oalib

Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99

Submit

Any time

2017 ( 1 )

2016 ( 1 )

2015 ( 5 )

2014 ( 11 )

Custom range...

Search Results: 1 - 10 of 95 matches for " Yuchio Yanagawa "
All listed articles are free for downloading (OA Articles)
Page 1 /95
Display every page Item
2,5-Dihydro-2,4,5-Trimethylthiazoline (TMT)-Induced Neuronal Activation Pattern and Behavioral Fear Response in GAD67 Mice  [PDF]
Kathrin Janitzky, Olaf Prellwitz, Herbert Schwegler, Yuchio Yanagawa, Thomas Roskoden
Journal of Behavioral and Brain Science (JBBS) , 2015, DOI: 10.4236/jbbs.2015.57032
Abstract: The synthetic predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) was used to induce innate fear in male GAD67 mice and behavioral changes were correlated with c-fos mRNA levels as marker for neuronal activation to reveal underlying activated fear circuits. Results show the same amount of increased freezing and decreased rearing and grooming behavior of TMT-exposed GAD67 mice and wild type littermates, and therefore suggest that heterozygous knock-in of GFP in the GAD67 gene that is associated with a fifty percent decreased GAD67 protein level in the brain, has no impact on TMT-induced behavioral effects. Exposure to TMT significantly increased the number of c-fos mRNA positive cells in the main olfactory bulb (MOB), the lateral septum (LS), the bed nucleus of the stria terminalis (BNST), the central amygdala (CeA), the anterior-ventral (MeAav), the anterior-dorsal (MeAad) and the posterior-ventral (MeApv) part of the medial amygdala in GAD67 mice. Thus, to further investigate the role of GABAergic neurons in TMT-induced uncontrollable stress responses GAD67 mice that provide the advantage of prelabeled GABAergic neurons through the GABA neuron specific expression of GFP could be a suitable model organism.
Local Connections of Layer 5 GABAergic Interneurons to Corticospinal Neurons
Yasuyo H. Tanaka,Yasuhiro R. Tanaka,Yuchio Yanagawa,Takeshi Kaneko
Frontiers in Neural Circuits , 2011, DOI: 10.3389/fncir.2011.00012
Abstract: In the local circuit of the cerebral cortex, GABAergic inhibitory interneurons are considered to work in collaboration with excitatory neurons. Although many interneuron subgroups have been described in the cortex, local inhibitory connections of each interneuron subgroup are only partially understood with respect to the functional neuron groups that receive these inhibitory connections. In the present study, we morphologically examined local inhibitory inputs to corticospinal neurons (CSNs) in motor areas using transgenic rats in which GABAergic neurons expressed fluorescent protein Venus. By analysis of biocytin-filled axons obtained with whole-cell recording/staining in cortical slices, we classified fast-spiking (FS) neurons in layer (L) 5 into two types, FS1 and FS2, by their high and low densities of axonal arborization, respectively. We then investigated the connections of FS1, FS2, somatostatin (SOM)-immunopositive, and other (non-FS/non-SOM) interneurons to CSNs that were retrogradely labeled in motor areas. When close appositions between the axon boutons of the intracellularly labeled interneurons and the somata/dendrites of the retrogradely labeled CSNs were examined electron-microscopically, 74% of these appositions made symmetric synaptic contacts. The axon boutons of single FS1 neurons were two- to fourfold more frequent in appositions to the somata/dendrites of CSNs than those of FS2, SOM, and non-FS/non-SOM neurons. Axosomatic appositions were most frequently formed with axon boutons of FS1 and FS2 neurons (approximately 30%) and least frequently formed with those of SOM neurons (7%). In contrast, SOM neurons most extensively sent axon boutons to the apical dendrites of CSNs. These results might suggest that motor outputs are controlled differentially by the subgroups of L5 GABAergic interneurons in cortical motor areas.
Roles of taurine-mediated tonic GABAA receptor activation in the radial migration of neurons in the fetal mouse cerebral cortex
Tomonori Furukawa,Junko Yamada,Tenpei Akita,Yuchio Yanagawa,Atsuo Fukuda
Frontiers in Cellular Neuroscience , 2014, DOI: 10.3389/fncel.2014.00088
Abstract: γ-Aminobutyric acid (GABA) depolarizes embryonic cerebrocortical neurons and continuous activation of the GABAA receptor (GABAAR) contributes to their tonic depolarization. Although multiple reports have demonstrated a role of GABAAR activation in neocortical development, including in migration, most of these studies have used pharmacological blockers. Herein, we performed in utero electroporation in GABA synthesis-lacking homozygous GAD67-GFP knock-in mice (GAD67GFP/GFP) to label neurons born in the ventricular zone. Three days after electroporation, there were no differences in the distribution of labeled cells between the genotypes. The dose–response properties of labeled cells to GABA were equivalent among genotypes. However, continuous blockade of GABAAR with the GABAAR antagonist SR95531 accelerated radial migration. This effect of GABAAR blockade in GAD67GFP/GFP mice suggested a role for alternative endogenous GABAAR agonists. Thus, we tested the role of taurine, which is derived from maternal blood but is abundant in the fetal brain. The taurine-evoked currents in labeled cells were mediated by GABAAR. Taurine uptake was blocked by a taurine transporter inhibitor, 2-(guanidino)ethanesulfonic acid (GES), and taurine release was blocked by a volume-sensitive anion channel blocker, 4-(2-butyl-6,7-dichlor-2-cyclopentylindan-1-on-5-yl) oxobutyric acid, as examined through high-performance liquid chromatography. GES increased the extracellular taurine concentration and induced an inward shift of the holding current, which was reversed by SR95531. In a taurine-deficient mouse model, the GABAAR-mediated tonic currents were greatly reduced, and radial migration was accelerated. As the tonic currents were equivalent among the genotypes of GAD67-GFP knock-in mice, taurine, rather than GABA, might play a major role as an endogenous agonist of embryonic tonic GABAAR conductance, regulating the radial migration of neurons in the developing neocortex.
Sour Taste Responses in Mice Lacking PKD Channels
Nao Horio,Ryusuke Yoshida,Keiko Yasumatsu,Yuchio Yanagawa,Yoshiro Ishimaru,Hiroaki Matsunami,Yuzo Ninomiya
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0020007
Abstract: The polycystic kidney disease-like ion channel PKD2L1 and its associated partner PKD1L3 are potential candidates for sour taste receptors. PKD2L1 is expressed in type III taste cells that respond to sour stimuli and genetic elimination of cells expressing PKD2L1 substantially reduces chorda tympani nerve responses to sour taste stimuli. However, the contribution of PKD2L1 and PKD1L3 to sour taste responses remains unclear.
Identification of a Neuropeptide S Responsive Circuitry Shaping Amygdala Activity via the Endopiriform Nucleus
Susanne Meis, Jorge Ricardo Bergado-Acosta, Yuchio Yanagawa, Kunihiko Obata, Oliver Stork, Thomas Munsch
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002695
Abstract: Neuropeptide S (NPS) and its receptor are thought to define a set of specific brain circuits involved in fear and anxiety. Here we provide evidence for a novel, NPS-responsive circuit that shapes neural activity in the mouse basolateral amygdala (BLA) via the endopiriform nucleus (EPN). Using slice preparations, we demonstrate that NPS directly activates an inward current in 20% of EPN neurons and evokes an increase of glutamatergic excitation in this nucleus. Excitation of the EPN is responsible for a modulation of BLA activity through NPS, characterized by a general increase of GABAergic inhibition and enhancement of spike activity in a subset of BLA projection neurons. Finally, local injection of NPS to the EPN interferes with the expression of contextual, but not auditory cued fear memory. Together, these data suggest the existence of a specific NPS-responsive circuitry between EPN and BLA, likely involved in contextual aspects of fear memory.
The role of the t-SNARE SNAP-25 in action potential-dependent calcium signaling and expression in GABAergic and glutamatergic neurons
Lawrence CR Tafoya, C William Shuttleworth, Yuchio Yanagawa, Kunihiko Obata, Michael C Wilson
BMC Neuroscience , 2008, DOI: 10.1186/1471-2202-9-105
Abstract: We found that neurons cultured from Snap25 homozygous null mutant (Snap25-/-) mice failed to develop synchronous network activity seen as spontaneous AP-dependent calcium oscillations and were unable to trigger glial transients following depolarization. Voltage-gated calcium channel (VGCC) mediated calcium transients evoked by depolarization, nevertheless, did not differ between soma of SNAP-25 deficient and control neurons. Furthermore, we observed that although the expression of SNAP-25 RNA transcripts varied among neuronal populations in adult brain, the relative ratio of the transcripts encoding alternatively spliced SNAP-25 variant isoforms was not different in GABAergic and glutamatergic neurons.We propose that the SNAP-25b isoform is predominantly expressed by both mature glutamatergic and GABAergic neurons and serves as a fundamental component of SNARE complex used for fast synaptic communication in excitatory and inhibitory circuits required for brain function. Moreover, SNAP-25 is required for neurons to establish AP-evoked synchronous network activity, as measured by calcium transients, whereas the loss of this t-SNARE does not affect voltage-dependent calcium entry.Regulated neurotransmission at chemical synapses underlies neural communication and is likely to contribute to complex brain functions, such as synaptic plasticity and memory storage. Neurotransmitter release requires fusion of synaptic vesicles that is mediated by the neuronal SNARE complex at release sites of presynaptic terminals [for review, see ref. [1,2]]. This core heteromeric protein assembly, comprised of the t-SNAREs syntaxin 1, and SNAP-25 situated at the target or plasma membrane and the v-SNARE VAMP-2/synaptobrevin on secreting vesicles, is responsible for membrane fusion that underlies the Ca2+-triggered neuroexocytosis that is required for AP-dependent neurotransmission signaling point-to-point communication between neurons, as well as the regulated secretion from neuroendocrine
Genetic Deficiency of GABA Differentially Regulates Respiratory and Non-Respiratory Motor Neuron Development
Matthew J. Fogarty, Karen L. Smallcombe, Yuchio Yanagawa, Kunihiko Obata, Mark C. Bellingham, Peter G. Noakes
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056257
Abstract: Central nervous system GABAergic and glycinergic synaptic activity switches from postsynaptic excitation to inhibition during the stage when motor neuron numbers are being reduced, and when synaptic connections are being established onto and by motor neurons. In mice this occurs between embryonic (E) day 13 and birth (postnatal day 0). Our previous work on mice lacking glycinergic transmission suggested that altered motor neuron activity levels correspondingly regulated motor neuron survival and muscle innervation for all respiratory and non respiratory motor neuron pools, during this period of development [1]. To determine if GABAergic transmission plays a similar role, we quantified motor neuron number and the extent of muscle innervation in four distinct regions of the brain stem and spinal cord; hypoglossal, phrenic, brachial and lumbar motor pools, in mice lacking the enzyme GAD67. These mice display a 90% drop in CNS GABA levels ( [2]; this study). For respiratory-based motor neurons (hypoglossal and phrenic motor pools), we have observed significant drops in motor neuron number (17% decline for hypoglossal and 23% decline for phrenic) and muscle innervations (55% decrease). By contrast for non-respiratory motor neurons of the brachial lateral motor column, we have observed an increase in motor neuron number (43% increase) and muscle innervations (99% increase); however for more caudally located motor neurons within the lumbar lateral motor column, we observed no change in either neuron number or muscle innervation. These results show in mice lacking physiological levels of GABA, there are distinct regional changes in motor neuron number and muscle innervation, which appear to be linked to their physiological function and to their rostral-caudal position within the developing spinal cord. Our results also suggest that for more caudal (lumbar) regions of the spinal cord, the effect of GABA is less influential on motor neuron development compared to that of glycine.
GABA Regulates the Multidirectional Tangential Migration of GABAergic Interneurons in Living Neonatal Mice
Hiroyuki Inada, Miho Watanabe, Taku Uchida, Hitoshi Ishibashi, Hiroaki Wake, Tomomi Nemoto, Yuchio Yanagawa, Atsuo Fukuda, Junichi Nabekura
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027048
Abstract: Cortical GABAergic interneurons originate from ganglionic eminences and tangentially migrate into the cortical plate at early developmental stages. To elucidate the characteristics of this migration of GABAergic interneurons in living animals, we established an experimental design specialized for in vivo time-lapse imaging of the neocortex of neonate mice with two-photon laser-scanning microscopy. In vesicular GABA/glycine transporter (VGAT)-Venus transgenic mice from birth (P0) through P3, we observed multidirectional tangential migration of genetically-defined GABAergic interneurons in the neocortical marginal zone. The properties of this migration, such as the motility rate (distance/hr), the direction moved, and the proportion of migrating neurons to stationary neurons, did not change through P0 to P3, although the density of GABAergic neurons at the marginal zone decreased with age. Thus, the characteristics of the tangential motility of individual GABAergic neurons remained constant in development. Pharmacological block of GABAA receptors and of the Na+-K+-Cl? cotransporters, and chelating intracellular Ca2+, all significantly reduced the motility rate in vivo. The motility rate and GABA content within the cortex of neonatal VGAT-Venus transgenic mice were significantly greater than those of GAD67-GFP knock-in mice, suggesting that extracellular GABA concentration could facilitate the multidirectional tangential migration. Indeed, diazepam applied to GAD67-GFP mice increased the motility rate substantially. In an in vitro neocortical slice preparation, we confirmed that GABA induced a NKCC sensitive depolarization of GABAergic interneurons in VGAT-Venus mice at P0-P3. Thus, activation of GABAAR by ambient GABA depolarizes GABAergic interneurons, leading to an acceleration of their multidirectional motility in vivo.
Cerebellar Globular Cells Receive Monoaminergic Excitation and Monosynaptic Inhibition from Purkinje Cells
Moritoshi Hirono, Fumihito Saitow, Moeko Kudo, Hidenori Suzuki, Yuchio Yanagawa, Masahisa Yamada, Soichi Nagao, Shiro Konishi, Kunihiko Obata
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0029663
Abstract: Inhibitory interneurons in the cerebellar granular layer are more heterogeneous than traditionally depicted. In contrast to Golgi cells, which are ubiquitously distributed in the granular layer, small fusiform Lugaro cells and globular cells are located underneath the Purkinje cell layer and small in number. Globular cells have not been characterized physiologically. Here, using cerebellar slices obtained from a strain of gene-manipulated mice expressing GFP specifically in GABAergic neurons, we morphologically identified globular cells, and compared their synaptic activity and monoaminergic influence of their electrical activity with those of small Golgi cells and small fusiform Lugaro cells. Globular cells were characterized by prominent IPSCs together with monosynaptic inputs from the axon collaterals of Purkinje cells, whereas small Golgi cells or small fusiform Lugaro cells displayed fewer and smaller spontaneous IPSCs. Globular cells were silent at rest and fired spike discharges in response to application of either serotonin (5-HT) or noradrenaline. The two monoamines also facilitated small Golgi cell firing, but only 5-HT elicited firing in small fusiform Lugaro cells. Furthermore, globular cells likely received excitatory monosynaptic inputs through mossy fibers. Because globular cells project their axons long in the transversal direction, the neuronal circuit that includes interplay between Purkinje cells and globular cells could regulate Purkinje cell activity in different microzones under the influence of monoamines and mossy fiber inputs, suggesting that globular cells likely play a unique modulatory role in cerebellar motor control.
Transient Neuronal Populations Are Required to Guide Callosal Axons: A Role for Semaphorin 3C
Mathieu Niquille,Sonia Garel,Fanny Mann,Jean-Pierre Hornung,Belkacem Otsmane,Sébastien Chevalley,Carlos Parras,Francois Guillemot,Patricia Gaspar,Yuchio Yanagawa,Cécile Lebrand
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000230
Abstract: The corpus callosum (CC) is the main pathway responsible for interhemispheric communication. CC agenesis is associated with numerous human pathologies, suggesting that a range of developmental defects can result in abnormalities in this structure. Midline glial cells are known to play a role in CC development, but we here show that two transient populations of midline neurons also make major contributions to the formation of this commissure. We report that these two neuronal populations enter the CC midline prior to the arrival of callosal pioneer axons. Using a combination of mutant analysis and in vitro assays, we demonstrate that CC neurons are necessary for normal callosal axon navigation. They exert an attractive influence on callosal axons, in part via Semaphorin 3C and its receptor Neuropilin-1. By revealing a novel and essential role for these neuronal populations in the pathfinding of a major cerebral commissure, our study brings new perspectives to pathophysiological mechanisms altering CC formation.
Page 1 /95
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.