Basic sketch of brain areas involved in language. Author: Reid Offringa creation date: 1/9/06
precentral gyrus. Primary motor cortex. Brodmann area 4
Author: Paul Wicks Source: My head! MRI Obtained in a 1.5T GE Scanner in 2003 Region highlighted = approximate location of the orbitofrontal cortex
Human brain view on transverse temporal and insular gyri
Doctor w:Oliver Sacks.
Doctor Oliver Sacks at TED 2009.
Neurologist and writer Oliver Sacks at the 2009 Brooklyn Book Festival.
The en:Nobel Prize diploma of en:Otto Loewi, displayed in the en:Royal Society, en:London. Copyright В© 2004 Kaihsu Tai.
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Emil Kraeelin
Frontispiece in the original 1909 edition of Brodmann's book
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Eric R. Kandel (left), director of the Center for Neurobiology and Behavior at Columbia University, is standing with Donald S. Fredrickson (right), director of the National Institutes of Health (NIH), at Eric Kandel's NIH lecture on cellular insights into behavior and learning
Eric Kandel, Austrian psychologist and neuroscientist
Donald Glaser
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diagram about Tononi's information integration theory of consciousness.
diagram about Tononi's information integration theory of consciousness.
diagram about Tononi's information integration theory of consciousness.
diagram about Tononi's information integration theory of consciousness.
diagram about Tononi's information integration theory of consciousness.
Giulio Tononi, M.D., Ph.D., is neuroscientist. He is a professor in the Department of Psychiatry at the University of Wisconsin-Madison Medical School.
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The en:Nobel Prize diploma of en:Henry Hallett Dale, awarded in 1936 and displayed in the en:Royal Society, en:London. Copyright 2004 Kaihsu Tai.
Maclyn McCarty (June 9, 1911, to January 2, 2005) with Francis Crick and James D. Watson
Panel discussion
Patricia Churchland on NIH's STEP(The staff training in extramural programs) program 2005.
Patricia Churchland on NIH's STEP(The staff training in extramural programs) program 2005.
Paul Broca, scientist
Patrick Aebischer
Patrick Aebischer
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Das Wirkungsprinzip der Farbwahrnehmung - Das Grundgesetz der Farbenlehre
Scheme of blood-brain barrier
Transmission electron microscope image of a thin section cut through the developing brain tissue (telencephalic hemisphere) of an 11.5 day mouse embryo. This image of the luminal surface of the telencephalon, shows junctional complexes and pinocytotic vesicles. The junctional complex is divided into three types of junctions: 1) the most apical is the tight junction, which controls and/or restricts the movement of molecules across epithelial layers and helps maintain polarity, 2) the zonula adherens, which also includes the numerous actin filaments seen in the apical cytoplasm, and 3) the desmosome, which is a spot junction. The pinocytotic vesicles are formed from coated pits in the plasma membrane and are involved in endocytosis.
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Charles Smart Roy and Charles Scott Sherrington (right), at the door of the Old Pathological Laboratory, Cambridge, 1893
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Patricia Goldman-Rakic
Wolf Singer auf dem 17. Göttinger Literaturherbst.
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Vilayanur S. Ramachandran. Neurologist best known for his work in the fields of behavioral neurology and psychophysics. ヴィラヤヌル・S・ラマチャンドラン。インド出身のアメリカの神経科医、心理学・神経科学者。
Theodore
Solomon H. Snyder, American neuroscientist
Paul Greengard
Paul D. MacLean, American physician and neuroscientist
Michael T. Ullman (photo)
Photo of Daniel Levitin, 2006
Photos of Jean-Pierre Changeux
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Ernst von Fleischl-Marxow (1846-1891), Austrian physiologist Fleischl-Marxow, Ernst von
Александр Станиславович Догель (1852-1922) Polski Aleksander Stanisławowicz Dogel (1852-1922) English Alexander Stanislavovich Dogel (1852-1922)
This licensing tag was added to this file as part of the GFDL licensing update.
Neuroscientist David Eagleman
Placa que se encuentra en el frente de la casa donde viviГі RamГіn Carrillo en BelГ©m do ParГЎ
en:Vladimir Alekseyevich Betz source: http://klymenko.data-tec.net/Kyiv/Kyiv.Vydubytchi/IMG_2819.htm Image courtesy Sergiy Klymenko, klymenko.data-tec.net en:Category:Images of Ukraine
Anirvan Ghosh at the Duke University campus in Durham NC in 2007
Photo
From left to right, Jon Meacham of Newsweek (moderator), Marc Hauser, Daniel Dennett, Antonio Damasio, and Patricia Churchland.
w:Picower Institute for Learning and Memory at MIT
Diagram of processes which are a part of the resting state of a neuron.
Trailer housing Varian 4T fMRI at the University of California. The bent overhang, tiles on the walls, and bent chain-link fence were placed in jest to simulate the power of the magnet housed inside. Category:Neuroscience Category:Neuroimaging Category:University of California
Life Sciences Addition building at the University of California. Category:University of California
Coronal Nissl-counterstained sections of the rat brain showing anterograde labeling after a biotinylated dextran-amine injection into the posterolateral cortical amygdaloid nucleus. The Islands of Calleja are visualized under IC abbreviation.
Helen Wills Neuroscience Institute located within Barker Hall at the University of California. Category:University of California
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no original description
Head shot of Dr Peter John Snow
shows electrode location, names, and numbers of the custom 32-electrode cap used in the Neurocognition Lab at Tufts University.
100x light micrograph of Meissner's corpulsce at the tip of a dermal papillus
Ultra-structural analysis of synapses in the brainstem of wild-type (WT) and transforming growth factor (TGF)-β2 knock-out (KO) mice at embryonic day 18.5. Synapses of WT and TGF-β2 KO neurons in the pre-Bötzinger-complex area exhibit presynaptic vesicles (asterisks), a synaptic cleft and a distinct postsynaptic density (arrowheads). Scale bar, 250 nm. Heupel et al. Neural Development 2008 3:25 doi:10.1186/1749-8104-3-25
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Three-dimensional representations of DA modulatory landscapes with (B) and without (A, C, and D) chandelier cells. The strength of the inhibition by other GABAergic interneurons are also varied (A: 1.0, B: 1.0, C: 0.95, and D: 1.06). Note that the onset of the H mode is very quick (less than 100 ms), whereas the inverted-U mode profiles are very slow to evolve. Even at t = 1000 ms, the profiles of the inverted-U mode have not reached the equilibrium states. The profiles at equilibrium are shown in Figure 3.Tanaka BMC Neuroscience 2008 9:41 doi:10.1186/1471-2202-9-41
Summary of the pathways in motor neurons implicated in mediating a BC cell derived repellent signal that stops somal migration. Boundary cap cells (yellow) located at the MEP express repellent signals (red) that act either directly on motor neuron cell bodies or retrogradely via their axons to disengage somal migration from axon extension. Our data suggest that these signals comprise a combination of class 3 semaphorins and Sema6A (red). Plexin-A2 (purple) expressed by the motor neurons can function as a dual receptor for class 3 and class 6 semaphorins, the former in conjunction with Npn-2 (blue). In this scheme, MICAL3 (green), by linking Plexin-A to the cytoskeleton, is a key downstream mediator of the somal stabilising signal. As a result of cytoskeletal re-organisation, the force (green arrow) exerted from the axonal growth cone that leads to somal translocation in migrating neurons is disrupted. Bron et al. Neural Development 2007 2:21 doi:10.1186/1749-8104-2-21
wristwatch computer from http://wearcam.org/wristcam/dusting/
Stanislas Dehaene, Toward a Science of Consciousness conference, Tucson, Arizona.
EPSP spatial and temporal summation
Slc1a3 gene expressed in the Bergmann glia of the cerebellum of a mice aged 7 days; saggital section. The Gene Expression Nervous System Atlas (GENSAT) Project, NINDS Contract # N01NS02331 to The Rockefeller University (New York, NY)
Skinner box for rat
Examples of CNS Functional Measures. A. Schematic of cortical areas involved with pain processing. The highlighted areas summarize areas found active in previous functional imaging studies. Color-coding reflects the hypothesized role of each area in processing the different psychological dimensions of pain. Numbers in parentheses indicate the relative involvement of these areas during different temporal stages of the pain experience. Areas displayed include insula, anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), primary somatosensory cortex (SI), secondary somatosensory cortex (SII), inferior parietal lobe (Inf. Par), dorsolateral prefrontal cortex (DLPFC), pre-motor cortex (Pre-Mot), orbitofrontal cortex (OFC), medial prefrontal cortex (Med. PFC), posterior insula (P. Ins), anterior insula (A. Ins), hippocampus (Hip), entorhinal cortex (Ento). [Reprinted with permission from Casey and Tran, 2006]. For examples of brainstem involvement in pain processing, please refer to Tracey and Iannetti ([52]). B. Example of fMRI responses to painful phasic thermal stimulation to the forehead in a cohort of 12 subjects. (Moulton et al., unpublished observations). Borsook et al. Molecular Pain 2007 3:25 doi:10.1186/1744-8069-3-25
Schematic drawing of cellular regulation of extracellular glutamate concentrations ([Glu]ec) in normal brain function (left), and in the presence of the proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 (right). Possible pathophysiology underlying mental fatigue at the cellular level is outlined below. To the left: Two neuronal cell bodies with processes (white) make contact with each other through a synapse (center). Astrocytic (pink) processes encapsulate the synapse and cover also the abluminal side of the blood vessel wall (right). The endothelial cells covering the luminal (blood) side of the vessel wall and the astrocytic processes make up the blood brain barrier (BBB). An oligodendroglial cell (bluish), with its myelin encapsulating the axon, and a microglial cell (yellow) are seen. The astrocytes, with their high-affinity glutamate transporters, are the main site for keeping [Glu]ec low. Even neurons express glutamate transporters, as do oligodendroglial cells, and endothelial cells at their abluminal side. To the right: TNF-α, IL-1β and IL-6 attenuate astroglial glutamate uptake transport and disintegrate the BBB, allowing glutamate from the blood to enter the brain. The overall result is slightly increased [Glu]ec. Tumor necrosis factor-alfa also decreases oligodendroglial cell glutamate uptake [78], while microglial glutamate uptake has been demonstrated to increase (Persson, M., Hansson, E., and Rönnbäck, L, to be published), though not to levels to compensate for the decreased astroglial glutamate uptake capacity. Due to increased [Glu]ec, astroglial swelling is shown. Below: Hypothetic cellular events underlying mental fatigue. Slightly increased [Glu]ec could make the glutamate neurotransmission less distinct (decrease the signal-to-noise ratio). At the cellular level, there would be astroglial swelling, which in turn would decrease the local extracellular (ec) volume and, as a consequence, lead to further increased [Glu]ec. Astroglial swelling also depolarizes the astroglial cell membrane, which further attenuates the electrogenic glutamate uptake and, in addition, the astroglial K+ uptake capacity. As a consequence, even [K+]ec may rise. The increased [K+]ec, together with decreased glutamine production and reduced glucose uptake concomitant with the decreased glutamate uptake, could lead to decreased presynaptic glutamate release and thereby decreased glutamate transmission, which, according to our hypothesis, is one cellular correlate to mental fatigue/exhaustion. Increased extracellular glutamate levels in the prefrontal region could lead to inhibition of the brain stem nuclei locus coeruleus (LC) and raphe nuclei and thereby inhibit noradrenaline (NA) and serotonin (5-HT) release in the cerebral cortex resulting in decreased astroglial metabolism and neuronal metabolic supply. Increased neuronal excitability may be part of the loudness and light sensitivity often accompanying the mental fatigue. In addition, the decrease in noradrenaline and serotonin release might be part of decreased attention and the appearance of depression often accompanying the mental fatigue. Rönnbäck and Hansson Journal of Neuroinflammation 2004 1:22 doi:10.1186/1742-2094-1-22
Schematic Examples of CNS Structural Changes. Red circles signify decreased gray matter density relative to controls. A. Subjects with chronic back pain show decreases in gray matter density in bilateral dorsolateral prefrontal cortex (DLPFC) and right anterior thalamus (adapted from [25]). B. Patients with fibromyalgia show decreases in cingulate cortex (CC), medial prefrontal cortex (Med. PFC), parahippocampal gyrus (PHG) and insula (adapted from [27]). 3-D surface renderings were created using Freesurfer. Borsook et al. Molecular Pain 2007 3:25 doi:10.1186/1744-8069-3-25
In case this is not legally possible: Ceccomaster grants anyone the right to use this work for any purpose, without any conditions, unless such conditions are required by law.
(a) Head of a mouse showing the location of the brain and the rostral migratory stream, RMS, (in red) along which newly generated neuroblasts migrate from the SVZ of the lateral ventricle into the olfactory bulb (OB). (b) The migration of newly generated neuroblasts begins at the lateral ventricle, continues along the RMS and terminated in the OB, where mature interneuron populations are generated. (c) Schematic based on electron microscopy showing the cytoarchitecture of the SVZ along the ventricle. Ependymal cells (gray) form a monolayer along the ventricle with astrocytes (green), neuroblasts (red) and transitory amplifying progenitors (TAP) (purple) comprising the SVZ. (d) Schematic showing the migration of neuroblasts along the RMS. Astrocytes (green) ensheath the migrating neuroblasts (red) and are thought to restrict and contain the neuroblasts to their specific pathway. (e) Migrating neuroblasts enter the OB, migrate radially and give rise to granule or periglomerular cells. Lennington et al. Reproductive Biology and Endocrinology 2003 1:99 doi:10.1186/1477-7827-1-99
Repetitive transcranial magnetic stimulation (rTMS) is a technique for noninvasive stimulation of the adult brain. Stimulation is produced by generating a brief, high-intensity magnetic field by passing a brief electric current through a magnetic coil. Compared with the growing number of clinical trial with rTMS, there are surprisingly few animal studies on its basic mechanisms of action, constraining the ability to perform hypothesis-driven clinical studies. Arias-Carrión International Archives of Medicine 2008 1:2 doi:10.1186/1755-7682-1-2
Reelin-induced radial glial phenotype is dependent on γ-secretase activity. HNPCs were deprived of FGF and EGF for 24 hours prior to their transfection or treatment. a, g, HNPCs were transfected with empty vector or d, j NICD for 24 hours before fixation. The percentage of the BLBP-positive radial glia increased from 2.3% in the empty vector transfected cells to 6.2% in the NICD transfected cells, *p-value = 0.05. b, h, HNPCs were treated with partially purified control or c, i, partially purified Reelin for 24 hours before fixation. The percentage of the BLBP-positive radial glia increased from 3.4 % in the control-treated cells to 9.5% in the Reelin-treated cells, **p-value = 0.05. e, k, f, l, 10 μM of L-685,458 was used to inhibit the activity of γ-secretase for 24 hours in the control and the Reelin treated HNPCs. γ-secretase inhibition in the Reelin treated cells abolished Reelin's effect by reducing the percentage of the BLBP-positive radial glia back to 1.6 %, ***p-value = 0.05. The results represent the standard error of the mean ± SEM of at least three independent experiments. One-way ANOVA with Tukey's post hoc test for individual treatment differences was used for statistical analysis. Values that are significantly different from each other according to Tukey's test are indicated by asterisks. Scale bar for a-f is 100 μm and for g-l is 50 μm. Keilani and Sugaya BMC Developmental Biology 2008 8:69 doi:10.1186/1471-213X-8-69
Reelin treatment in vitro induces a radial glial phenotype similar to Notch-1 activation. A, HNPCs were deprived of FGF and EGF for 24 hours prior to their transfection or treatment. a, HNPCs were transfected with empty vector or b NICD for 24 hours before fixation. c, HNPCs were treated with control or d, partially purified Reelin for 24 hours before fixation. The cells were later stained against GFAP. Scale bar 200 μm. B, Control and Reelin conditioned-medium were collected from HEK293 cells transfected with either control empty vector or Reelin, respectively. Reelin was partially purified (P.P) from the medium by column centrifugation and its expression was verified by western blotting using anti-reelin clone G10. C, Reelin treatment of HNPCs in vitro (1:40) induced Reelin signaling by increasing Dab-1 phosphorylation on tyrosine residue 198. Keilani and Sugaya BMC Developmental Biology 2008 8:69 doi:10.1186/1471-213X-8-69
Reelin induces GFAP and FABP7 via Notch1. Part of an image from the Commons. From the article by Keilani and Sugaya, BMC Developmental Biology 2008 8:69 doi:10.1186/1471-213X-8-69
Activity of a grid cell in rat hippocampus
Pictomicrograph shows the “barrel field” in layer IV of the rat somatosensory cortex. Each “barrel” receives input from one whisker. The tissue in the image has been stained with cytochrome oxidase and is 50μm thick.
Phenotypes of proliferating cells in the RMS and DG. Double-labeled immunofluoresence studies showed that in the RMS most cells were BrdU+/nestin+ (arrow, a) and revealed the presence of GFAP+ filaments (arrow, b) surrounding BrdU+ cells (asterisk, b). In the DG, BrdU+/nestin+ cells (c) were seen and a few BrdU+/GFAP+ cells could also be found (arrow, d, e). BrdU (red); nestin, GFAP (green). Faiz et al. BMC Neuroscience 2005 6:26 doi:10.1186/1471-2202-6-26
Ultra-structural analysis of synapses in the brainstem of wild-type (WT)mice at embryonic day 18.5. Synapses of WT neurons in the pre-Bötzinger-complex area exhibit presynaptic vesicles (asterisks), a synaptic cleft and a distinct postsynaptic density (arrowheads). Scale bar, 250 nm. Heupel et al. Neural Development 2008 3:25 doi:10.1186/1749-8104-3-25
An increase of Reelin-positive cells changes morphology of migrating neurons.
Phenotypes of proliferating cells in the RMS and DG. Double-labeled immunofluoresence studies showed that in the RMS most cells were BrdU+/nestin+ (arrow, a) and revealed the presence of GFAP+ filaments (arrow, b) surrounding BrdU+ cells (asterisk, b). In the DG, BrdU+/nestin+ cells (c) were seen and a few BrdU+/GFAP+ cells could also be found (arrow, d, e). BrdU (red); nestin, GFAP (green). Faiz et al. BMC Neuroscience 2005 6:26 doi:10.1186/1471-2202-6-26
écriture avec le crayon orienté plus haut que la ligne d'écriture
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principle of patch clump
scanning electron microscope image of planar patch chip (Author: N. Fertig)
Crystal structure of the third repeat domain of reelin protein
Neurotrophin immunopositivity in the nondegenerate and degenerate intervertebral disc. Histograms illustrating the percentage of (a) positive nerve growth factor (NGF) cells and (b) brain-derived neurotrophic factor (BDNF) immunopositive cells in the nucleus pulposus (NP), inner annulus fibrosus (IAF) and outer annulus fibrosus (OAF) regions of nondegenerate, moderately degenerate and severely degenerate intervertebral disc (IVD) tissue. *Significance between disease states, **significance between regions of the IVD (P < 0.05). Data presented as the mean ± standard error of the mean. Purmessur et al. Arthritis Research & Therapy 2008 10:R99 doi:10.1186/ar2487
Neuropilin-2 (Nrp2) expression in normal breast and breast carcinoma tissue. (A) Nrp2 staining was observed in blood or lymph vessels. There was no staining in normal breast epithelium. (×100). (B) In cancer tissue, staining of the Nrp2 protein was identified not only in the vascular endothelial cells, but also in the cytoplasm of cancer cells. Almost all invasive cells were immunopositive for Nrp2. (×200). (C-D) Co-localized expression of Nrp2 (C) and CXCR4 (D) using serial sections of breast carcinoma tissue. (×100). Yasuoka et al. BMC Cancer 2009 9:220 doi:10.1186/1471-2407-9-220
Neurons used for studies on neuronal growth at different stages of Drosophila development. (a,c) Horizontal views of a Drosophila larva and adult fly, respectively, illustrating the position of the CNS (grey and cream) in relation to other body structures. (b,d) Three-dimensional extracts from the areas boxed in dark blue in (a,c), respectively. The cell body area of the CNS (cortex (CX)) is shown in light grey, and the neuritic/synaptic area (neuropile (NP)) in cream (only relevant neuropile structures are shown in (b,d)). Black arrows point anterior, morphological structures are annotated in colour code, and neuronal classes are explained in the box at bottom right. The various model neurons are marked with numbers in yellow circles, explained below. Many neurons of the larval trunk can be studied from their birth in the embryo through to the mature synaptic stage. Amongst these, motorneurons (1) project towards the dorsal zone of ipsilateral or ipsi- and contralateral connectives (where they form dendrites; double chevron), from where they enter specific branches of peripheral nerves leading towards their target muscles, on which they form neuromuscular junctions (NMJ; yellow circles represent chemical synapses). Projections of larval interneurons (2) are restricted to the neuropile. Sensory neurons of the trunk (3) project along tracheal branches and motoraxons towards the ventral nerve cord (vNC) where they innervate the ventral domain of connectives [192,195,196,198-200,236]. Sensory neurons in the embryonic trunk have been used, for example, to study the actin-microtubule linker molecule Short stop, signalling through Robo or Notch receptors, or the spatial arrangement of axons in the neuropile [197,202,203,255]. Projections of neurons 1, 2 and 3 in the neuropile of the ventral nerve cord can be classified with respect to their anteroposterior extension within the segment (white curved arrow) or across segments (black curved arrow), their dorsoventral and mediolateral position in connectives (green and red double arrows, respectively), their ipsilateral (neuron 3) versus contralateral (neurons 1 and 2) nature, and their projection through anterior (white arrowhead) versus posterior commissure (black arrowhead; see details in 'Signalling mechanisms involved in axonal pathfinding in Drosophila' above). In the embryonic/larval head region (4), the Bolwig organ has been used for studies of neuronal growth. It contains somata of 12 photoreceptor cells [306], the axons of which form the Bolwig nerve projecting over the antennal and eye discs via the optic stalk into the optic lobe anlage (OLA) [26,307]. The Bolwig nerve is joined by successively outgrowing waves of axons of photoreceptor neurons (5), which are specified in the eye disc during larval and pupal stages. The optic lobe pioneer neuron (6), a projection neuron of embryonic origin, seems to be used as a guide within the OLA by the Bolwig nerve and photoreceptor axons [308,309]. Sensory neurons of the adult trunk (7) develop de novo during larval and pupal stages (with a few exceptions) [310] and terminate in the vNC neuropile (T1-3 and A indicate the three thoracic and fused abdominal segments). They can be analysed from the time of birth through to the fully differentiated stage [311,312], and have been used to study features, such as segment-specific growth regulation (homeotic genes), or the influence of adhesive interactions (Dscam), axonal transport (cut up, the dynein light chain) or of size alterations (gigas) on neuronal growth behaviour [311,313-315]. Photoreceptor cells in the adult compound eye (8) form a precise retinotopic map in the optic lobe (OL: grey 1, lamina; 2, medulla; 3, lobula; 4, lobula plate) established during larval (see neuron 5) and pupal stages, and the genetic mechanisms regulating these precise growth decisions are beginning to be unravelled [316-318]. Interneurons postsynaptic to photoreceptor neurons are well described [317,319] but seem not to have been used for studies of growth mechanisms so far, with the exception of a group of 20–30 dorsal cluster neurons (9; targeted by atoGal4-14A), which form dendrites in the ipsilateral optic lobe and project through the dorsal commissure to innervate the contralateral lobula and medulla [320-322]. Olfactory neurons in the third antennal segment (10) and the maxillary palp (not shown) project from the antenna into the antennal lobe (AL) where they terminate in specific glomeruli in a reproducible pattern correlating with the class of odorant receptor they express; the genetic regulation of this growth behaviour is under investigation [39]. The major output from the AL is constituted by projection neurons (11), which are postsynaptic to olfactory neurons and innervate the lateral horn (red double chevron) and the calyx (blue double chevron), a dorsal structure of the mushroom bodies (MB) [39]. The mushroom bodies are the brain structures responsible for olfactory learning in Drosophila [323,324], and its intrinsic interneurons (Kenyon cells (12)) project through the calyx and pedunculus where many of them bifurcate to project into the vertical α/α'-and the horizontal β/β'/γ-lobes, simultaneously [325]. The large giant fibre neuron (13) connects the optic system via a large diameter axon with motorneurons in the second thoracic segment (14), innervating the tergotrochanteral muscle (TTM; responsible for the visually induced jump escape response) via chemical and electrical (orange triangle) synapses [326]. Giant fibre axons grow out during late larval/pupal stages and have been used to study growth regulatory mechanism, such as the influence of Rho-like GTPases or the role of the E2 ubiquitin ligase Bendless [326]. Ocellar photoreceptor neurons do not send out their own axons but are connected to the brain via large interneurons, the cell bodies of which are located in the brain originally, but migrate into the periphery during pupal development (15). The pathfinding of these interneurons depends on a set of short-lived pioneer neurons that, in turn, require the extracellular matrix molecule laminin, the transmembrane receptor neurotactin and its ligand Amalgam for proper outgrowth [21,239,241]. Further potentially attractive models for studies of neuronal growth that are not shown here are auditory sensory neurons [327], and axonal fascicles in the ventral nerve cord of late Drosophila larvae representing paused interneurons of the future adult CNS (not shown) [209]. Sánchez-Soriano et al. Neural Development 2007 2:9 doi:10.1186/1749-8104-2-9
Neurobionics illustrating picture
Na-K exchange pump
showing equilibrium state of Na+ ion
NOGO-A expression during cell migration. A) H&E staining of optic tectum at HH30(E7) showing the generative zone (GZ), the migrating zone (MZ) and the first neuronal lamina (L1). B) Section in situ hybridization (sISH) of NOGO-A in an adjacent section demonstrating a corresponding radial pattern of expression in the region of migration. High magnification of the MZ (from boxed region in
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Reconstruction of a biocytin-filled chandelier cell from a mouse neocortical brain slice. Soma and dendrites labeled in blue, axon arbor in red. Chandelier cells have characteristic terminal portions of their axon, which form short vertical rows of boutons resembling candlesticks. Each candlestick innervates a single axon initial segment of a pyramidal cell. PLoS Biol. 2008 September; 6(9): e243. Published online 2008 September 23. doi: 10.1371/journal.pbio.0060243.
MIT Media Lab entrance
Metabolic interactions between astrocytes and neurons with major reactions. Thick arrows show uptake and release reactions. Dashed arrows indicate shuttle of metabolites between two cell types. Glutamate and α-ketoglutarate in transamination reactions are abbreviated as GLU and AKG, respectively. All reactions considered in the modeling are given in additional file 1. The reaction numbers in the figure refer to the numbering in the reaction list of additional file 1. Here we only depict major reactions for simplicity. Çakιr et al. Theoretical Biology and Medical Modelling 2007 4:48 doi:10.1186/1742-4682-4-48
Low Ca2+ buffering and excitotoxicity under physiological stress and pathophysiological conditions in motor neuron (MNs). Low Ca2+ buffering in amyotrophic lateral sclerosis (ALS) vulnerable hypoglossal MNs exposes mitochondria to higher Ca2+ loads compared to highly buffered cells. Under normal physiological conditions, the neurotransmitter opens glutamate, NMDA and AMPA receptor channels, and voltage dependent Ca2+ channels (VDCC) with high glutamate release, which is taken up again by EAAT1 and EAAT2. This results in a small rise in intracellular calcium that can be buffered in the cell. In ALS, a disorder in the glutamate receptor channels leads to high calcium conductivity, resulting in high Ca2+ loads and increased risk for mitochondrial damage. This triggers the mitochondrial production of reactive oxygen species (ROS), which then inhibit glial EAAT2 function. This leads to further increases in the glutamate concentration at the synapse and further rises in postsynaptic calcium levels, contributing to the selective vulnerability of MNs in ALS. Jaiswal et al. BMC Neuroscience 2009 10:64 doi:10.1186/1471-2202-10-64
Laser capture microdissection of four cell populations from the embryonic E15 mouse brain. a. Subplate (SP) and lower cortical plate (CP) from anterior and posterior cortex are isolated from 20 μm cryosection using a PALM Microbeam. b. Microdissected tissue strips are harvested in RNA stabilization solution and can be visualized in the cap of the collection tube. Scalebars: a. 500 μm. b. 200 μm. Wang et al. BMC Molecular Biology 2009 10:69 doi:10.1186/1471-2199-10-6
Comparison of four staining methods. Images were taken directly on the PALM Microbeam to demonstrate the staining and image quality available to identify the different cell populations. a. Hematoxylin. b. Hematoxylin and Eosin. c. 0.1% cresyl violet in H2O. d. 1% cresyl violet in H2O. For hematoxylin and H&E staining (a, b), sections were rinsed with 70% EtOH and H2O, stained with Mayer's hematoxylin for 15 sec, rinsed with H2O and 70% EtOH and stained with Accustain Eosin Y for 10 sec (for H&E only). For cresyl violet staining (c, d), sections were rehydrated in decreasing concentrations of ethanol, stained in cresyl violet for 45 sec and dehydrated in increasing concentrations of ethanol. 1% cresyl violet (d) provided the best morphological details and allowed clear distinction between cortical plate and subplate. e&f. Localization of the subplate at E15. Depth and width of the subplate layer on cresyl violet stained sections (e) were confirmed with immunohistochemistry against Nurr1 (f). Scalebars: 100 μm. MZ = marginal zone, CP = cortical plate, SP = subplate, IZ = intermediate zone, SVZ = subventricular zone, VZ = ventricular zone. Wang et al. BMC Molecular Biology 2009 10:69 doi:10.1186/1471-2199-10-69
This is the PSMBF sub-field of the “barrel field” in the rat somatosensory cortex. Each “barrel” received input from one major whisker on the snout of the rat. The tissue in the image has been stained with cytochrome oxidase and is 50μm thick. Layer IV. White circles are empty areas left by emptied blood vessels. Barrels have been labeled to match with their correspondent vibrissa. (Cartoon of vibrissa not shown.)
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showing equilibrium state of K+ ion
Neural progenitor cells (small-size jpg version of Journal.pone.0001604.g001.png) : After forming a neurosphere, embryonic neural progenitor cells spread out into a monolayer. A. Neurosphere consisting of SVZ cells isolated at E15 that have aggregated in suspension after 2 days in culture. Scale bar: 100 µm. B. Neurosphere of SVZ cells derived at E15 that has attached to the floor of the culture flask after 4 days in culture. Note cells migrating away from the neurosphere. Scale bar: 100 µm. C. Cells at the periphery of neurospheres were chosen for electrophysiological recording. Most of the recorded cells extended processes. Arrows indicate the location of recording (left) and puffer (right) pipettes. Scale bar: 20 µm.
Jeffress model of Delay Lines with coincidence detectors
Figure 2 Hypothesized Propagation of Activity in Human Neocortex An action potential in a pyramidal neuron (cell 1) elicits a spike in a chandelier cell (2) via a strong connection, in turn evoking a third-order spike in a downstream pyramidal cell (3). This spike results in a trisynaptic EPSP being recorded in a postsynaptic pyramidal cell (cell 4, event A). At the same time, cell 3 drives both a basket cell (5) and chandelier cell (6) to threshold. The basket cell evokes a hyperpolarizing IPSP on the postsynaptically recorded pyramidal cell (cell 4, event B), four synapses removed from the original spike. The spiking chandelier cell (6) triggers yet another pyramidal neuron to fire (7), which produces an EPSP on the recorded neuron (cell 4, event C), five synapses away from the original spike. The result seen in the postsynaptic pyramidal neuron (cell 4) is a delayed EPSP-IPSP-EPSP sequence (events A, B, and C), traveling through three, four, and five synapses respectively. Molnár et al. propose that polysynaptic pathways similar to this one can be activated by a single action potential in a cortical pyramidal cell.
A) H&E staining of chicken optic tectum at HH30(E7) showing the generative zone (GZ), the migrating zone (MZ) and the first neuronal lamina (L1). Scale bar 200 μm in A, B; 50 μm in C, D, E, F. Caltharp et al. BMC Developmental Biology 2007 7:32 doi:10.1186/1471-213X-7-32
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Glial distribution of Cu/Zn SOD immunoreactivity in intact immature brain. Cu/Zn SOD was not observed in the GFAP-expressing astrocyte population of the brain parenchyma (A: cortex, confocal image). However, GFAP-expressing astrocytes showed co-localization with Cu/Zn SOD in the glia limitans (C, confocal image) and in the ventricle walls (B: third ventricle; arrow: tanycyte). Microglial cells and endothelium (arrow), identified with tomato lectin histochemistry, were negative for Cu/Zn SOD (D: cortex; confocal image). Scale bars in A: 40 μm; in B, C and D: 20 μm. Peluffo et al. Journal of Neuroinflammation 2005 2:12 doi:10.1186/1742-2094-2-12
Glial distribution of Cu/Zn SOD immunoreactivity in intact immature brain. Cu/Zn SOD was not observed in the GFAP-expressing astrocyte population of the brain parenchyma (A: cortex, confocal image). However, GFAP-expressing astrocytes showed co-localization with Cu/Zn SOD in the glia limitans (C, confocal image) and in the ventricle walls (B: third ventricle; arrow: tanycyte). Microglial cells and endothelium (arrow), identified with tomato lectin histochemistry, were negative for Cu/Zn SOD (D: cortex; confocal image). Scale bars in A: 40 μm; in B, C and D: 20 μm. Peluffo et al. Journal of Neuroinflammation 2005 2:12 doi:10.1186/1742-2094-2-12
Glial distribution of Cu/Zn SOD immunoreactivity in intact immature brain. Cu/Zn SOD was not observed in the GFAP-expressing astrocyte population of the brain parenchyma (A: cortex, confocal image). However, GFAP-expressing astrocytes showed co-localization with Cu/Zn SOD in the glia limitans (C, confocal image) and in the ventricle walls (B: third ventricle; arrow: tanycyte). Microglial cells and endothelium (arrow), identified with tomato lectin histochemistry, were negative for Cu/Zn SOD (D: cortex; confocal image). Scale bars in A: 40 μm; in B, C and D: 20 μm. Peluffo et al. Journal of Neuroinflammation 2005 2:12 doi:10.1186/1742-2094-2-12
Coronal section in the forebrain of an embryonic mouse at 12.5 days of gestation (preplate stage), showing the lateral and medial ganglionic eminences (LGE, MGE) from which GABAergic interneurons migrate to the cortical anlage (left, yellow). Glutamatergic neurons destined for the cortex are generated locally in the cortical ventricular zone and migrate radially (right, red). Courtesy of V. Pachnis.
Gad1 transcripts in the developing vibrissae. (A, B) Expression at E12.5. (A) Gad1 RNA in the supra-orbital (black arrow at top of panel), lateral nasal/maxillary (white arrow) and postoral (black arrow bottom of panel) rows of vibrissae are indicated. (B) Higher magnification view of lateral nasal/maxillary vibrissal rows. The placode corresponding to the β vibrissa follicle [29] is indicated. (C-F) Gad1 transcripts in the vibrissae at E13.5 (C, D) and E14.5 (E, F). The initial faint expression in the rhinal (white arrow) and anterior maxillary vibrissae (black arrow) at E13.5 is indicated in panel C. (G, H) Coronal sections through the snout of E12.5 embryos hybridized to the Gad1 probe prior to sectioning. Scale bar: A, C, F 750 μm; E 1.5 mm; B 450 μm; D 400 μm; G 200 μm; H 25 μm. Maddox and Condie BMC Developmental Biology 2001 1:1 doi:10.1186/1471-213X-1-1
Mode diagrams. A: Control. B: With chandelier cells. C: Weaker GABAergic interneurons other than chandelier cells. D: Stronger GABAergic interneurons other than chandelier cells. The chandelier cells are dysfunctional in A, C and D. Tanaka BMC Neuroscience 2008 9:41 doi:10.1186/1471-2202-9-41
Zelfgemaakt schema
G-CSF receptor is expressed in the embryonic nervous system. The expression shows characteristics of radial glia cells in terms of long processes and termination in end-feet. A E11 forebrain, B E12 spinal cord with dorsal root ganglion, axon root and muscle, C E14 hindbrain, D E16 spinal cord with dorsal root ganglion, E E19 spinal cord, F E19 spinal cord, G E19 hindbrain, H E21 olfactory bulb, I E21 diencephalon, (Immunohistochemical staining of 10 μm paraffin sections, scale bar = 50 μm, d: dorsal, E: embryonic day, v: ventral). Kirsch et al. BMC Developmental Biology 2008 8:32 doi:10.1186/1471-213X-8-32
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The Frontal Lobes
This licensing tag was added to this file as part of the GFDL licensing update.
This licensing tag was added to this file as part of the GFDL licensing update.
This licensing tag was added to this file as part of the GFDL licensing update.
EEG with 32 elektrodes
Research Participant with 32 electrode EEG
Comparison of standardized expression patterns. Projection view on standardized expression patterns (ok107/201y/mb247). Gal4 lines were crossed to UAS-EGFP2 for visualization, scanned with a Leica-SP1 confocal microscope (8-bit tifs) and standardized using VIBdiffusionTransformation(DT). On the left the standardized expression patterns are visualized in grey values (Nok107 = 17, N201y/mb247 = 15). On the right the same images are superimposed and color coded (ok107 red, 201y green, mb247 blue). In structures common to all three expression patterns colors add up to white (e.g. γ-lobes of the mushroom body Gal4-positiv in all lines displayed (white), α'/(β') and medial bundle Gal4-positive in ok107 only (red), besides strong Gal4 expression in the pars intercerebralis (PI) in ok107 some cell bodies are Gal4-positive as well in 201y (green)), Scale bar 100 μm Jenett et al. BMC Bioinformatics 2006 7:544 doi:10.1186/1471-2105-7-544
Drosophila growth cones and the (potential) factors regulating their cytoskeletal dynamics. (a) Growth cones of aCC (arrows) and RP2 motorneurons (double chevrons; cell bodies named) in two consecutive segments of the trunk of a Drosophila embryo, stained with a cell-specifically expressed membrane marker. (b,b') Cultured Drosophila growth cone stained for microtubules (green) and filamentous actin (magenta); some filopodia lack microtubules (curved arrows), whereas others are deeply invaded (arrow heads indicate microtubule tips). (c) Schematic representation of the cytoskeletal organisation in Drosophila growth cones as extrapolated from work on growth cones in other species (detailed in the section 'Principal structure and function of growth cones'): veil-like lamellipodia (black arrowhead) contain mesh-like networks of actin filaments (randomly oriented red lines), whereas pointed filopodia (white arrowhead) contain bundled actin filaments (parallel red lines); microtubules (blue lines) are bundled in the axon, but single splayed microtubules extend into the periphery of the growth cone (curved white arrows indicate splayed microtubule tips), reaching into filopodia, as was similarly reported for growth cones of other species or migrating cells [63,330]. (d) Details of the boxed area in (c); circled numbers correlate with the numbers in Table 1 and represent the following molecular activities: 1, actin filament nucleation by Arp2/3 (which subsequently stays with the pointed ends); 2, actin filament nucleation and elongation by formins (which stay with barbed ends); 3, actin monomer binding; 4, barbed-end capping; 5, pointed end-depolymerisation/severing; 6, actin filament bundling; 7, retrograde flow of actin cytoskeleton; 8, microtubule plus end binding; 9, microtubule stabilising; 10, actin-microtubule linkage. Black straight arrows indicate growth of actin filaments or microtubules, grey straight arrows shrinkage, black curved arrows addition of actin monomers, grey curved arrows removal of actin monomers or filamentous fragments, hatched arrows indicate direction of retrograde actin flow, and the grey dashed curved double arrow linkage of actin and microtubules. (e) Current view of the effectors downstream of the Slit receptor Robo mediating repulsion from the midline of the ventral nerve cord. Robo (top right) habours five immunoglobulin domains (half elipses) and three fibronectin type III domains (blue boxes) extracellularly, and four conserved cytoplasmic (CC) domains (light to dark green) intracellularly. Robo induces growth cone repulsion by controlling cytoskeletal dynamics via either Abelson kinase (Abl) and Enabled (Ena), or Rac activity. Ena binds at CC2 and acts most likely through Chickadee/Profilin on actin dynamics. Abl binding to Robo at CC3 influences actin dynamics via Capulet and microtubule dynamics via the +TIP protein Chromosome Bows (Chb/Orbit/MAST). Simultaneously, Abl phosphorylates CC1 to antagonise Robo function. The regulation of Rac activity through Robo occurs through CC2/3 recruitment of the SH3-SH2 adaptor molecule Dreadlocks (Dock) which, in turn, activates Rac through both Pak and the GEF Sos. In parallel, active Robo can influence Rac activity via the binding of RhoGAP93B (vilse/CrGAP) to CC2, but it remains unclear whether RhoGAP93B is positively or negatively regulated by Robo. Paradoxically, both decrease and increase of Rac activation levels can cause midline crossing, suggesting that: Rac might influence other effectors to cause repulsion; a precise Rac activation level is required to mediate Slit-induced repulsion; or a sequential modification of Rac in response to Robo activation has to occur, such as an initial role to prevent extension towards the source of the repellent and another role to encourage extension away from the Slit source. Calmodulin and GEF64C have additionally been identified as modifiers of Robo activity, although it is not clear yet how they influence Robo signalling (calmodulin possibly through Chic). Sánchez-Soriano et al. Neural Development 2007 2:9 doi:10.1186/1749-8104-2-9
demielinisation plaque
Dr. Jean Decety Santiago, Chile, November 2008
drg_chicken_e7.jpg
This licensing tag was added to this file as part of the GFDL licensing update.
Photography of Neuroscientist Prof. Dr. Christian Keysers by his wife Valeria Gazzola
Mode diagrams and state transition. A: When the chandelier cells are dysfunctional but the GABAergic inhibition by the other interneurons is normal, the transition from the inverted-U mode to the H mode hardly occurs because of a gap between the two modes. The gap becomes wider in the existence of chandelier cells. B: When the chandelier cells are dysfunctional and the GABAergic inhibition by the other interneurons is reduced, the two modes are connected, so that the transition to the H mode would occur readily. Tanaka BMC Neuroscience 2008 9:41 doi:10.1186/1471-2202-9-41
This is the PSMBF sub-field of the “barrel field” in the rat somatosensory cortex. Each “barrel” received input from one major whisker on the snout of the rat. The tissue in the image has been stained with cytochrome oxidase and is 50μm thick. Layer IV. White circles are empty areas left by emptied blood vessels.
Bereitschaftspotential (also pre-motor potential or readiness potential); Kornhuber and Deecke (Uploaded by Lueder Deecke)
Sketch of bat brain and auditory cortex
Axonal pathfinding and fasciculation behaviour in the embryonic ventral nerve cord. (a) In the ventral nerve cord of stage 13/14 embryos, growth cones of identified neurons (aCC, curved arrow; pCC, arrow; RP2, arrow head) navigate in stereotypic positions (stippled line, midline; asterisk, somata of aCC and pCC). (b) Schematic representations of early growing neurons vMP2, dMP2, MP1, aCC and pCC (colour coded): at stage 13, their axons are partly guided by glia cells (grey circles) and Netrin A and B (light green) bound to lateral fields of Frazzled expression (wave pattern); MP1s and dMP2s grow jointly posteriorward, whereas vMP2s and pCCs fasciculate and grow together anteriorward until all four neurons contact one another midway between adjacent neuromeres and establish a single longitudinal fascicle (stage 13) that splits (stage 14), re-fasciculates (stage 15) and splits again (stage 16), partly mediated by glia cells (pCCs, dMP2s, vMP2s form a common fascicle close to the midline, MP1s a distinct axon tract further lateral; grey stippled line represents the lateral Fas2 fascicle of unknown identity; compare Figure 4, ix). (c,d) The neuroblast lineage NB1-2 [190] illustrates the stereotypic pathfinding choices of individual neurons (curved arrow, ipsilateral longitudinal path; AC/PC, anterior/posterior commissure; arrow, medial contralateral longitudinal; double chevron, lateral contralateral longitudinal; arrow head, soma of identified TB neuron; CX, cortex; NP, neuropile). (e) Regulation of midline crossing and mediolateral longitudinal path choice: ipsilateral neurons don't express Commissureless (Comm), and their combinatorial Robo receptor code determines the mediolateral positioning of their axons; contralateral neurons express Comm (black T), thus preventing transport of Robo receptors to the growth cone (curved red arrow); subsequent downregulation of Comm activity permits the Robo-mediated fascicle choice. (f) Choice of anterior versus posterior commissure during midline crossing is partly determined by posterior expression of Wnt5 (Figure 4, xx), which repels growth cones of Derailed expressing neurons. (c,d) Kindly provided by Janina Seibert, Christoph Rickert and Gerd Technau; (b) redrawn from Hidalgo and Booth [223]. Sánchez-Soriano et al. Neural Development 2007 2:9 doi:10.1186/1749-8104-2-9
A two photon image of an axon showing arborization.
Activity of a grid cell in rat (entorhinal cortex)
Astrocyte in vitro stained with GFAP to show filaments
Andamento di E_m in un modello a cavo
GFAP stained cortex from a TgAPP mouse showing activated astrocytes
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Photo by Steve M. Potter chronic multi-wire probe
A network of capillaries supply brain cells with nutrients. Tight seals in their walls keep blood toxins—and many beneficial drugs—out of the brain. From: Bridging the Blood-Brain Barrier: New Methods Improve the Odds of Getting Drugs to the Brain Cells That Need Them Ferber D PLoS Biology Vol. 5, No. 6, e169 doi:10.1371/journal.pbio.0050169
Magnetic resonance imaging of central neurocytoma. axial MRI. T2
Magnetic resonance imaging of central neurocytoma. On axial T1 upon gadolinium enhancement, heterogeneous weak contrast enhancement of the tumor can be appreciated.
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Magnetic resonance imaging (T1) : lacunar infarcts, Multi-infarct dementia (Leukoaraiosis)
leukoaraiosis : Magnetic resonance imaging (T2) : lacunar infarcts, Multi-infarct dementia (Leukoaraiosis)
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Cerebral angiography, injection in the left vertebral artery, with retrograde flow in the contralateral vertebral artery, the basilar artery and the posterior communicating artery. The posterior cerebral circulation can be seen, including the posterior part of the arterial circle of Willis.
Angiograph of an aneurysm in a cerebral artery.
Crystal structure of two repeat fragment of reelin
Visual cortical implant designed by Profesor Mohamad Sawan



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