

Publication Types:

PMID: 16260743 [PubMed – indexed for MEDLINE]

PMCID: PMC1297516


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Interaction between tissue oxygen tension and NADH imaging during synaptic stimulation and hypoxia in rat hippocampal slices.

Foster KA, Beaver CJ, Turner DA.

Research and Surgery Services, Durham Veterans Affairs Medical Center, Durham, NC 27710, USA. fosterka@duke.edu

Oxygen and NADH are essential components in the production of ATP in the CNS. This study examined the dynamic interaction between tissue oxygen tension (pO(2)) and NADH imaging changes within hippocampal tissue slices, during metabolic stresses including hypoxia and synaptic activation. The initiation of abrupt hypoxia (from 95% O(2) to 95% N(2)) caused a rapid decrease in pO(2), onset of hypoxic spreading depression (hsd; at 6.7+/-1.3 mm Hg; n=15), and a monophasic increase in NADH. Provided that reoxygenation was prompt, synaptic responses, pO(2) and NADH levels returned to baseline following hsd. Longer hypoxia caused irreversible neuronal dysfunction, an increase in pO(2) beyond baseline (due to decreased tissue demand), and hyperoxidation of NADH (10+/-2% decrease below baseline; n=7). Synaptic activation in ambient 95% O(2) caused a decrease or ‘initial dip’ in pO(2) and a biphasic NADH response (oxidation followed by reduction). The oxidizing phase of the NADH response was mitochondrial as it was synchronous with the ‘initial’ dip in pO(2). Following slow graded reductions in ambient oxygen levels to 8%, four of seven slices developed hsd following synaptic stimulation. The hypoxic threshold for graded oxygen reductions occurred at 7.9+/-5.8 mm Hg O(2) (n=7). Our hypoxic threshold range (6.7-7.9 mm Hg O(2) from abrupt and graded oxygen reduction, respectively) correlates well with reported in vivo values of <12 mm Hg O(2). The major findings of this study include: 1) determination of the critical physiological threshold of pO(2) (based upon hsd), which is a marker of imminent neuronal death if oxygen is not rapidly restored; 2) NADH hyperoxidation and an increase in pO(2) beyond baseline levels following longer periods of hypoxia; and 3) the occurrence of a pO(2) ‘dip’ during synaptic stimulation, which correlates with the early oxidizing phase of the biphasic NADH response.

Publication Types:

PMID: 15837126 [PubMed – indexed for MEDLINE]


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Modeling the hemodynamic response to brain activation.

Buxton RB, Uludağ K, Dubowitz DJ, Liu TT.

Department of Radiology, 0677, and Center for Functional MRI, University of California-San Diego, La Jolla, CA 92093-0677, USA. rbuxton@ecsd.edu

Neural activity in the brain is accompanied by changes in cerebral blood flow (CBF) and blood oxygenation that are detectable with functional magnetic resonance imaging (fMRI) techniques. In this paper, recent mathematical models of this hemodynamic response are reviewed and integrated. Models are described for: (1) the blood oxygenation level dependent (BOLD) signal as a function of changes in cerebral oxygen extraction fraction (E) and cerebral blood volume (CBV); (2) the balloon model, proposed to describe the transient dynamics of CBV and deoxy-hemoglobin (Hb) and how they affect the BOLD signal; (3) neurovascular coupling, relating the responses in CBF and cerebral metabolic rate of oxygen (CMRO(2)) to the neural activity response; and (4) a simple model for the temporal nonlinearity of the neural response itself. These models are integrated into a mathematical framework describing the steps linking a stimulus to the measured BOLD and CBF responses. Experimental results examining transient features of the BOLD response (post-stimulus undershoot and initial dip), nonlinearities of the hemodynamic response, and the role of the physiologic baseline state in altering the BOLD signal are discussed in the context of the proposed models. Quantitative modeling of the hemodynamic response, when combined with experimental data measuring both the BOLD and CBF responses, makes possible a more specific and quantitative assessment of brain physiology than is possible with standard BOLD imaging alone. This approach has the potential to enhance numerous studies of brain function in development, health, and disease.

Publication Types:

PMID: 15501093 [PubMed – indexed for MEDLINE]


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Coupling of changes in cerebral blood flow with neural activity: what must initially dip must come back up.

Ances BM.

Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA. beau.ances@uphs.upenn.edu

Activation flow coupling, increases in neuronal activity leading to changes in cerebral blood flow (CBF), is the basis of many neuroimaging methods. An early rise in deoxygenation, the « initial dip, » occurs before changes in CBF and cerebral blood volume (CBV) and may provide a better spatial localizer of early neuronal activity compared with subsequent increases in CBF. Imaging modality, anesthetic, degree of oxygenation, and species can influence the magnitude of this initial dip. The observed initial dip may reflect a depletion of mitochondrial oxygen (O(2)) buffers caused by increased neuronal activity. Changes in CBF mediated by nitric oxide (NO) or other metabolites and not caused by a lack of O(2) or energy depletion most likely lead to an increased delivery of capillary O(2) in an attempt to maintain intracellular O(2) buffers.

Publication Types:

PMID: 14688611 [PubMed – indexed for MEDLINE]


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