Frontiers in neuroenergetics最新文献

{"title":"Spatial Relationship between Flavoprotein Fluorescence and the Hemodynamic Response in the Primary Visual Cortex of Alert Macaque Monkeys.","authors":"Yevgeniy B Sirotin,&nbsp;Aniruddha Das","doi":"10.3389/fnene.2010.00006","DOIUrl":"https://doi.org/10.3389/fnene.2010.00006","url":null,"abstract":"<p><p>Flavoprotein fluorescence imaging (FFI) is a novel intrinsic optical signal that is steadily gaining ground as a valuable imaging tool in neuroscience research due to its closer relationship with local metabolism relative to the more commonly used hemodynamic signals. We have developed a technique for FFI imaging in the primary visual cortex (V1) of alert monkeys. Due to the nature of neurovascular coupling, hemodynamic signals are known to spread beyond the locus of metabolic activity. To determine whether FFI signals could provide a more focal measure of cortical activity in alert animals, we compared FFI and hemodynamic point spreads (i.e. responses to a minimal visual stimulus) and functional mapping signals over V1 in macaques performing simple fixation tasks. FFI responses were biphasic, with an early and focal fluorescence increase followed by a delayed and spatially broader fluorescence decrease. As expected, the early fluorescence increase, indicating increased local oxidative metabolism, was somewhat narrower than the simultaneously observed hemodynamic response. However, the later FFI decrease was broader than the hemodynamic response and started prior to the cessation of visual stimulation suggesting different mechanisms underlying the two phases of the fluorescence signal. FFI mapping signals were free of vascular artifacts and comparable in amplitude to hemodynamic mapping signals. These results indicate that the FFI response may be a more local and direct indicator of cortical metabolism than the hemodynamic response in alert animals.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"2 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2010-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/fnene.2010.00006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29080406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurovascular Uncoupling: Much Ado about Nothing.","authors":"Nikos K Logothetis","doi":"10.3389/fnene.2010.00002","DOIUrl":"https://doi.org/10.3389/fnene.2010.00002","url":null,"abstract":"The vast majority of human fMRI studies measure Blood-Oxygen-Level-Dependent (BOLD) contrast, which reflects regional changes in cerebral blood flow (CBF), cerebral blood volume (CBV) and blood oxygenation; all three vascular responses reflect local increases in neural activity (Logothetis and Wandell, 2004). Understanding the exact mechanism (often referred to as neurovascular coupling) by means of which changes in neural activity alter hemodynamics is obviously of paramount importance for the meaningful interpretation of fMRI results. Not surprisingly, over the last decade an increasing number of researchers investigated the neurovascular coupling by combining fMRI with electroencephalography (EEG) or magnetoencephalography (MEG) in humans, e.g. (Dale and Halgren, 2001) as well as with intracortical recordings in animals (Logothetis et al., 2001; Goense and Logothetis, 2008; Logothetis, 2008; Rauch et al., 2008). This neurovascular coupling can also be studied with the optical imaging of intrinsic signals (OIS) (Bonhoeffer and Grinvald, 1996), an excellent invasive method of high spatiotemporal resolution that can measure changes in oxygenation and/or blood volume.","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"2 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2010-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/fnene.2010.00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29200805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pericyte-mediated regulation of capillary diameter: a component of neurovascular coupling in health and disease.","authors":"Nicola B Hamilton,&nbsp;David Attwell,&nbsp;Catherine N Hall","doi":"10.3389/fnene.2010.00005","DOIUrl":"https://doi.org/10.3389/fnene.2010.00005","url":null,"abstract":"<p><p>Because regional blood flow increases in association with the increased metabolic demand generated by localized increases in neural activity, functional imaging researchers often assume that changes in blood flow are an accurate read-out of changes in underlying neural activity. An understanding of the mechanisms that link changes in neural activity to changes in blood flow is crucial for assessing the validity of this assumption, and for understanding the processes that can go wrong during disease states such as ischaemic stroke. Many studies have investigated the mechanisms of neurovascular regulation in arterioles but other evidence suggests that blood flow regulation can also occur in capillaries, because of the presence of contractile cells, pericytes, on the capillary wall. Here we review the evidence that pericytes can modulate capillary diameter in response to neuronal activity and assess the likely importance of neurovascular regulation at the capillary level for functional imaging experiments. We also discuss evidence suggesting that pericytes are particularly sensitive to damage during pathological insults such as ischaemia, Alzheimer's disease and diabetic retinopathy, and consider the potential impact that pericyte dysfunction might have on the development of therapeutic interventions and on the interpretation of functional imaging data in these disorders.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"2 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2010-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/fnene.2010.00005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29202438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent mitochondrial damage by nitric oxide and its derivatives: neuropathological implications.","authors":"Juan P Bolaños,&nbsp;Simon J R Heales","doi":"10.3389/neuro.14.001.2010","DOIUrl":"https://doi.org/10.3389/neuro.14.001.2010","url":null,"abstract":"<p><p>Approximately 15 years ago we reported that cytochrome c oxidase (CcO) was persistently inhibited as a consequence of endogenous induction and activation of nitric oxide ((*)NO) synthase-2 (NOS2) in astrocytes. Furthermore, the reactive nitrogen species implicated was peroxynitrite. In contrast to the reversible inhibition by (*)NO, which occurs rapidly, in competition with O(2), and has signaling regulatory implications, the irreversible CcO damage by peroxynitrite is progressive in nature and follows and/or is accompanied by damage to other key mitochondrial bioenergetic targets. In purified CcO it has been reported that the irreversible inhibition occurs through a mechanism involving damage of the heme a(3)-Cu(B) binuclear center leading to an increase in the K(m) for oxygen. Astrocyte survival, as a consequence of peroxynitrite exposure, is preserved due to their robust bioenergetic and antioxidant defense mechanisms. However, by releasing peroxynitrite to the neighboring neurons, whose antioxidant defense can, under certain conditions, be fragile, activated astrocytes trigger bioenergetic stress leading to neuronal cell death. Thus, such irreversible inhibition of CcO by peroxynitrite may be a plausible mechanism for the neuronal death associated with neurodegenerative diseases, in which the activation of astrocytes plays a crucial role.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"2 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2010-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.001.2010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28719189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Possible Role of CO(2) in Producing A Post-Stimulus CBF and BOLD Undershoot.","authors":"Meryem A Yücel,&nbsp;Anna Devor,&nbsp;Ata Akin,&nbsp;David A Boas","doi":"10.3389/neuro.14.007.2009","DOIUrl":"https://doi.org/10.3389/neuro.14.007.2009","url":null,"abstract":"<p><p>Comprehending the underlying mechanisms of neurovascular coupling is important for understanding the pathogenesis of neurodegenerative diseases related to uncoupling. Moreover, it elucidates the casual relation between the neural signaling and the hemodynamic responses measured with various imaging modalities such as functional magnetic resonance imaging (fMRI). There are mainly two hypotheses concerning this mechanism: a metabolic hypothesis and a neurogenic hypothesis. We have modified recent models of neurovascular coupling adding the effects of both NO (nitric oxide) kinetics, which is a well-known neurogenic vasodilator, and CO(2) kinetics as a metabolic vasodilator. We have also added the Hodgkin-Huxley equations relating the membrane potentials to sodium influx through the membrane. Our results show that the dominant factor in the hemodynamic response is NO, however CO(2) is important in producing a brief post-stimulus undershoot in the blood flow response that in turn modifies the fMRI blood oxygenation level-dependent post-stimulus undershoot. Our results suggest that increased cerebral blood flow during stimulation causes CO(2) washout which then results in a post-stimulus hypocapnia induced vasoconstrictive effect.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2009-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.007.2009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28607787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steady-state brain glucose transport kinetics re-evaluated with a four-state conformational model.","authors":"João M N Duarte,&nbsp;Florence D Morgenthaler,&nbsp;Hongxia Lei,&nbsp;Carol Poitry-Yamate,&nbsp;Rolf Gruetter","doi":"10.3389/neuro.14.006.2009","DOIUrl":"https://doi.org/10.3389/neuro.14.006.2009","url":null,"abstract":"<p><p>Glucose supply from blood to brain occurs through facilitative transporter proteins. A near linear relation between brain and plasma glucose has been experimentally determined and described by a reversible model of enzyme kinetics. A conformational four-state exchange model accounting for trans-acceleration and asymmetry of the carrier was included in a recently developed multi-compartmental model of glucose transport. Based on this model, we demonstrate that brain glucose (G(brain)) as function of plasma glucose (G(plasma)) can be described by a single analytical equation namely comprising three kinetic compartments: blood, endothelial cells and brain. Transport was described by four parameters: apparent half saturation constant K(t), apparent maximum rate constant T(max), glucose consumption rate CMR(glc), and the iso-inhibition constant K(ii) that suggests G(brain) as inhibitor of the isomerisation of the unloaded carrier. Previous published data, where G(brain) was quantified as a function of plasma glucose by either biochemical methods or NMR spectroscopy, were used to determine the aforementioned kinetic parameters. Glucose transport was characterized by K(t) ranging from 1.5 to 3.5 mM, T(max)/CMR(glc) from 4.6 to 5.6, and K(ii) from 51 to 149 mM. It was noteworthy that K(t) was on the order of a few mM, as previously determined from the reversible model. The conformational four-state exchange model of glucose transport into the brain includes both efflux and transport inhibition by G(brain), predicting that G(brain) eventually approaches a maximum concentration. However, since K(ii) largely exceeds G(plasma), iso-inhibition is unlikely to be of substantial importance for plasma glucose below 25 mM. As a consequence, the reversible model can account for most experimental observations under euglycaemia and moderate cases of hypo- and hyperglycaemia.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2009-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.006.2009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28607785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering neuron-glia compartmentalization in cortical energy metabolism.","authors":"Renaud Jolivet,&nbsp;Pierre J Magistretti,&nbsp;Bruno Weber","doi":"10.3389/neuro.14.004.2009","DOIUrl":"https://doi.org/10.3389/neuro.14.004.2009","url":null,"abstract":"<p><p>Energy demand is an important constraint on neural signaling. Several methods have been proposed to assess the energy budget of the brain based on a bottom-up approach in which the energy demand of individual biophysical processes are first estimated independently and then summed up to compute the brain's total energy budget. Here, we address this question using a novel approach that makes use of published datasets that reported average cerebral glucose and oxygen utilization in humans and rodents during different activation states. Our approach allows us (1) to decipher neuron-glia compartmentalization in energy metabolism and (2) to compute a precise state-dependent energy budget for the brain. Under the assumption that the fraction of energy used for signaling is proportional to the cycling of neurotransmitters, we find that in the activated state, most of the energy ( approximately 80%) is oxidatively produced and consumed by neurons to support neuron-to-neuron signaling. Glial cells, while only contributing for a small fraction to energy production ( approximately 6%), actually take up a significant fraction of glucose (50% or more) from the blood and provide neurons with glucose-derived energy substrates. Our results suggest that glycolysis occurs for a significant part in astrocytes whereas most of the oxygen is utilized in neurons. As a consequence, a transfer of glucose-derived metabolites from glial cells to neurons has to take place. Furthermore, we find that the amplitude of this transfer is correlated to (1) the activity level of the brain; the larger the activity, the more metabolites are shuttled from glia to neurons and (2) the oxidative activity in astrocytes; with higher glial pyruvate metabolism, less metabolites are shuttled from glia to neurons. While some of the details of a bottom-up biophysical approach have to be simplified, our method allows for a straightforward assessment of the brain's energy budget from macroscopic measurements with minimal underlying assumptions.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2009-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.004.2009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28332840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Energetics of (Dis)Assembly of the Ternary SNARE Complex.","authors":"Wei Liu,&nbsp;Vladimir Parpura","doi":"10.3389/neuro.14.005.2009","DOIUrl":"https://doi.org/10.3389/neuro.14.005.2009","url":null,"abstract":"The soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE) complex (Sollner et al., 1993) plays a central role in the process of exocytosis whereby vesicles fuse with the plasma membrane to release their cargo of transmitter molecules into the extracellular space. In the majority of neurons, this complex is composed of the vesicular protein synaptobrevin 2 (Sb2), and two proteins located at the plasma membrane, syntaxin (Sx) and synaptosome-associated protein of 25 kDa (SNAP25). The energetics of (dis)assembly of the ternary SNARE complex is critical for understanding of exocytosis, in particular to their role in mediating vesicular fusions to and/or pinching off the plasma membrane. \u0000 \u0000The energy required for disassembly of the ternary SNARE complex has been recently assessed by two different groups (Li et al., 2007; Liu et al., 2009). In both studies SNARE proteins were immobilized to surfaces. One surface contained a Sx-SNAP25 binary complex, while the other Sb2. These surfaces were brought into contact allowing for the formation of the ternary complex, before the surfaces were pulled apart to dismantle the complex. Using surface force apparatus (SFA), Li et al. (2007) revealed a change in free, presumably Gibbs (ΔG), energy of 21 kcal mol−1 (35 kBT) assigned to a disassembly of single SNARE complex. Liu et al. (2009) using Atomic Force Microscopy (AFM) in force spectroscopy mode reported the enthalpic changes (ΔH) of 25.7 kcal mol−1 (43 kBT), as well changes in free energy (ΔG) of 13.8–18.0 kcal mol−1 (23–30 kBT) and entropy (−TΔS) for a disassembly of single ternary SNARE complex (Table ​(Table1).1). Both SFA and AFM approaches, however, could not be used to measure the energetics of the assembly of the complex. \u0000 \u0000 \u0000 \u0000Table 1 \u0000 \u0000Energy measurements for (dis)assembly of the ternary SNARE complex. \u0000 \u0000 \u0000 \u0000Wiederhold and Fasshauer (2009) investigated the ternary SNARE complex assembly by isothermal titration calorimetry (ITC). Various combinations of SNARE proteins were put in a thermally insulated cell and syringe, and then were mixed by injection from the syringe to the cell, while measuring the thermodynamic properties. To avoid formation of the Sx1 SNAP25 binary complex with 2:1 stoichiometry, referred to as a “dead-end species” (Weninger et al., 2008) since it does not represent a reactive Sb2 binding site (Pobbati et al., 2006), SNAP25A was injected into a mixture of Sx1A (H3 domain) and Sb2 [cytosolic domain; amino acids (aa) 1–96] to form the ternary SNARE complex. In these conditions there was extremely large favorable ΔH of −112.8 kcal mol−1 recorded with the positive entropy changes (102.4 kcal mol−1), reflecting the major conformation change during complex assembly, and resulting in ΔG of −10.4 kcal mol−1 (−17.4 kBT) (Table ​(Table11). \u0000 \u0000The ITC measurements above represent energetics of a non-sequential ternary SNARE complex formation, rather than the sequential interactions in which Sb2 binds to a p","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2009-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.005.2009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28302956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Energetics of (Dis)Assembly of the Ternary SNARE Complex","authors":"Wei Liu, V. Parpura","doi":"10.3389/neuro.14/005.2009","DOIUrl":"https://doi.org/10.3389/neuro.14/005.2009","url":null,"abstract":"The soluble N-ethylmaleimidesensitive fusion protein attachment protein receptor (SNARE) complex (Sollner et al., 1993) plays a central role in the process of exocytosis whereby vesicles fuse with the plasma membrane to release their cargo of transmitter molecules into the extracellular space. In the majority of neurons, this complex is composed of the vesicular protein synaptobrevin 2 (Sb2), and two proteins located at the plasma membrane, syntaxin (Sx) and synaptosome-associated protein of 25 kDa (SNAP25). The energetics of (dis)assembly of the ternary SNARE complex is critical for understanding of exocytosis, in particular to their role in mediating vesicular fusions to and/or pinching off the plasma membrane. The energy required for disassembly of the ternary SNARE complex has been recently assessed by two different groups (Li et al., 2007; Liu et al., 2009). In both studies SNARE proteins were immobilized to surfaces. One surface contained a SxSNAP25 binary complex, while the other Sb2. These surfaces were brought into contact allowing for the formation of the ternary complex, before the surfaces were pulled apart to dismantle the complex. Using surface force apparatus (SFA), Li et al. (2007) revealed a change in free, presumably Gibbs (ΔG), energy of 21 kcal mol (35 k B T) assigned to a disassembly of single SNARE complex. Liu et al. (2009) using Atomic Force Microscopy (AFM) in force spectroscopy mode reported the enthalpic changes (ΔH) of 25.7 kcal mol (43 k B T), as well changes in free energy (ΔG) of 13.8–18.0 kcal mol (23–30 k B T) and entropy (−TΔS) for a disassembly of single ternary SNARE complex (Table 1). Both SFA and AFM approaches, however, could not be used to measure the energetics of the assembly of the complex. Wiederhold and Fasshauer (2009) investigated the ternary SNARE complex assembly by isothermal titration calorimetry (ITC). Various combinations of SNARE proteins were put in a thermally insulated cell and syringe, and then were mixed by injection from the syringe to the cell, while measuring the thermodynamic properties. To avoid formation of the Sx1-SNAP25 binary complex with 2:1 stoichiometry, referred to as a “dead-end species” (Weninger et al., 2008) since it does not represent a reactive Sb2 binding site (Pobbati et al., 2006), SNAP25A was injected into a mixture of Sx1A (H3 domain) and Sb2 [cytosolic domain; amino acids (aa) 1–96] to form the ternary SNARE complex. In these conditions there was extremely large favorable ΔH of −112.8 kcal mol recorded with the positive entropy changes (102.4 kcal mol), refl ecting the major conformation change during complex assembly, and resulting in ΔG of −10.4 kcal mol (−17.4 k B T) (Table 1). The ITC measurements above represent energetics of a non-sequential ternary SNARE complex formation, rather than the sequential interactions in which Sb2 binds to a preformed Sx1-SNAP25 binary complex with 1:1 stoichiometry. To addrsess this issue the authors cleverly designed experiment","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2009-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69829935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A model for transient oxygen delivery in cerebral cortex.","authors":"David Ress,&nbsp;Jeffrey K Thompson,&nbsp;Bas Rokers,&nbsp;Reswanul K Khan,&nbsp;Alexander C Huk","doi":"10.3389/neuro.14.003.2009","DOIUrl":"https://doi.org/10.3389/neuro.14.003.2009","url":null,"abstract":"<p><p>Popular hemodynamic brain imaging methods, such as blood oxygen-level dependent functional magnetic resonance imaging (BOLD fMRI), would benefit from a detailed understanding of the mechanisms by which oxygen is delivered to the cortex in response to brief periods of neural activity. Tissue oxygen responses in visual cortex following brief visual stimulation exhibit rich dynamics, including an early decrease in oxygen concentration, a subsequent large increase in concentration, and substantial late-time oscillations (\"ringing\"). We introduce a model that explains the full time-course of these observations made by Thompson et al. (2003). The model treats oxygen transport with a set of differential equations that include a combination of flow and diffusion in a three-compartment (intravascular, extravascular, and intracellular) system. Blood flow in this system is modeled using the impulse response of a lumped linear system that includes an inertive element; this provides a simple biophysical mechanism for the ringing. The model system is solved numerically to produce excellent fits to measurements of tissue oxygen. The results give insight into the dynamics of cerebral oxygen transfer, and can serve as the starting point to understand BOLD fMRI measurements.</p>","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2009-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.003.2009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28304099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}