15. Vascularización cerebral
Control de la circulación sistémica
Autorregulación vascularización
cerebral
5
martes 15 de noviembre de 2011
16. Vascularización cerebral
Control de la circulación sistémica
Autorregulación vascularización
cerebral
Distribución del flujo
5
martes 15 de noviembre de 2011
47. Vascularización intracerebral
Arteriolas (50-100 µm)
Arteriolas terminales (10-100µm)
31
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48. Vascularización intracerebral
Arteriolas (50-100 µm)
Arteriolas terminales (10-100µm)
Vénulas (± 30 µm)
31
martes 15 de noviembre de 2011
49. Vascularización intracerebral
Arteriolas (50-100 µm)
Arteriolas terminales (10-100µm)
Vénulas (± 30 µm)
Capilares (<30 µm)
31
martes 15 de noviembre de 2011
50. Vascularización cortical
Red capilar
640 km (reducida en Alzheimer)
Un capilar por neurona
Barrera hematoencefálica
Mecanismos estructurales
Mecanismos metabólicos
martes 15 de noviembre de 2011
59. a
Tipos de transporte
b c d e
Paracellular aqueous Transcellular Transport proteins Receptor-mediated Adsorptive
pathway lipophilic transcytosis transcytosis
pathway
Water-soluble Lipid-soluble Glucose, Vinca alkaloids, Insulin, Albumin, other
agents agents amino acids, Cyclosporin A, transferrin plasma proteins
nucleosides AZT
+++
+ +
+++
Blood –––– +
–+ + –
+ +
–+ + –
+
Tight
junction
–+ + + –
+ +
Texto –+ + + –
– –
Endothelium – –
+++
Brain + +
+++
Astrocyte Astrocyte
Figure 3 | Pathways across the blood–brain barrier. A schematic diagram of the endothelial cells that form the blood–
brain barrier (BBB) and their associations with the perivascular endfeet of astrocytes. The main routes for molecular
traffic across the BBB are shown. a | Normally, the tight junctions severely restrict penetration of water-soluble
martes 15 de noviembre de 2011
61. at the BBB is observed in starvation and hypoxia53,54.
Blood Ligand Tight
junction
Receptor
↑Ca2+ ↑Ca2+
Endothelial cell
Pericyte
Smooth muscle
Basal Microglia
lamina
Neuron Astrocyte Neuron
Figure 5 | Complex cell–cell signalling at the blood–brain barrier. A portion of a
brain capillary wall, showing the main cell types present with the potential to signal to
each other. Pericytes are enclosed within the endothelial basal lamina and form the
closest associations with endothelium. The endfeet of astrocytic glial cells are apposed
martes 15 de noviembre de 2011
62. Review
Figure 3. A Simplified Molecular Atlas of the BBB
(A) Tight junctions. Claudins (claudin-3, -5, and -12) and occludin have four transmembrane domains with two extracellular loops. The junctional adhesion m
ecule A (JAM-A) and the endothelial cell-selective adhesion molecule (ESMA) are members of the Ig superfamily. Zonula occludens proteins (ZO-1, ZO-2, and ZO
and the calcium-dependent serine protein kinase (CASK) are first-order cytoplasmic adaptor proteins that contain PDZ binding domains for the C terminus of
intramembrane proteins. Cingulin, multi-PDZ protein 1 (MUPP1), and the membrane-associated guanylate kinase with an inverted orientation of protein-prot
martes 15 de noviembre de 2011
interaction domain (MAGI) are examples of second-order adaptor molecules. The first- and second-order adaptor molecules together with signaling molecu
64. Box 3 | Pathological states involving BBB breakdown or disorder permeability (little or no aquaporin)88–90, it is likely that
the excess metabolic water joins the ISF being secreted
Several pathologies of the CNS involve disturbance of blood–brain barrier (BBB) into the pericapillary space by the endothelium5. ISF out-
function, and, in many of these, astrocyte–endothelial cooperation is also abnormal. flow involves perivascular spaces around large vessels,
Stroke and clearance routes either through the CSF or following
• Astrocytes secrete transforming growth factor-β (TGFβ), which downregulates brain alternative pathways to neck lymphatics.
capillary endothelial expression of fibrinolytic enzyme tissue plasminogen activator Neurotransmitter recycling can also lead to local
(tPA) and anticoagulant thrombomodulin (TM)150. changes in ions and water. Glutamate is the major
excitatory transmitter of the brain, and astrocyte proc-
Barrera hematoencefálica • Proteolysis of the vascular basement membrane/matrix151.
• Induction of aquaporin 4 (AQP4) mRNA and protein at BBB disruption152. esses surrounding synapses can take up glutamate
• Decrease in BBB permeability after treatment with arginine vasopressin V1 receptor through transport proteins (particularly EAAT1 and 2);
antagonist in a stroke model153. the transport is Na+-dependent and accompanied by
net uptake of ions and water, again contributing to
Trauma water clearance at the BBB85. Glutamate is converted
• Bradykinin, a mediator of inflammation, is produced and stimulates production and to glutamine within the astrocyte and recycled to the
release of interleukin-6 (IL-6) from astrocytes, which leads to opening of the BBB102. neurons. The slight astrocytic cell swelling that accom-
Infectious or inflammatory processes panies neuronal activity, resulting from activation by
Examples include bacterial infections, meningitis, encephalitis and sepsis. glutamate or ion uptake, leads to several cellular mech-
• The bacterial protein lipopolysaccharide affects the permeability of BBB tight anisms that contribute to the recovery of ionic balance
junctions. This is mediated by the production of free radicals, IL-6 and IL-1β154. and cell volume, some of which involve elevated intra-
• Interferon-β prevents BBB disruption155. cellular Ca2+ concentration66,91,92. Hence, there are many
links between the signalling and regulatory processes
Multiple sclerosis that occur in the neurovascular unit.
• Breakdown of the BBB97.
• Downregulation of laminin in the basement membrane156. BBB changes in pathology
• Selective loss of claudin 1/3 in experimental autoimmune encephalomyelitis94. In a number of pathologies, the function of the BBB is
altered (BOX 3), and several disorders appear to involve
HIV
disturbances of endothelial–glial interaction. Thus,
• BBB tight junction disruption157,158. the capillaries of many glial tumours are more leaky
Alzheimer’s disease than those of normal brain tissue, either as a result
• Increased glucose transport, upregulation of glucose transporter GLUT1, altered of a lack of inductive factors, or owing to the release
agrin levels, upregulation of AQP4 expression95,159. of permeability factors such as vascular endothelial
• Accumulation of amyloid-β, a key neuropathological feature of Alzheimer’s disease,
growth factor (VEGF). Moreover, the tight junction
by decreased levels of P-glycoprotein transporter expression160. protein claudin 1/3 is downregulated in some brain
tumours93,94.
• Altered cellular relations at the BBB, and changes in the basal lamina and amyloid-β
clearance100. In BBB disruption, agrin is lost from the abluminal
surface of the brain endothelial cells adjacent to astro-
Parkinson’s disease cytic endfeet11; this may contribute to BBB damage in
• Dysfunction of the BBB by reduced efficacy of P-glycoprotein101. Alzheimer’s disease95, and to the redistribution of astro-
Epilepsy
cytic AQP4 in glioblastomas96. Astrocytic AQP4 expres-
sion is upregulated in brain oedema triggered by BBB
• Transient BBB opening in epileptogenic foci, and upregulated expression of
breakdown. Such upregulation could be adaptive in
P-glycoprotein and other drug efflux transporters in astrocytes and endothelium98,99.
helping to clear the accumulating fluid, but the associ-
Brain tumours ated cell swelling would tend to exacerbate the problem
• Breakdown of the BBB161,162. under extreme conditions. Indeed, AQP4–/– mice show
• Downregulation of tight junction protein claudin 1/3; redistribution of astrocyte protection against ischaemic brain oedema48. Some
AQP4 and Kir4.1 (inwardly rectifying K+ channel)20,93,96. chronic neuropathologies such as multiple sclerosis may
involve an early phase of BBB disturbance (involving
Pain
the downregulation of claudin 1/3 (REF. 11)) that precedes
• Inflammatory pain alters BBB tight junction protein expression and BBB neuronal damage, which suggests that vascular damage
permeability108.
can lead to secondary neuronal disorder97.
In epilepsy, the normal pattern of brain ABC trans-
porter expression may change, with upregulation of
martes 15 de noviembre de 2011 buffer) when neural activity ceases. Astrocytes can also Pgp on astrocytes and brain endothelium98,99; this may
+ + +
65. ronal groups in the regulation of neuroendocrine three families: sel
functions. related receptors
lar inflammation
PMN and other
developing infarc
Barrera hematoencefálica the microvascula
artery occlusion
contribute to mic
mation during t
Adherence and
through the po
sequential intera
sion molecule (I
family consists o
endothelial cells
L-selectin (leuko
and platelets me
cytes and monoc
sion molecules
adhesion proper
leukocyte transm
the interaction
endothelial cell I
Fig. 14. Midline sagittal schematic drawing of the brain show- endothelial cell I
ing circumventricular organs (dark shaded structures): NH, LFA-1).
neurohypophysis; ME, median eminence; OVLT, organum
vasculosum of lamina terminales; SFO, subfornicial organ; 4.3.2. CYTOKINE
PI, pineal gland or body; SCO, subcommissural organ; AP,
area postrema; CP, choroid plexus; OC, optic chiasm; AC, Ischemic cereb
anterior commissure; CC, corpus callosum (lightly shaded oxide free radic
areas). These are stimula
martes 15 de noviembre de 2011
67. 1 junctions, bradykini
leading to the releas
Barrera hematoencefálica NF-κB
B2
Bradykinin
3
amplify the effect by
ET-1 Tumour necrosis fa
TNFα
Microglial cell permeability by dir
and indirect effects
lL-6 2 production and IL
TNFα •O2–
lL-1β LPS complex immunore
Substance P can exacerbate CNS
[Ca2+]i↑ 5-HT multiple sclerosis b
Histamine activation of already
ATP
some mechanisms e
PGs
B2 Indeed, the ability of
contribute to the lin
tPA
disease106.
tPA It has recently be
Capillary cytes and microglia
Tight 4 pain107. As astrocyt
junction TGFβ↓
connectivity and for
gested that glia ma
pain sensation. In in
Endothelial from central and pe
cell sue cells and blood
Agrin? such as substance P
K+ (CGRP), serotonin,
AQP4 Glu BBB from both the b
For example, the re
Basal lamina Astrocyte 5 concentration or alt
tion protein occludi
Figure 6 | Astroglial–endothelial signalling under pathological conditions. TNFα, histamine an
Examples of astroglial–endothelial signalling in infection or inflammation, stroke or matory pain can also
trauma, leading to opening of the blood–brain barrier (BBB) and disturbance of brain permeability108.
martes 15 de noviembre de 2011
function. bradykinin, produced during inflammation in stroke or brain trauma, acts on
68. 42
Endotelio cerebral
martes 15 de noviembre de 2011
69. 42
Endotelio cerebral
Rico en mitocondrias
martes 15 de noviembre de 2011
70. 42
Endotelio cerebral
Rico en mitocondrias
Ausencia de pinocitosis
martes 15 de noviembre de 2011
71. 42
Endotelio cerebral
Rico en mitocondrias
Ausencia de pinocitosis
Ausencia de fenestraciones
martes 15 de noviembre de 2011
72. 42
Endotelio cerebral
Rico en mitocondrias
Ausencia de pinocitosis
Ausencia de fenestraciones
martes 15 de noviembre de 2011
73. l. Encircling the basal lamina of
43
or the pericyte are numerous pro-
joined to one another by gap
Endotelio
d-Brain Barrier Refers to a
cerebral
of Physical, Metabolic, and
operties of the Capillary
Endothelium
barrier is a complex anatomic or
ogic and osmotic barrier protect-
ulating macromolecules, such as
min, do not cross the endothelial
illaries. This contrasts with the
ulating macromolecules that nor-
extracranial tissues. The original
blood-brain barrier is attributed
1885, observed that intravenous
blue, a dye that circulates bound
the diffuse distribution of the dye
n and tissue except the brain and
blood-brain barrier describes the
ing macromolecules to enter the
or interstitial fluid of the brain
he mechanical component of the Fig. 13. Normal rat brain capillary (original magnification
ed primarily to structural charac- Â7000). The inset shows a close-up view of the capillary wall
helial capillary lining of the brain to demonstrate a tight junction (arrows) (original magnifica-
at are lacking in the endothelial tion Â32,200).
martes 15 de noviembre de 2011
82. 45
Pericitos
Identidad oscura
Células
pluripotenciales
Participación en
inducción y
maduración de la
BHE
martes 15 de noviembre de 2011
83. LETTER
46
doi:10.1038/nature09522
Pericytes regulate the blood–brain barrier
Annika Armulik1, Guillem Genove1, Maarja Mae1, Maya H. Nisancioglu1, Elisabet Wallgard1{, Colin Niaudet1, Liqun He1{,
´ ¨
Jenny Norlin1, Per Lindblom2, Karin Strittmatter1{, Bengt R. Johansson3 & Christer Betsholtz1
The blood–brain barrier (BBB) consists of specific physical barriers, (Fig. 1g, h, j and Supplementary Fig. 5a–c). Similarly, the fluorescent
enzymes and transporters, which together maintain the necessary dye cadaverine Alexa Fluor-555 accumulated significantly in the brain
extracellular environment of the central nervous system (CNS)1. parenchyma of Pdgfbret/ret and R26P1/0 mice (Fig. 1j and Supplemen-
The main physical barrier is found in the CNS endothelial cell, tary Fig. 5d, h, i). Additionally, fluorescently labelled albumin, 70 kDa
and depends on continuous complexes of tight junctions combined dextran and IgG passed the BBB in Pdgfbret/ret and R26P1/0 mice, but not
with reduced vesicular transport2. Other possible constituents of the in controls or in R26P1/1 mice (Fig. 1j and Supplementary Fig. 5e–g).
BBB include extracellular matrix, astrocytes and pericytes3, but the These experiments establish a close correlation between pericyte density
relative contribution of these different components to the BBB and permeability across the BBB for a range of tracers of different
remains largely unknown1,3. Here we demonstrate a direct role of molecular masses (Supplementary Table 1).
pericytes at the BBB in vivo. Using a set of adult viable pericyte- Permeability in CNS vessels is impeded by continuous complexes of
deficient mouse mutants we show that pericyte deficiency increases endothelial junctions13,14. We studied such complexes in adult pericyte-
the permeability of the BBB to water and a range of low-molecular- deficient mutants using markers for adherens (VE-cadherin) and tight
mass and high-molecular-mass tracers. The increased permeability (ZO-1 and claudin 5) junctions. Pdgfbret/ret, R26P1/0 and controls
occurs by endothelial transcytosis, a process that is rapidly arrested showed junctional marker expression at similar levels as judged by
by the drug imatinib. Furthermore, we show that pericytes function immunostaining and western blotting (Supplementary Fig. 6a–c and
at the BBB in at least two ways: by regulating BBB-specific gene data not shown). The junctional markers were distributed in a pattern
expression patterns in endothelial cells, and by inducing polariza- consistent with continuous junction complexes in both mutants and
tion of astrocyte end-feet surrounding CNS blood vessels. Our controls; however, mutants displayed focally increased junctional width
results indicate a novel and critical role for pericytes in the integ- and undulation. These patterns were confirmed by transmission elec-
ration of endothelial and astrocyte functions at the neurovascular tron microscopy, which failed to reveal any apparent abnormalities in
unit, and in the regulation of the BBB. the ultrastructure of endothelial junctions, with the exception that
Platelet-derived growth factor (PDGF)-B/PDGF receptor-b (PDGFR- longer and irregular stretches of endothelial overlap were commonly
b) signalling is necessary for pericyte recruitment during angiogenesis4,5. found in pericyte-deficient mutants (Fig. 2c and Supplementary Fig. 6e).
Perinatal lethality precludes analysis of postnatal processes in Pdgfb or Because continuity, ultrastructure and marker expression were con-
Pdgfrb null mice6,7, but several other mouse mutants of this pathway are sistent with retained integrity of endothelial junctions in the absence of
viable postnatally. Two such mutants were used here: PDGF-B retention pericytes, we took advantage of the fixable nature of the fluorescent
motif knockouts (Pdgfbret/ret) where PDGF-B binding to heparan sul- tracers to explore the route of extravasation in Pdgfbret/ret and R26P1/0
phate proteoglycans was disrupted8; and mutants in which Pdgfb null mice in more detail. Cadaverine Alexa Fluor-555 accumulated in
martes 15 de complemented by one or two copies of a conditionally silent
alleles were noviembre de 2011 endothelial cells and in the brain parenchyma in Pdgfbret/ret and
84. LETTER
46
doi:10.1038/nature09522
Pericytes regulate the blood–brain barrier
Annika Armulik1, Guillem Genove1, Maarja Mae1, Maya H. Nisancioglu1, Elisabet Wallgard1{, Colin Niaudet1, Liqun He1{,
´ ¨
Jenny Norlin1, Per Lindblom2, Karin Strittmatter1{, Bengt R. Johansson3 & Christer Betsholtz1
The blood–brain barrier (BBB) consists of specific physical barriers, (Fig. 1g, h, j and Supplementary Fig. 5a–c). Similarly, the fluorescent
enzymes and transporters, which together maintain the necessary dye cadaverine Alexa Fluor-555 accumulated significantly in the brain
extracellular environment of the central nervous system (CNS)1. parenchyma of Pdgfbret/ret and R26P1/0 mice (Fig. 1j and Supplemen-
The main physical barrier is found in the CNS endothelial cell, tary Fig. 5d, h, i). Additionally, fluorescently labelled albumin, 70 kDa
and depends on continuous complexes of tight junctions combined dextran and IgG passed the BBB in Pdgfbret/ret and R26P1/0 mice, but not
Su deficit incrementa permeabilidad agua y otras moléculas
with reduced vesicular transport2. Other possible constituents of the
BBB include extracellular matrix, astrocytes and pericytes3, but the
in controls or in R26P1/1 mice (Fig. 1j and Supplementary Fig. 5e–g).
These experiments establish a close correlation between pericyte density
mediante transcitosis
relative contribution of these different components to the BBB
remains largely unknown1,3. Here we demonstrate a direct role of
and permeability across the BBB for a range of tracers of different
molecular masses (Supplementary Table 1).
pericytes at the BBB in vivo. Using a set of adult viable pericyte- Permeability in CNS vessels is impeded by continuous complexes of
Regula la expresión génica de genes endoteliales de BHE
deficient mouse mutants we show that pericyte deficiency increases
the permeability of the BBB to water and a range of low-molecular-
endothelial junctions13,14. We studied such complexes in adult pericyte-
deficient mutants using markers for adherens (VE-cadherin) and tight
mass and high-molecular-mass tracers. The increased permeability (ZO-1 and claudin 5) junctions. Pdgfbret/ret, R26P1/0 and controls
Induce polarización de pies astrocitarios
occurs by endothelial transcytosis, a process that is rapidly arrested showed junctional marker expression at similar levels as judged by
by the drug imatinib. Furthermore, we show that pericytes function immunostaining and western blotting (Supplementary Fig. 6a–c and
at the BBB in at least two ways: by regulating BBB-specific gene data not shown). The junctional markers were distributed in a pattern
expression patterns in endothelial cells, and by inducing polariza- consistent with continuous junction complexes in both mutants and
Participación en inducción y maduración de la BHE
tion of astrocyte end-feet surrounding CNS blood vessels. Our
results indicate a novel and critical role for pericytes in the integ-
controls; however, mutants displayed focally increased junctional width
and undulation. These patterns were confirmed by transmission elec-
regulando la relación astrocito-endotelio
ration of endothelial and astrocyte functions at the neurovascular
unit, and in the regulation of the BBB.
tron microscopy, which failed to reveal any apparent abnormalities in
the ultrastructure of endothelial junctions, with the exception that
Platelet-derived growth factor (PDGF)-B/PDGF receptor-b (PDGFR- longer and irregular stretches of endothelial overlap were commonly
b) signalling is necessary for pericyte recruitment during angiogenesis4,5. found in pericyte-deficient mutants (Fig. 2c and Supplementary Fig. 6e).
Perinatal lethality precludes analysis of postnatal processes in Pdgfb or Because continuity, ultrastructure and marker expression were con-
Pdgfrb null mice6,7, but several other mouse mutants of this pathway are sistent with retained integrity of endothelial junctions in the absence of
viable postnatally. Two such mutants were used here: PDGF-B retention pericytes, we took advantage of the fixable nature of the fluorescent
motif knockouts (Pdgfbret/ret) where PDGF-B binding to heparan sul- tracers to explore the route of extravasation in Pdgfbret/ret and R26P1/0
phate proteoglycans was disrupted8; and mutants in which Pdgfb null mice in more detail. Cadaverine Alexa Fluor-555 accumulated in
martes 15 de complemented by one or two copies of a conditionally silent
alleles were noviembre de 2011 endothelial cells and in the brain parenchyma in Pdgfbret/ret and
100. 55
Barrera hematoencefálica
Células
martes 15 de noviembre de 2011
101. 55
Barrera hematoencefálicaS
REVIEW
Basal lamina
Neuron
Interneuron
Tight
junction Astrocyte
Tight junction
Células
Pericyte Capillary
A belt-like region of adhesion Astrocyte
Endothelial
between adjacent cells. Tight
cell
junctions regulate paracellular
flux, and contribute to the b LIF
maintenance of cell polarity by
stopping molecules from a Tight
diffusing within the plane of the TGFβ
junction
membrane.
Tight ? bFGF
GLUT1
Abluminal membrane junction
Capillary
The endothelial cell membrane ANG1
that faces away from the vessel
Capillary Endothelial
lumen, towards the brain. Microglia LAT1
cell
Meninges
Endothelial Pgp GDNF
cell
The complex arrangement of
EAAT1–3 Astrocyte
three protective membranes
surrounding the brain, with a Basal
thick outer connective tissue lamina
layer (dura) overlying the ET1 TIE2 P2Y2 5-HT
barrier layer (arachnoid), and
Figure 2 | Cellular constituents of the blood–brain barrier. The barrier is formed by capillary endothelial cells,
finally the thin layer covering
the glia limitans (pia). The sub-
surrounded by basal lamina and astrocytic perivascular endfeet. Astrocytes provide the cellular link to the neurons.
arachnoid layer has a sponge-
The figure also shows pericytes and microglial cells. a | Brain endothelial cell features observed in cell culture. The
like structure filled with CSF.
martes 15 de noviembre cells express a number of transporters and receptors, some of which are shown. EAAT1–3, excitatory amino acid
de 2011
102. 56
Regulación de la permeabilidad
vascular
martes 15 de noviembre de 2011
103. 56
Regulación de la permeabilidad
vascular
martes 15 de noviembre de 2011
104. 57
Unidad neurogliovascular
euron
Review
ure 4. Schematic of the Neurovascular Unit
Endothelial cells and pericytes are separated by the basement membrane. Pericyte processes sheathe most of the outer side of the basement membr
nts of contact, pericytes communicate directly with endothelial cells through the synapse-like peg-socket contacts. Astrocytic endfoot processes uns
microvessel wall, which is made up of endothelial cells and pericytes. Resting microglia have a ‘‘ramified’’ shape. In cases of neuronal disorders th
imary vascular origin, circulating neurotoxins may cross the BBB to reach their neuronal targets, or proinflammatory signals from the vascular cells or r
illary blood flow may disrupt normal synaptic transmission and trigger neuronal injury (arrow 1). Microglia recruited from the blood or within the brain
martes 15 de noviembre de 2011
105. 58
Red capilar
martes 15 de noviembre de 2011
106. 58
Red capilar
martes 15 de noviembre de 2011
107. Desarrollo vascular
Extracraneal
Intracraneal
Troncos perpendiculares
Arborización
martes 15 de noviembre de 2011
125. Angio(glio?)neurins
“Angioneurins can be broadly defined as
molecules that affect both neural and
vascular cell functions; these effects might
include, but are not restricted to, the
regulation of angiogenesis, blood–brain
barrier (BBB) integrity, vascular perfusion,
neuroprotection, neuroregeneration and
synaptic plasticity”
Zacchigna et al., Nature Reviews Neuroscience. 2008
martes 15 de noviembre de 2011
127. VEGF
Vascular Endothelial Growth Factor
I. Inductor de:
• Proliferación endotelial
• Migración endotelial
• Inhibición apotosis
II. Efectos neurotróficos
y neuroprotectores
III. Permeabilidad
vascular
martes 15 de noviembre de 2011
128. VEGF
Vascular Endothelial Growth Factor
martes 15 de noviembre de 2011
129. VEGF
Vascular Endothelial Growth Factor
martes 15 de noviembre de 2011
144. Mechanism of BOLD Functional MRI
Brain activity
Oxygen consumption Cerebral blood flow
Oxyhemoglobin
Deoxyhemoglobin
Magnetic susceptibility
T2*
MRI signal intesity
martes 15 de noviembre de 2011
145. Oxyhemoglobin and
Deoxyhemoglobin in Veins during
Brain Activation
Rest Activation
Normal blood flow High blood flow
Oxyhemoglobin
Deoxyhemoglobin
martes 15 de noviembre de 2011
146. Signal Intensity
Time Series and Activation Maps
Off On Off On Off On Off On
Scan Number
martes 15 de noviembre de 2011
151. martes 15 de noviembre de 2011
All images courtesy of Johann Wolfgang G oethe University Hospital,
152. BOLD MRI MAPP
BrainLA B is the o
of B O LD MRI func
imaging (DTI) for u
integration of both
tion not only abou
white matter struc
The result is a com
completely new in
ning that sets the
MORE COMPRE
MRI DATA
West Virginia Universi
A. Puce, PhD, Profess
Center for Advanced I
W. Boling, MD, Neuros
M. Parson, PhD, Depa
Functional MRI pl
cedures in or nea
imaging based on
martes 15 de noviembre de 2011
153. Neural correlates of admiration and compassion.
Immordino-Yang MH, McColl A, Damasio H, Damasio A. Proc Natl Acad Sci U S A. 2009 May 12;106
(19):8021-6.
martes 15 de noviembre de 2011
