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Thomas J Feuerstein - One of the best experts on this subject based on the ideXlab platform.
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Exogenous and Endogenous Cannabinoids Suppress Inhibitory Neurotransmission in the Human Neocortex
Neuropsychopharmacology, 2012Co-Authors: Flora E Kovacs, Thomas J Feuerstein, Thomas M. Freiman, Josef Zentner, Tim Knop, Michal J Urbanski, Ilka Freiman, Bela SzaboAbstract:Activation of CB_1 receptors on axon terminals by exogenous cannabinoids (eg, Δ^9-tetrahydrocannabinol) and by endogenous cannabinoids (endocannabinoids) released by postsynaptic neurons leads to presynaptic inhibition of neurotransmission. The aim of this study was to characterize the effect of cannabinoids on GABAergic synaptic transmission in the Human Neocortex. Brain slices were prepared from neocortical tissues surgically removed to eliminate epileptogenic foci. Spontaneous GABAergic inhibitory postsynaptic currents (sIPSCs) were recorded in putative pyramidal neurons using patch-clamp techniques. To enhance the activity of cannabinoid-sensitive presynaptic axons, muscarinic receptors were continuously stimulated by carbachol. The synthetic cannabinoid receptor agonist WIN55212-2 decreased the cumulative amplitude of sIPSCs. The CB_1 antagonist rimonabant prevented this effect, verifying the involvement of CB_1 receptors. WIN55212-2 decreased the frequency of miniature IPSCs (mIPSCs) recorded in the presence of tetrodotoxin, but did not change their amplitude, indicating that the neurotransmission was inhibited presynaptically. Depolarization of postsynaptic pyramidal neurons induced a suppression of sIPSCs. As rimonabant prevented this suppression, it is very likely that it was due to endocannabinods acting on CB_1 receptors. This is the first demonstration that an exogenous cannabinoid inhibits synaptic transmission in the Human Neocortex and that endocannabinoids released by postsynaptic neurons suppress synaptic transmission in the Human brain. Interferences of cannabinoid agonists and antagonists with synaptic transmission in the cortex may explain the cognitive and memory deficits elicited by these drugs.
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Reactive oxygen species (ROS) in the Human Neocortex: role of aging and cognition.
Brain research bulletin, 2009Co-Authors: Bianca Brawek, Rolf Jackisch, Marlene Löffler, Kathrin Wagner, Hans-jürgen Huppertz, Anne-sophie Wendling, Astrid Weyerbrock, Thomas J FeuersteinAbstract:Reactive oxygen species (ROS), formed during normal aerobic metabolism, are involved in signal transduction and cognitive functions, but highly increased ROS concentrations may also have detrimental effects. The aim of the present study was to investigate whether aging and cognitive functions are associated with ROS generation in Human Neocortex obtained from neurosurgical patients. ROS formation in mitochondria from fresh and re-thawed neocortical specimens was measured by monitoring ROS-mediated conversion of dihydrorhodamine 123 to fluorescent rhodamine 123. The validity of this technique was characterized in rat brain mitochondria. The increase in the concentration-response curve of the complex I inhibitor rotenone on ROS generation, as measured by rhodamine 123 (Rh123) fluorescence, was much more pronounced than that of rotenone on mitochondrial [(3)H]-choline uptake [which indicates changes in the mitochondrial membrane potential (DeltaPsi(M))]. Thus, mitochondrial ROS generation can be shown by Rh123 fluorescence although this fluorescence may also reflect changes in DeltaPsi(M) to some extent. ROS formation in Human brain mitochondria positively correlated with the age of patients. Moreover, an age-corrected positive correlation of ROS formation with presurgical cognitive performance was observed. Our data suggest a mild increase in ROS formation with aging possibly reflecting a physiological compensation of mitochondrial function. Furthermore, higher cognitive performances in tests of executive functions may be paralleled by slightly increased ROS levels.
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Functional characterization of muscarinic autoreceptors in rat and Human Neocortex.
Journal of neurochemistry, 2009Co-Authors: Christoph Stoll, Thomas J Feuerstein, Josef Zentner, Manfrid Eltze, Günter Lambrecht, Rolf JackischAbstract:Electrically evoked overflow of [3H]acetylcholine in slices of rat Neocortex and of Human Neocortex (freshly obtained during neurosurgical treatment of epilepsy or deep-seated tumors) was used to functionally characterize the muscarinic receptor subtype, which mediates autoinhibition of acetylcholine release in these tissues. In the rat Neocortex, the following pKB values [CI95] were calculated from the shifts to the right of the concentration–response curves of the full agonist oxotremorine in presence of subtype preferring muscarinic receptor antagonists: tripitramine: 9.1 [8.8, 9.4], tripinamide: 8.6 [8.5, 8.7], AQ-RA 741 (11-[[4-[4-(diethylamino)butyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H-pyrido(2,3-b)[1,4]benzodiazepine-6-one): 8.2 [8.0, 8.4], himbacine: 8.0 [7.9, 8.1], 4-diphenylacetoxy-N-methylpiperidine methobromide: 8.0 [7.8, 8.1], methoctramine: 7.5 [7.4, 7.6], AF-DX 116 (11[[2-[(diethyl-amino)methyl]-1-piperidinyl] acetyl] 5,11-dihydro-6H-pyrido(2,3-b)[1,4]benzodiazepine-6-one): 7.1 [7.0, 7.3], hexahydro-sila-difenidol: 6.8 [6.7, 6.9], pirenzepine: 6.6 [6.4, 6.7], and 3,6a,11,14-tetrahydro-9-methoxy-2-methyl-12H-isoquino[1,2-b]pyrrolo[3,2-f] [1,3]benzoxazine-1-carboxylic acid ethyl ester (PD 102807): 6.0 [5.8, 6.2]. In the Human Neocortex the following values were found: tripitramine: 9.4 [9.3, 9.6], tripinamide: 9.0 [8.9, 9.2], AF-DX 116: 6.7 [6.4, 6.9], hexahydro-sila-difenidol: 6.6 [6.2, 6.9], and PD 102807: 6.5 [6.3, 6.6]. In correlation plots, these pKB values correspond best to published binding data on native or recombinant M2 receptors but not to those on M1, M3, M4, and M5 receptors, suggesting that muscarinic autoreceptors of both the rat and Human Neocortex belong to the M2 subtype. This observation lends further support to the development of M2 receptor selective brain penetrating antagonists for application in Alzheimer’s disease.
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GABA(A) autoreceptors enhance GABA release from Human Neocortex: towards a mechanism for high-frequency stimulation (HFS) in brain?
Naunyn-Schmiedeberg's archives of pharmacology, 2009Co-Authors: Michela Mantovani, Josef Zentner, Andreas Moser, Carola A. Haas, Thomas J FeuersteinAbstract:High-frequency stimulation (HFS) in Human neocortical slices induces γ-aminobutyric acid (GABA) release via GABAA receptor (GABAAR) activation. The mechanism of this effect and the localization of these GABAARs were now studied. Fresh Human neocortical slices were subjected to HFS (130 Hz) in the presence of veratridine (3 µM). As measured by high-performance liquid chromatography, only GABA but not glutamate outflow was affected by HFS/veratridine stimulation. The evoked GABA overflow was abolished by tetrodotoxin and furosemide, suggesting an involvement of action potentials and plasmalemmal chloride gradients. Double immunolabeling showed that GABAARs are localized on soma and dendrites of GABAergic neurons in the Human Neocortex. Moreover, in support of a terminal localization of GABAARs, the K+-evoked [3H]-GABA release from synaptosomes was enhanced by the GABAAR agonist muscimol (antagonized by GABAAR blockers). We conclude that HFS in Human brain Neocortex leads to a specific increase of GABA release, which is mediated by facilitatory GABAA autoreceptors located on soma, dendrites, and axon terminals of GABAergic neurons.
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Fatty acid amidohydrolase in Human Neocortex-activity in epileptic and non-epileptic brain tissue and inhibition by putative endocannabinoids.
Neuroscience letters, 2005Co-Authors: Marc Steffens, Andreas Schulze-bonhage, Rainer Surges, Thomas J FeuersteinAbstract:Abstract Increased levels of the endocannabinoid anandamide (AEA) have been observed in connection with neuronal disorders like epilepsy. In order to investigate whether an impaired enzymatic AEA hydrolysis contributes to this phenomenon, the present study determined the activity of fatty acid amidohydrolase (FAAH) in epileptic and non-epileptic Human neocortical brain tissue. Additionally, we investigated whether other putative endocannabinoids (2-arachidonylglycerol (2-AG), noladin ether, virodhamine) may also interact with FAAH. AEA hydrolysis was measured by the formation of the product [ 3 H]-ethanolamine after separation from the substrate using activated charcoal. FAAH activity was found to be similar in epileptic and non-epileptic Human Neocortex (0.29 and 0.37 nmol ethanolamine/mg protein/min, respectively). FAAH activity was about 55% higher in rat Neocortex. While in Human, Neocortex noladin ether did not influence AEA hydrolysis, FAAH activity was concentration-dependently inhibited by AEA, 2-AG and virodhamine (IC 50 values 3.3, 3.5 and 13.8 μM, respectively). Our results suggest that, in the course of epilepsy, increased AEA levels are likely due to enhanced formation and not due to decreased hydrolysis. To further increase endocannabinoid activity, the application of FAAH inhibitors might be therapeutically useful in the treatment of neuronal hyperexcitability. Whereas noladin ether did not interact with AEA hydrolysis, this compound, 2-AG and virodhamine may share common enzymatic inactivation mechanisms in Human Neocortex.
Maurizio Raiteri - One of the best experts on this subject based on the ideXlab platform.
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RANTES modulates the release of glutamate in Human Neocortex.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008Co-Authors: Veronica Musante, Fabio Longordo, Elisa Neri, Marco Pedrazzi, Fotios Kalfas, Paolo Severi, Maurizio Raiteri, Anna PittalugaAbstract:The effects of the recombinant chemokine Human RANTES (hRANTES) on the release of glutamate from Human Neocortex glutamatergic nerve endings were investigated. hRANTES facilitated the spontaneous release of d [3H]d-aspartate ([3H]dASP-) by binding Pertussis toxin-sensitive G-protein-coupled receptors (GPCRs), whose activation caused Ca2+ mobilization from inositol trisphosphate-sensitive stores and cytosolic tyrosine kinase-mediated phosphorylations. Facilitation of release switched to inhibition when the effects of hRANTES on the 12 mm K+-evoked [3H]d-ASP exocytosis were studied. Inhibition of exocytosis relied on activation of Pertussis toxin-sensitive GPCRs negatively coupled to adenylyl cyclase. Both hRANTES effects were prevented by met-RANTES, an antagonist at the chemokine receptors (CCRs) of the CCR1, CCR3, and CCR5 subtypes. Interestingly, Human Neocortex glutamatergic nerve endings seem to possess all three receptor subtypes. Blockade of CCR1 and CCR5 by antibodies against the extracellular domain of CCRs prevented both the hRANTES effect on [3H]d-ASP release, whereas blockade of CCR3 prevented inhibition, but not facilitation, of release. The effects of RANTES on the spontaneous and the evoked release of [3H]d-ASP were also observed in experiments with mouse cortical synaptosomes, which may therefore represent an appropriate animal model to study RANTES-induced effects on neurotransmission. It is concluded that glutamate transmission can be modulated in opposite directions by RANTES acting at distinct CCR receptor subtypes coupled to different transduction pathways, consistent with the multiple and sometimes contrasting effects of the chemokine.
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direct evidence that release stimulating α7 nicotinic cholinergic receptors are localized on Human and rat brain glutamatergic axon terminals
Journal of Neurochemistry, 2002Co-Authors: Mario Marchi, Concetta Viola, Paolo Cavazzani, Francesca Risso, Maurizio RaiteriAbstract:The existence on glutamatergic nerve endings of nicotinic acetylcholine receptors (nAChRs) mediating enhancement of glutamate release has often been suggested but not demonstrated directly. Here, we study the effects of nAChR agonists on [3H]-d-aspartate ([3H]-d-ASP) release from synaptosomes superfused in conditions known to prevent indirect effects. Nicotinic receptor agonists, while unable to modify the basal [3H]-d-ASP release from Human Neocortex or rat striatal synaptosomes, enhanced the Ca2+-dependent exocytotic release evoked by K+ (12 mm) depolarization. Their rank order of potency were anatoxin-a > epibatidine > nicotine > ACh (+ atropine). The anatoxin-a effect, both in Human and rat synaptosomes, was antagonized by mecamylamine, α-bungarotoxin or methyllycaconitine. The basal release of [3H]ACh from Human cortical synaptosomes was increased by (–)-nicotine (EC50 = 1.16 ± 0.33 µm) or by ACh plus atropine (EC50 = 2.0 ± 0.04 µm). The effect of ACh plus atropine was␣insensitive to α-bungarotoxin, methyllycaconitine or α-conotoxin MII, whereas it was totally antagonized by mecamylamine or dihydro-β-erythroidine. To conclude, glutamatergic axon terminals in Human Neocortex and in rat striatum possess α7* nicotinic heteroreceptors mediating enhancement of glutamate release. Release-enhancing cholinergic autoreceptors in Human Neocortex are nAChRs with a pharmacological profile compatible with the α4β2 subunit combination.
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serotonin inhibition of the nmda receptor nitric oxide cyclic gmp pathway in Human Neocortex slices involvement of 5 ht2c and 5 ht1a receptors
British Journal of Pharmacology, 2000Co-Authors: Guido Maura, Concetta Viola, Manuela Marcoli, Olimpia Pepicelli, Christian Rosu, Maurizio RaiteriAbstract:The NMDA receptor/nitric oxide (NO)/cyclic GMP pathway and its modulation by 5-hydroxytryptamine (5-HT) was studied in slices of neocortical samples obtained from patients undergoing neurosurgery. The cyclic GMP elevation produced by 100 μM NMDA was blocked by 100 μM of the NO synthase inhibitor NG-nitro-L-arginine (L-NOARG) or by 10 μM of the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-α] quinoxaline-1-one (ODQ). The NMDA effect was prevented by 5-HT or by the 5-HT2 agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane ((±)-DOI; EC50=22 nM). The (±)-DOI inhibition was insensitive to the 5-HT2A receptor antagonist MDL 100907 or the 5-HT2B antagonist rauwolscine; it was largely prevented by 1 μM of the non-selective 5-HT2C antagonists mesulergine (5-HT2A,B,C), ketanserin (5-HT2A,C) or SB 200646A (5-HT2B,C); it was completely abolished by 0.1 μM of the selective 5-HT2C receptor antagonist SB 242084. The NMDA-induced cyclic GMP elevation also was potently inhibited by the selective 5-HT2C agonist RO 60-0175 and by the antidepressant trazodone, both added at 1 μM, in an SB 242084-sensitive manner. Finally, the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT; 1 μM) inhibited the NMDA-evoked cyclic GMP response, an effect blocked by the selective 5-HT1A receptor antagonist WAY 100635. In conclusion, the NMDA receptor/NO/cyclic GMP pathway in Human Neocortex slices can be potently inhibited by activation of 5-HT2C or 5-HT1A receptors. British Journal of Pharmacology (2000) 130, 1853–1858; doi:10.1038/sj.bjp.0703510
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Release of dopamine from Human Neocortex nerve terminals evoked by different stimuli involving extra- and intraterminal calcium.
British journal of pharmacology, 2000Co-Authors: Giambattista Bonanno, Roberta Sala, Laura Cancedda, Paolo Cavazzani, Massimo Cossu, Maurizio RaiteriAbstract:The release of [3H]-dopamine ([3H]-DA) from Human Neocortex nerve terminals was studied in synaptosomes prepared from brain specimens removed in neurosurgery and exposed during superfusion to different releasing stimuli. Treatment with 15 mM KCl, 100 μM 4-aminopyridine, 1 μM ionomycin or 30 mM caffeine elicited almost identical overflows of tritium. Removal of external Ca2+ ions abolished the overflow evoked by K+ or ionomycin and largely prevented that caused by 4-aminopyridine; the overflow evoked by caffeine was completely independent of external Ca2+. Exposure of synaptosomes to 25 μM of the broad spectrum calcium channel blocker CdCl2 strongly inhibited the 4-aminopyridine-induced tritium overflow while that evoked by ionomycin remained unaffected. The Ca2+ chelator, 1,2-bis-(2-aminophenoxy)ethane-N,N,N′,N′ tetraacetic acid (BAPTA), reduced significantly the K+- and the caffeine-induced tritium overflow. The effect of caffeine was attenuated by exposure to the ryanodine receptor blocker dantrolene or when the membrane-impermeant inositol trisphosphate receptor antagonist, heparin, was entrapped into synaptosomes; the combined treatment with dantrolene and heparin abolished the release elicited by caffeine. Tetanus toxin, entrapped into Human Neocortex synaptosomes to avoid prolonged incubation, inhibited in a concentration-dependent manner the K+- or the 4-aminopyridine-evoked tritium overflow; in contrast, the release stimulated by ionomycin and by caffeine were both totally insensitive to the same concentrations of tetanus toxin. Western blot analysis showed about 50% reduction of the content of the vesicular protein, synaptobrevin, in synaptosomes poisoned with tetanus toxin. In conclusion, the release of dopamine from Human Neocortex nerve terminals can be triggered by Ca2+ ions originating from various sources. It seems that stimuli not leading to activation of voltage-sensitive Ca2+ channels elicit Ca2+-dependent, probably exocytotic, release that is insensitive to tetanus toxin. British Journal of Pharmacology (2000) 129, 1780–1786; doi:10.1038/sj.bjp.0703251
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Serotonin inhibition of the NMDA receptor/nitric oxide/cyclic GMP pathway in Human Neocortex slices: involvement of 5-HT2C and 5-HT1A receptors
British journal of pharmacology, 2000Co-Authors: Guido Maura, Concetta Viola, Manuela Marcoli, Olimpia Pepicelli, Christian Rosu, Maurizio RaiteriAbstract:The NMDA receptor/nitric oxide (NO)/cyclic GMP pathway and its modulation by 5-hydroxytryptamine (5-HT) was studied in slices of neocortical samples obtained from patients undergoing neurosurgery. The cyclic GMP elevation produced by 100 microM NMDA was blocked by 100 microM of the NO synthase inhibitor N(G)-nitro-L-arginine (L-NOARG) or by 10 microM of the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-alpha] quinoxaline-1-one (ODQ). The NMDA effect was prevented by 5-HT or by the 5-HT(2) agonist (+/-)-1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane ((+/-)-DOI; EC(50)=22 nM). The (+/-)-DOI inhibition was insensitive to the 5-HT(2A) receptor antagonist MDL 100907 or the 5-HT(2B) antagonist rauwolscine; it was largely prevented by 1 microM of the non-selective 5-HT(2C) antagonists mesulergine (5-HT(2A,B,C)), ketanserin (5-HT(2A,C)) or SB 200646A (5-HT(2B,C)); it was completely abolished by 0.1 microM of the selective 5-HT(2C) receptor antagonist SB 242084. The NMDA-induced cyclic GMP elevation also was potently inhibited by the selective 5-HT(2C) agonist RO 60-0175 and by the antidepressant trazodone, both added at 1 microM, in an SB 242084-sensitive manner. Finally, the 5-HT(1A) agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT; 1 microM) inhibited the NMDA-evoked cyclic GMP response, an effect blocked by the selective 5-HT(1A) receptor antagonist WAY 100635. In conclusion, the NMDA receptor/NO/cyclic GMP pathway in Human Neocortex slices can be potently inhibited by activation of 5-HT(2C) or 5-HT(1A) receptors.
Rolf Jackisch - One of the best experts on this subject based on the ideXlab platform.
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Reactive oxygen species (ROS) in the Human Neocortex: role of aging and cognition.
Brain research bulletin, 2009Co-Authors: Bianca Brawek, Rolf Jackisch, Marlene Löffler, Kathrin Wagner, Hans-jürgen Huppertz, Anne-sophie Wendling, Astrid Weyerbrock, Thomas J FeuersteinAbstract:Reactive oxygen species (ROS), formed during normal aerobic metabolism, are involved in signal transduction and cognitive functions, but highly increased ROS concentrations may also have detrimental effects. The aim of the present study was to investigate whether aging and cognitive functions are associated with ROS generation in Human Neocortex obtained from neurosurgical patients. ROS formation in mitochondria from fresh and re-thawed neocortical specimens was measured by monitoring ROS-mediated conversion of dihydrorhodamine 123 to fluorescent rhodamine 123. The validity of this technique was characterized in rat brain mitochondria. The increase in the concentration-response curve of the complex I inhibitor rotenone on ROS generation, as measured by rhodamine 123 (Rh123) fluorescence, was much more pronounced than that of rotenone on mitochondrial [(3)H]-choline uptake [which indicates changes in the mitochondrial membrane potential (DeltaPsi(M))]. Thus, mitochondrial ROS generation can be shown by Rh123 fluorescence although this fluorescence may also reflect changes in DeltaPsi(M) to some extent. ROS formation in Human brain mitochondria positively correlated with the age of patients. Moreover, an age-corrected positive correlation of ROS formation with presurgical cognitive performance was observed. Our data suggest a mild increase in ROS formation with aging possibly reflecting a physiological compensation of mitochondrial function. Furthermore, higher cognitive performances in tests of executive functions may be paralleled by slightly increased ROS levels.
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Functional characterization of muscarinic autoreceptors in rat and Human Neocortex.
Journal of neurochemistry, 2009Co-Authors: Christoph Stoll, Thomas J Feuerstein, Josef Zentner, Manfrid Eltze, Günter Lambrecht, Rolf JackischAbstract:Electrically evoked overflow of [3H]acetylcholine in slices of rat Neocortex and of Human Neocortex (freshly obtained during neurosurgical treatment of epilepsy or deep-seated tumors) was used to functionally characterize the muscarinic receptor subtype, which mediates autoinhibition of acetylcholine release in these tissues. In the rat Neocortex, the following pKB values [CI95] were calculated from the shifts to the right of the concentration–response curves of the full agonist oxotremorine in presence of subtype preferring muscarinic receptor antagonists: tripitramine: 9.1 [8.8, 9.4], tripinamide: 8.6 [8.5, 8.7], AQ-RA 741 (11-[[4-[4-(diethylamino)butyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H-pyrido(2,3-b)[1,4]benzodiazepine-6-one): 8.2 [8.0, 8.4], himbacine: 8.0 [7.9, 8.1], 4-diphenylacetoxy-N-methylpiperidine methobromide: 8.0 [7.8, 8.1], methoctramine: 7.5 [7.4, 7.6], AF-DX 116 (11[[2-[(diethyl-amino)methyl]-1-piperidinyl] acetyl] 5,11-dihydro-6H-pyrido(2,3-b)[1,4]benzodiazepine-6-one): 7.1 [7.0, 7.3], hexahydro-sila-difenidol: 6.8 [6.7, 6.9], pirenzepine: 6.6 [6.4, 6.7], and 3,6a,11,14-tetrahydro-9-methoxy-2-methyl-12H-isoquino[1,2-b]pyrrolo[3,2-f] [1,3]benzoxazine-1-carboxylic acid ethyl ester (PD 102807): 6.0 [5.8, 6.2]. In the Human Neocortex the following values were found: tripitramine: 9.4 [9.3, 9.6], tripinamide: 9.0 [8.9, 9.2], AF-DX 116: 6.7 [6.4, 6.9], hexahydro-sila-difenidol: 6.6 [6.2, 6.9], and PD 102807: 6.5 [6.3, 6.6]. In correlation plots, these pKB values correspond best to published binding data on native or recombinant M2 receptors but not to those on M1, M3, M4, and M5 receptors, suggesting that muscarinic autoreceptors of both the rat and Human Neocortex belong to the M2 subtype. This observation lends further support to the development of M2 receptor selective brain penetrating antagonists for application in Alzheimer’s disease.
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Characterization of nicotinic receptors inducing noradrenaline release and absence of nicotinic autoreceptors in Human Neocortex
Brain research bulletin, 2004Co-Authors: Florian Amtage, Thomas J Feuerstein, Bogdan Neughebauer, J. Michael Mcintosh, Thomas M. Freiman, Josef Zentner, Rolf JackischAbstract:Abstract Presynaptic facilitatory nicotinic receptors (nAChRs) on noradrenergic axon terminals were studied in slices of Human or rat Neocortex and of rat hippocampus preincubated with [ 3 H ]noradrenaline ([ 3 H ]NA). During superfusion of the slices, stimulation by nicotinic agonists for 2 min only slightly increased [ 3 H ]NA outflow in the rat Neocortex, but caused a tetrodotoxin-sensitive, Ca2+-dependent release of [ 3 H ]NA in rat hippocampus and Human Neocortex. In both tissues a similar rank order of potency of nicotinic agonists was found: epibatidine⪢DMPP>nicotine∼cytisine≥acetylcholine; choline was ineffective. In Human Neocortex, the effects of nicotine (100 μM) were reduced by mecamylamine, methyllycaconitine, di-hydro-β-erythroidine (10 μM, each) and the α3β2/α6βx-selective α-conotoxin MII (100/200 nM). The α3β4 selective α-conotoxin AuIB (1 μM), and the α7 selective α-conotoxin ImI (200 nM) as well as α-bungarotoxin (125 nM) were ineffective. Glutamate receptor antagonists (300 μM AP-5, 100 μM DNQX) acted inhibitory, suggesting the participation of nAChRs on glutamatergic neurons. On the other hand, nAChR agonists were unable to evoke exocytotic release of [ 3 H ]acetylcholine from Human and rat neocortical slices preincubated with [ 3 H ]choline. In conclusion: (1) α3β2 and/or α6 containing nAChRs are at least partially responsible for presynaptic cholinergic facilitation of noradrenergic transmission in Human Neocortex; (2) nicotinic autoreceptors were not detectable in rat and Human Neocortex.
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High potassium-induced activation of choline-acetyltransferase in Human Neocortex: implications and species differences.
Brain research bulletin, 2003Co-Authors: J.-p. Sigle, Rolf Jackisch, J. Zander, Andreas Ehret, J. Honegger, Thomas J FeuersteinAbstract:Abstract The role of electrical and potassium (K + )-induced depolarisation on choline-acetyltransferase (ChAT) activity in Human and mouse neocortical slices was studied. When [ 3 H ]-ACh release was evoked by two K + stimulations in Human Neocortex, the mean S 2 / S 1 ratio was significantly below unity. ChAT inhibitors, like bromo-acetylcholine and ocadaic acid, raised this ratio by 79 and 63%, respectively, suggesting that the diminished S 2 / S 1 value in the absence of ChAT inhibitors reflected an increased ChAT activity at S 2 following K + depolarisation at S 1 . When stimulated electrically, however, the S 2 / S 1 ratio in Human Neocortex was near unity and ocadaic acid remained without effect. In parallel experiments on mouse neocortical slices, the S 2 / S 1 ratio was near unity in both electrically or K + -evoked [ 3 H ]-ACh release and was not altered by ChAT inhibition. ChAT activity following K + depolarisation was also determined directly. ChAT activation in Human neocortical slices was highest at 10 and 20 mM K + . ChAT activity in mouse neocortical tissue was not altered by K + depolarisation. These results suggest that in Human, but not in mouse, Neocortex ChAT activity may be increased due to ongoing K + depolarisation. This increase of ChAT activity supports a cholinergic degeneration hypothesis which has been entitled “autocannibalism” by Wurtman [TINS 15 (1992) 177].
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Evaluation of autoreceptor-mediated control of [3H]acetylcholine release in rat and Human Neocortex
Experimental brain research, 1999Co-Authors: C Albrecht, Rolf Jackisch, H. G. Bloss, Thomas J FeuersteinAbstract:In order to assess the autoinhibitory control of endogenous acetylcholine (ACh) in rat and Human Neocortex, slices of these tissues were prelabelled with [3H]choline, superfused continuously and stimulated electrically using various frequencies in the presence or absence of drugs. The autoinhibitory feedback control of [3H]ACh release was operative – despite the absence of blockers of ACh esterase – at stimulation frequencies ≥3 Hz in rat and ≥6 Hz in Human Neocortex tissue. At these frequencies the muscarinic antagonist atropine (0.1 µM) disinhibited the release of [3H]ACh in both species. Estimation of the biophase concentration of ACh near the autoreceptor in the rat Neocortex from concentration-response curves of the muscarinic agonist oxotremorine revealed that at 3 Hz about 25% of the autoreceptors were activated by endogenously released ACh. This estimation is consistent with an increase in [3H]ACh release to about 120% of control values by complete blockade of autoreceptors with atropine. The observation that in Human neocortical tissue presynaptic autoinhibition of [3H]ACh release is operative at stimulation frequencies ≥6 Hz suggests that selective blockade of autoinhibition may also increase ACh release in the cortex of Alzheimer’s disease patients, without additional blockade of the enzyme acetylcholinesterase.
Cees A. J. Broere - One of the best experts on this subject based on the ideXlab platform.
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A detailed comparison of the cytoarchitectonic and myeloarchitectonic maps of the Human Neocortex produced by the Vogt–Vogt school
Brain Structure and Function, 2020Co-Authors: Rudolf Nieuwenhuys, Cees A. J. BroereAbstract:The comprehensive research programme of the Vogt–Vogt (V–V) school, which was active during the period 1900–1970, included detailed cytoarchitectonic and myeloarchitectonic analyses of the Human cerebral cortex, with the aim to integrate the data obtained into a map, showing a parcellation of the Human cerebral cortex into fundamental structural and potentially functional units. The cytoarchitectonic V–V analyses yielded two maps of the Human cerebral cortex, the famous map of Brodmann (Vergleichende Lokalisationslehre der Grosshirnrinde in ihren Prinzipien dargestellt auf Grund des Zellenbaues. Barth, Leipzig, 1909), Brodmann (in: Bruns P (ed) Neue deutsche Chirurgie, Enke, Stuttgart, 1914), and the less known, but more detailed map of Sarkisov et al. (Cytoarchitecture of the Human cortex cerebri. Medgiz, Moscow, 1949). Sarkisov et al. used in their cytoarchitectonic parcellation of the cortex the same numbering scheme as Brodmann. They confirmed the presence of most of the areas delineated by the latter, but they subdivided several of these areas into two or more separate areas or subareas. Within the realm of the myeloarchitectonic V–V analyses, numerous meticulous studies of the cortex of individual cerebral lobes were carried out, but these were not united into a single map. Consequently, the envisioned integration of cytoarchitectonic and myeloarchitectonic data mentioned above was never realized. Some years ago, we (Nieuwenhuys et al. in Brain Struct Funct 220:2551–2573, 2015a, Nieuwenhuys et al. in Brain Struct Funct 220:3753–3755, 2015b) reanalyzed the V–V myeloarchitectonic data, and succeeded in constructing a complete myeloarchitectonic map of the Human Neocortex from these data. Because the data provided by the V–V school were derived from many different brains, a standard brain had to be introduced as a template to which all data available could be transferred. As such the MNI305 template was selected. Having made available now the cytoarchitectonic maps of Brodmann and Sarkisov et al. and the recently prepared myeloarchitectonic map, an attempt is made here to realize at last the original aim of the V–V school, viz. the preparation of a single, combined (cyto + myelo) architectonic map of the Human cortex. To this end, the following three steps have been made. First, Brodmann’s (BR) map, and the map of Sarkisov et al. (SA) were harmoniously transferred to the same template brain as the one used during the construction of our myeloarchitectonic map. Second, the standardized BR and our myeloarchitectonic (NI) map were compared, and the data contained within these maps were integrated into a single standardized combined BR–NI map (Fig. 11). The standardized SA and NI maps were subjected to the same procedure (Fig. 12). Finally, the standardized combined BR–NI and SA–NI maps were united into a single combined BR–SA–NI map (Fig. 13). This map renders it possible to make direct comparisons between the results of the architectonic studies of the V–V school and current parcellations of the Human Neocortex.
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A detailed comparison of the cytoarchitectonic and myeloarchitectonic maps of the Human Neocortex produced by the Vogt-Vogt school.
Brain structure & function, 2020Co-Authors: Rudolf Nieuwenhuys, Cees A. J. BroereAbstract:The comprehensive research programme of the Vogt-Vogt (V-V) school, which was active during the period 1900-1970, included detailed cytoarchitectonic and myeloarchitectonic analyses of the Human cerebral cortex, with the aim to integrate the data obtained into a map, showing a parcellation of the Human cerebral cortex into fundamental structural and potentially functional units. The cytoarchitectonic V-V analyses yielded two maps of the Human cerebral cortex, the famous map of Brodmann (Vergleichende Lokalisationslehre der Grosshirnrinde in ihren Prinzipien dargestellt auf Grund des Zellenbaues. Barth, Leipzig, 1909), Brodmann (in: Bruns P (ed) Neue deutsche Chirurgie, Enke, Stuttgart, 1914), and the less known, but more detailed map of Sarkisov et al. (Cytoarchitecture of the Human cortex cerebri. Medgiz, Moscow, 1949). Sarkisov et al. used in their cytoarchitectonic parcellation of the cortex the same numbering scheme as Brodmann. They confirmed the presence of most of the areas delineated by the latter, but they subdivided several of these areas into two or more separate areas or subareas. Within the realm of the myeloarchitectonic V-V analyses, numerous meticulous studies of the cortex of individual cerebral lobes were carried out, but these were not united into a single map. Consequently, the envisioned integration of cytoarchitectonic and myeloarchitectonic data mentioned above was never realized. Some years ago, we (Nieuwenhuys et al. in Brain Struct Funct 220:2551-2573, 2015a, Nieuwenhuys et al. in Brain Struct Funct 220:3753-3755, 2015b) reanalyzed the V-V myeloarchitectonic data, and succeeded in constructing a complete myeloarchitectonic map of the Human Neocortex from these data. Because the data provided by the V-V school were derived from many different brains, a standard brain had to be introduced as a template to which all data available could be transferred. As such the MNI305 template was selected. Having made available now the cytoarchitectonic maps of Brodmann and Sarkisov et al. and the recently prepared myeloarchitectonic map, an attempt is made here to realize at last the original aim of the V-V school, viz. the preparation of a single, combined (cyto + myelo) architectonic map of the Human cortex. To this end, the following three steps have been made. First, Brodmann's (BR) map, and the map of Sarkisov et al. (SA) were harmoniously transferred to the same template brain as the one used during the construction of our myeloarchitectonic map. Second, the standardized BR and our myeloarchitectonic (NI) map were compared, and the data contained within these maps were integrated into a single standardized combined BR-NI map (Fig. 11). The standardized SA and NI maps were subjected to the same procedure (Fig. 12). Finally, the standardized combined BR-NI and SA-NI maps were united into a single combined BR-SA-NI map (Fig. 13). This map renders it possible to make direct comparisons between the results of the architectonic studies of the V-V school and current parcellations of the Human Neocortex.
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A map of the Human Neocortex showing the estimated overall myelin content of the individual architectonic areas based on the studies of Adolf Hopf.
Brain structure & function, 2016Co-Authors: Rudolf Nieuwenhuys, Cees A. J. BroereAbstract:During the period extending from 1910 to 1970, Oscar and Cecile Vogt and their numerous collaborators published a large number of myeloarchitectonic studies on the cortex of the various lobes of the Human cerebrum. In a previous publication [Nieuwenhuys et al (Brain Struct Funct 220:2551-2573, 2015; Erratum in Brain Struct Funct 220: 3753-3755, 2015)], we used the data provided by the Vogt-Vogt school for the composition of a myeloarchitectonic map of the entire Human Neocortex. Because these data were derived from many different brains, a standard brain had to be introduced to which all data available could be transferred. As such the Colin 27 structural scan, aligned to the MNI305 template was selected. The resultant map includes 180 myeloarchitectonic areas, 64 frontal, 30 parietal, 6 insular, 17 occipital and 63 temporal. Here we present a supplementary map in which the overall density of the myelinated fibers in the individual architectonic areas is indicated, based on a meta-analysis of data provided by Adolf Hopf, a prominent collaborator of the Vogts. This map shows that the primary sensory and motor regions are densely myelinated and that, in general, myelination decreases stepwise with the distance from these primary regions. The map also reveals the presence of a number of heavily myelinated formations, situated beyond the primary sensory and motor domains, each consisting of two or more myeloarchitectonic areas. These formations were provisionally designated as the orbitofrontal, intraparietal, posterolateral temporal, and basal temporal dark clusters. Recently published MRI-based in vivo myelin content mappings show, with regard to the primary sensory and motor regions, a striking concordance with our map. As regards the heavily myelinated clusters shown by our map, scrutiny of the current literature revealed that correlates of all of these clusters have been identified in in vivo structural MRI studies and appear to correspond either entirely or largely to known cytoarchitectonic entities. Moreover, functional neuroimaging studies indicate that all of these clusters are involved in vision-related cognitive functions.
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A new myeloarchitectonic map of the Human Neocortex based on data from the Vogt–Vogt school
Brain Structure and Function, 2015Co-Authors: Rudolf Nieuwenhuys, Cees A. J. Broere, Leonardo CerlianiAbstract:The Human cerebral cortex contains numerous myelinated fibres, the arrangement and density of which is by no means homogeneous throughout the cortex. Local differences in the spatial organization of these fibres render it possible to recognize areas with a different myeloarchitecture. The neuroanatomical subdiscipline aimed at the identification and delineation of such areas is known as myeloarchitectonics. During the period extending from 1910 to 1970, Oscar and Cécile Vogt and their numerous collaborators (The Vogt–Vogt school) published a large number of myeloarchitectonic studies on the cortex of the various lobes of the Human cerebrum. Recently, one of us (Nieuwenhuys in Brain Struct Funct 218: 303–352, 2013 ) extensively reviewed these studies. It was concluded that the data available are adequate and sufficient for the composition of a myeloarchitectonic map of the entire Human Neocortex. The present paper is devoted to the creation of this map. Because the data provided by the Vogt–Vogt school are derived from many different brains, a standard brain had to be introduced to which all data available could be transferred. As such, the colin27 structural scan, aligned to the MNI305 template was selected. The procedure employed in this transfer involved computer-aided transformations of the lobar maps available in the literature, to the corresponding regions of the standard brain, as well as local adjustments in the border zones of the various lobes. The resultant map includes 180 myeloarchitectonic areas, 64 frontal, 30 parietal, 6 insular, 17 occipital and 63 temporal. The designation of the various areas with simple Arabic numbers, introduced by Oscar Vogt for the frontal and parietal cortices, has been extended over the entire Neocortex. It may be expected that combination of the myeloarchitectonic data of the Vogt–Vogt school, as expressed in our map, with the results of the detailed cytoarchitectonic and receptor architectonic studies of Karl Zilles and Katrin Amunts and their numerous associates, will yield a comprehensive ‘supermap’ of the structural organization of the Human Neocortex. For the time being, i. e., as long as this ‘supermap’ is not yet available, our map may provide a tentative frame of reference for (a) the morphological interpretation of the results of functional neuroimaging studies; (b) the selection of starting points (seed voxels, regions-of-interest) in diffusion tractography studies and (c) the interpretation of putative myeloarchitectonic features, visualized by in vivo and ex vivo mappings of the cerebral cortex with high-field magnetic resonance imaging.
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A new myeloarchitectonic map of the Human Neocortex based on data from the Vogt-Vogt school
Brain structure & function, 2014Co-Authors: Rudolf Nieuwenhuys, Cees A. J. Broere, Leonardo CerlianiAbstract:The Human cerebral cortex contains numerous myelinated fibres, the arrangement and density of which is by no means homogeneous throughout the cortex. Local differences in the spatial organization of these fibres render it possible to recognize areas with a different myeloarchitecture. The neuroanatomical subdiscipline aimed at the identification and delineation of such areas is known as myeloarchitectonics. During the period extending from 1910 to 1970, Oscar and Cecile Vogt and their numerous collaborators (The Vogt-Vogt school) published a large number of myeloarchitectonic studies on the cortex of the various lobes of the Human cerebrum. Recently, one of us (Nieuwenhuys in Brain Struct Funct 218: 303-352, 2013) extensively reviewed these studies. It was concluded that the data available are adequate and sufficient for the composition of a myeloarchitectonic map of the entire Human Neocortex. The present paper is devoted to the creation of this map. Because the data provided by the Vogt-Vogt school are derived from many different brains, a standard brain had to be introduced to which all data available could be transferred. As such, the colin27 structural scan, aligned to the MNI305 template was selected. The procedure employed in this transfer involved computer-aided transformations of the lobar maps available in the literature, to the corresponding regions of the standard brain, as well as local adjustments in the border zones of the various lobes. The resultant map includes 180 myeloarchitectonic areas, 64 frontal, 30 parietal, 6 insular, 17 occipital and 63 temporal. The designation of the various areas with simple Arabic numbers, introduced by Oscar Vogt for the frontal and parietal cortices, has been extended over the entire Neocortex. It may be expected that combination of the myeloarchitectonic data of the Vogt-Vogt school, as expressed in our map, with the results of the detailed cytoarchitectonic and receptor architectonic studies of Karl Zilles and Katrin Amunts and their numerous associates, will yield a comprehensive 'supermap' of the structural organization of the Human Neocortex. For the time being, i. e., as long as this 'supermap' is not yet available, our map may provide a tentative frame of reference for (a) the morphological interpretation of the results of functional neuroimaging studies; (b) the selection of starting points (seed voxels, regions-of-interest) in diffusion tractography studies and
Rudolf Nieuwenhuys - One of the best experts on this subject based on the ideXlab platform.
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A detailed comparison of the cytoarchitectonic and myeloarchitectonic maps of the Human Neocortex produced by the Vogt–Vogt school
Brain Structure and Function, 2020Co-Authors: Rudolf Nieuwenhuys, Cees A. J. BroereAbstract:The comprehensive research programme of the Vogt–Vogt (V–V) school, which was active during the period 1900–1970, included detailed cytoarchitectonic and myeloarchitectonic analyses of the Human cerebral cortex, with the aim to integrate the data obtained into a map, showing a parcellation of the Human cerebral cortex into fundamental structural and potentially functional units. The cytoarchitectonic V–V analyses yielded two maps of the Human cerebral cortex, the famous map of Brodmann (Vergleichende Lokalisationslehre der Grosshirnrinde in ihren Prinzipien dargestellt auf Grund des Zellenbaues. Barth, Leipzig, 1909), Brodmann (in: Bruns P (ed) Neue deutsche Chirurgie, Enke, Stuttgart, 1914), and the less known, but more detailed map of Sarkisov et al. (Cytoarchitecture of the Human cortex cerebri. Medgiz, Moscow, 1949). Sarkisov et al. used in their cytoarchitectonic parcellation of the cortex the same numbering scheme as Brodmann. They confirmed the presence of most of the areas delineated by the latter, but they subdivided several of these areas into two or more separate areas or subareas. Within the realm of the myeloarchitectonic V–V analyses, numerous meticulous studies of the cortex of individual cerebral lobes were carried out, but these were not united into a single map. Consequently, the envisioned integration of cytoarchitectonic and myeloarchitectonic data mentioned above was never realized. Some years ago, we (Nieuwenhuys et al. in Brain Struct Funct 220:2551–2573, 2015a, Nieuwenhuys et al. in Brain Struct Funct 220:3753–3755, 2015b) reanalyzed the V–V myeloarchitectonic data, and succeeded in constructing a complete myeloarchitectonic map of the Human Neocortex from these data. Because the data provided by the V–V school were derived from many different brains, a standard brain had to be introduced as a template to which all data available could be transferred. As such the MNI305 template was selected. Having made available now the cytoarchitectonic maps of Brodmann and Sarkisov et al. and the recently prepared myeloarchitectonic map, an attempt is made here to realize at last the original aim of the V–V school, viz. the preparation of a single, combined (cyto + myelo) architectonic map of the Human cortex. To this end, the following three steps have been made. First, Brodmann’s (BR) map, and the map of Sarkisov et al. (SA) were harmoniously transferred to the same template brain as the one used during the construction of our myeloarchitectonic map. Second, the standardized BR and our myeloarchitectonic (NI) map were compared, and the data contained within these maps were integrated into a single standardized combined BR–NI map (Fig. 11). The standardized SA and NI maps were subjected to the same procedure (Fig. 12). Finally, the standardized combined BR–NI and SA–NI maps were united into a single combined BR–SA–NI map (Fig. 13). This map renders it possible to make direct comparisons between the results of the architectonic studies of the V–V school and current parcellations of the Human Neocortex.
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A detailed comparison of the cytoarchitectonic and myeloarchitectonic maps of the Human Neocortex produced by the Vogt-Vogt school.
Brain structure & function, 2020Co-Authors: Rudolf Nieuwenhuys, Cees A. J. BroereAbstract:The comprehensive research programme of the Vogt-Vogt (V-V) school, which was active during the period 1900-1970, included detailed cytoarchitectonic and myeloarchitectonic analyses of the Human cerebral cortex, with the aim to integrate the data obtained into a map, showing a parcellation of the Human cerebral cortex into fundamental structural and potentially functional units. The cytoarchitectonic V-V analyses yielded two maps of the Human cerebral cortex, the famous map of Brodmann (Vergleichende Lokalisationslehre der Grosshirnrinde in ihren Prinzipien dargestellt auf Grund des Zellenbaues. Barth, Leipzig, 1909), Brodmann (in: Bruns P (ed) Neue deutsche Chirurgie, Enke, Stuttgart, 1914), and the less known, but more detailed map of Sarkisov et al. (Cytoarchitecture of the Human cortex cerebri. Medgiz, Moscow, 1949). Sarkisov et al. used in their cytoarchitectonic parcellation of the cortex the same numbering scheme as Brodmann. They confirmed the presence of most of the areas delineated by the latter, but they subdivided several of these areas into two or more separate areas or subareas. Within the realm of the myeloarchitectonic V-V analyses, numerous meticulous studies of the cortex of individual cerebral lobes were carried out, but these were not united into a single map. Consequently, the envisioned integration of cytoarchitectonic and myeloarchitectonic data mentioned above was never realized. Some years ago, we (Nieuwenhuys et al. in Brain Struct Funct 220:2551-2573, 2015a, Nieuwenhuys et al. in Brain Struct Funct 220:3753-3755, 2015b) reanalyzed the V-V myeloarchitectonic data, and succeeded in constructing a complete myeloarchitectonic map of the Human Neocortex from these data. Because the data provided by the V-V school were derived from many different brains, a standard brain had to be introduced as a template to which all data available could be transferred. As such the MNI305 template was selected. Having made available now the cytoarchitectonic maps of Brodmann and Sarkisov et al. and the recently prepared myeloarchitectonic map, an attempt is made here to realize at last the original aim of the V-V school, viz. the preparation of a single, combined (cyto + myelo) architectonic map of the Human cortex. To this end, the following three steps have been made. First, Brodmann's (BR) map, and the map of Sarkisov et al. (SA) were harmoniously transferred to the same template brain as the one used during the construction of our myeloarchitectonic map. Second, the standardized BR and our myeloarchitectonic (NI) map were compared, and the data contained within these maps were integrated into a single standardized combined BR-NI map (Fig. 11). The standardized SA and NI maps were subjected to the same procedure (Fig. 12). Finally, the standardized combined BR-NI and SA-NI maps were united into a single combined BR-SA-NI map (Fig. 13). This map renders it possible to make direct comparisons between the results of the architectonic studies of the V-V school and current parcellations of the Human Neocortex.
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A map of the Human Neocortex showing the estimated overall myelin content of the individual architectonic areas based on the studies of Adolf Hopf.
Brain structure & function, 2016Co-Authors: Rudolf Nieuwenhuys, Cees A. J. BroereAbstract:During the period extending from 1910 to 1970, Oscar and Cecile Vogt and their numerous collaborators published a large number of myeloarchitectonic studies on the cortex of the various lobes of the Human cerebrum. In a previous publication [Nieuwenhuys et al (Brain Struct Funct 220:2551-2573, 2015; Erratum in Brain Struct Funct 220: 3753-3755, 2015)], we used the data provided by the Vogt-Vogt school for the composition of a myeloarchitectonic map of the entire Human Neocortex. Because these data were derived from many different brains, a standard brain had to be introduced to which all data available could be transferred. As such the Colin 27 structural scan, aligned to the MNI305 template was selected. The resultant map includes 180 myeloarchitectonic areas, 64 frontal, 30 parietal, 6 insular, 17 occipital and 63 temporal. Here we present a supplementary map in which the overall density of the myelinated fibers in the individual architectonic areas is indicated, based on a meta-analysis of data provided by Adolf Hopf, a prominent collaborator of the Vogts. This map shows that the primary sensory and motor regions are densely myelinated and that, in general, myelination decreases stepwise with the distance from these primary regions. The map also reveals the presence of a number of heavily myelinated formations, situated beyond the primary sensory and motor domains, each consisting of two or more myeloarchitectonic areas. These formations were provisionally designated as the orbitofrontal, intraparietal, posterolateral temporal, and basal temporal dark clusters. Recently published MRI-based in vivo myelin content mappings show, with regard to the primary sensory and motor regions, a striking concordance with our map. As regards the heavily myelinated clusters shown by our map, scrutiny of the current literature revealed that correlates of all of these clusters have been identified in in vivo structural MRI studies and appear to correspond either entirely or largely to known cytoarchitectonic entities. Moreover, functional neuroimaging studies indicate that all of these clusters are involved in vision-related cognitive functions.
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A new myeloarchitectonic map of the Human Neocortex based on data from the Vogt–Vogt school
Brain Structure and Function, 2015Co-Authors: Rudolf Nieuwenhuys, Cees A. J. Broere, Leonardo CerlianiAbstract:The Human cerebral cortex contains numerous myelinated fibres, the arrangement and density of which is by no means homogeneous throughout the cortex. Local differences in the spatial organization of these fibres render it possible to recognize areas with a different myeloarchitecture. The neuroanatomical subdiscipline aimed at the identification and delineation of such areas is known as myeloarchitectonics. During the period extending from 1910 to 1970, Oscar and Cécile Vogt and their numerous collaborators (The Vogt–Vogt school) published a large number of myeloarchitectonic studies on the cortex of the various lobes of the Human cerebrum. Recently, one of us (Nieuwenhuys in Brain Struct Funct 218: 303–352, 2013 ) extensively reviewed these studies. It was concluded that the data available are adequate and sufficient for the composition of a myeloarchitectonic map of the entire Human Neocortex. The present paper is devoted to the creation of this map. Because the data provided by the Vogt–Vogt school are derived from many different brains, a standard brain had to be introduced to which all data available could be transferred. As such, the colin27 structural scan, aligned to the MNI305 template was selected. The procedure employed in this transfer involved computer-aided transformations of the lobar maps available in the literature, to the corresponding regions of the standard brain, as well as local adjustments in the border zones of the various lobes. The resultant map includes 180 myeloarchitectonic areas, 64 frontal, 30 parietal, 6 insular, 17 occipital and 63 temporal. The designation of the various areas with simple Arabic numbers, introduced by Oscar Vogt for the frontal and parietal cortices, has been extended over the entire Neocortex. It may be expected that combination of the myeloarchitectonic data of the Vogt–Vogt school, as expressed in our map, with the results of the detailed cytoarchitectonic and receptor architectonic studies of Karl Zilles and Katrin Amunts and their numerous associates, will yield a comprehensive ‘supermap’ of the structural organization of the Human Neocortex. For the time being, i. e., as long as this ‘supermap’ is not yet available, our map may provide a tentative frame of reference for (a) the morphological interpretation of the results of functional neuroimaging studies; (b) the selection of starting points (seed voxels, regions-of-interest) in diffusion tractography studies and (c) the interpretation of putative myeloarchitectonic features, visualized by in vivo and ex vivo mappings of the cerebral cortex with high-field magnetic resonance imaging.
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A new myeloarchitectonic map of the Human Neocortex based on data from the Vogt-Vogt school
Brain structure & function, 2014Co-Authors: Rudolf Nieuwenhuys, Cees A. J. Broere, Leonardo CerlianiAbstract:The Human cerebral cortex contains numerous myelinated fibres, the arrangement and density of which is by no means homogeneous throughout the cortex. Local differences in the spatial organization of these fibres render it possible to recognize areas with a different myeloarchitecture. The neuroanatomical subdiscipline aimed at the identification and delineation of such areas is known as myeloarchitectonics. During the period extending from 1910 to 1970, Oscar and Cecile Vogt and their numerous collaborators (The Vogt-Vogt school) published a large number of myeloarchitectonic studies on the cortex of the various lobes of the Human cerebrum. Recently, one of us (Nieuwenhuys in Brain Struct Funct 218: 303-352, 2013) extensively reviewed these studies. It was concluded that the data available are adequate and sufficient for the composition of a myeloarchitectonic map of the entire Human Neocortex. The present paper is devoted to the creation of this map. Because the data provided by the Vogt-Vogt school are derived from many different brains, a standard brain had to be introduced to which all data available could be transferred. As such, the colin27 structural scan, aligned to the MNI305 template was selected. The procedure employed in this transfer involved computer-aided transformations of the lobar maps available in the literature, to the corresponding regions of the standard brain, as well as local adjustments in the border zones of the various lobes. The resultant map includes 180 myeloarchitectonic areas, 64 frontal, 30 parietal, 6 insular, 17 occipital and 63 temporal. The designation of the various areas with simple Arabic numbers, introduced by Oscar Vogt for the frontal and parietal cortices, has been extended over the entire Neocortex. It may be expected that combination of the myeloarchitectonic data of the Vogt-Vogt school, as expressed in our map, with the results of the detailed cytoarchitectonic and receptor architectonic studies of Karl Zilles and Katrin Amunts and their numerous associates, will yield a comprehensive 'supermap' of the structural organization of the Human Neocortex. For the time being, i. e., as long as this 'supermap' is not yet available, our map may provide a tentative frame of reference for (a) the morphological interpretation of the results of functional neuroimaging studies; (b) the selection of starting points (seed voxels, regions-of-interest) in diffusion tractography studies and