The Experts below are selected from a list of 69 Experts worldwide ranked by ideXlab platform

Atsuo Fukuda - One of the best experts on this subject based on the ideXlab platform.

  • Accumulation of GABAergic Neurons, Causing a Focal Ambient GABA Gradient, and Downregulation of KCC2 Are Induced During Microgyrus Formation in a Mouse Model
    2016
    Co-Authors: Of Polymicrogyria, Tianying Wang, Tatsuro Kumada, Toshitaka Morishima, Satomi Iwata, Takeshi Kaneko, Yuchio Yanagawa, Sachiko Yoshida, Atsuo Fukuda
    Abstract:

    Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration under-lying such malformations. A focal freeze-lesion (FFL) of the post-natal day zero (P0) glutamic acid decarboxylase–green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered micro-gyrus at P7. GABAergic interneurons accumulated around the necro-sis including the superficial region during Microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 Microgyrus. GABA imaging showed that an extracellular GABA level temporally in-creased in the GABAergic neuron-positive area, including the necro-tic center, at P4. The expression of the Cl – transporter KCC2 wa

  • accumulation of gabaergic neurons causing a focal ambient gaba gradient and downregulation of kcc2 are induced during Microgyrus formation in a mouse model of polymicrogyria
    Cerebral Cortex, 2014
    Co-Authors: Tianying Wang, Tatsuro Kumada, Toshitaka Morishima, Satomi Iwata, Takeshi Kaneko, Yuchio Yanagawa, Sachiko Yoshida, Atsuo Fukuda
    Abstract:

    Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration underlying such malformations. A focal freeze-lesion (FFL) of the postnatal day zero (P0) glutamic acid decarboxylase–green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered Microgyrus at P7. GABAergic interneurons accumulated around the necrosis including the superficial region during Microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 Microgyrus. GABA imaging showed that an extracellular GABA level temporally increased in the GABAergic neuron-positive area, including the necrotic center, at P4. The expression of the Cl – transporter KCC2 was downregulated in the Microgyrus-forming GABAergic and E17.5born glutamatergic neurons at P4; these cells may need a high intracellular Cl – concentration to induce depolarizing GABA effects. Bicuculline decreased the frequency of spontaneous Ca 2+ oscillations in these Microgyrus-forming cells. Thus, neonatal FFL causes specific neuronal accumulation, preceded by an increase in ambient GABA during Microgyrus formation. This GABA increase induces GABAA receptor-mediated Ca 2+ oscillation in KCC2-downregulated Microgyrus-forming cells, as seen in migrating cells during early neocortical development.

  • changes in the expression of cation cl cotransporters nkcc1 and kcc2 during cortical malformation induced by neonatal freeze lesion
    Neuroscience Research, 2007
    Co-Authors: Chigusa Shimizuokabe, Akihito Okabe, Werner Kilb, Kohji Sato, Heiko J Luhmann, Atsuo Fukuda
    Abstract:

    Focal cortical malformations comprise a heterogeneous group of disturbances in brain development, often associated with intractable epilepsy. A focal freeze-lesion of cerebral cortex in newborn rat produces a cortical malformation that resembles human polymicrogyria, clinical conditions that results from abnormal neuronal migration. The change in GABAergic functions that occurs during early brain development is induced by an alteration in Cl− homeostasis and plays important roles in neocortical development by modulating such events as laminar organization and synaptogenesis. We therefore investigated the relationship between pathogenesis of polymicrogyria and ontogeny of Cl− homeostasis in developing parietal cortex after creation of a freeze-lesion at P0. We demonstrated, by in situ hybridization histochemistry for cation-Cl− cotrtansporters, that NKCC1 mRNA expression was upregulated and KCC2 mRNA expression downregulated at P4 in “bridge” structure (formed in lesion site across the gap in intact exofocal cortex) as compared to exfocal cortex. Immunohistochemical investigation revealed a colocalization of NKCC1 and neuron specific enolase (NSE) within this structure, while BrdU-positive cells express GFAP and NKCC1 appeared beneath it. These results suggest that immature cortical plate neurons might produce “bridge” structure during formation of Microgyrus, and that altered neuronal Cl− homeostasis might be involved in neuronal migration disorder that ultimately results in cortical malformations.

John R Huguenard - One of the best experts on this subject based on the ideXlab platform.

  • Advance Access publication March 25, 2010 Enhanced Infragranular and Supragranular Synaptic Input onto Layer 5 Pyramidal Neurons in a Rat Model of Cortical Dysplasia
    2016
    Co-Authors: Julia Brill, John R Huguenard
    Abstract:

    Cortical dysplasias frequently underlie neurodevelopmental disorders and epilepsy. Rats with a neonatally induced cortical Microgyrus [freeze-lesion (FL)], a model of human polymicrogyria, display epileptiform discharges in vitro. We probed excitatory and inhibitory connectivity onto neocortical pyramidal neurons in layers 2/3 and 5 of postnatal day 16--22 rats, approximately 1--2 mm lateral of the lesion, using laser scanning photostimulation (LSPS)/glutamate uncaging. Excitatory input from deep and supragranular layers to layer 5 pyramidal cells was greater in FL cortex, while no significant differences were seen in layer 2/3 cells. The increased input was due to a greater number of LSPS-evoked excitatory postsynaptic currents (EPSCs), without differences in amplitude or kinetics. Inhibitory input was increased in a region-specific manner in pyramidal cells in FL cortex, due to an increased inhibitory postsynaptic current (IPSC) amplitude. Connectivity within layer 5, parts of which are destroyed during lesioning, was more severely affected than connectivity in layer 2/3. Thus, we observed 2 distinct mechanisms of altered synaptic input: 1) increased EPSC frequency suggesting an increased number of excitatory synapses and 2) higher IPSC amplitude, suggesting an increased strength of inhibitory synapses. These increases in both excitatory and inhibitory connectivity may limit the extent of circuit hyperexcitability

  • Cerebral Cortex doi:10.1093/cercor/bhq040 Enhanced Infragranular and Supragranular Synaptic Input onto Layer 5 Pyramidal Neurons in a Rat Model of Cortical Dysplasia
    2016
    Co-Authors: Julia Brill, John R Huguenard
    Abstract:

    Cortical dysplasias frequently underlie neurodevelopmental disorders and epilepsy. Rats with a neonatally induced cortical Microgyrus [freeze-lesion (FL)], a model of human polymicrogyria, display epileptiform discharges in vitro. We probed excitatory and inhibitory connectivity onto neocortical pyramidal neurons in layers 2/3 and 5 of postnatal day 16--22 rats, approximately 1--2 mm lateral of the lesion, using laser scanning photostimulation (LSPS)/glutamate uncaging. Excitatory input from deep and supragranular layers to layer 5 pyramidal cells was greater in FL cortex, while no significant differences were seen in layer 2/3 cells. The increased input was due to a greater number of LSPS-evoked excitatory postsynaptic currents (EPSCs), without differences in amplitude or kinetics. Inhibitory input was increased in a region-specific manner in pyramidal cells in FL cortex, due to an increased inhibitory postsynaptic current (IPSC) amplitude. Connectivity within layer 5, parts of which are destroyed during lesioning, was more severely affected than connectivity in layer 2/3. Thus, we observed 2 distinct mechanisms of altered synaptic input: 1) increased EPSC frequency suggesting an increased number of excitatory synapses and 2) higher IPSC amplitude, suggesting an increased strength of inhibitory synapses. These increases in both excitatory and inhibitory connectivity may limit the extent of circuit hyperexcitability

  • enhanced infragranular and supragranular synaptic input onto layer 5 pyramidal neurons in a rat model of cortical dysplasia
    Cerebral Cortex, 2010
    Co-Authors: Julia Brill, John R Huguenard
    Abstract:

    Cortical dysplasias frequently underlie neurodevelopmental disorders and epilepsy. Rats with a neonatally induced cortical Microgyrus [freeze-lesion (FL)], a model of human polymicrogyria, display epileptiform discharges in vitro. We probed excitatory and inhibitory connectivity onto neocortical pyramidal neurons in layers 2/3 and 5 of postnatal day 16-22 rats, approximately 1-2 mm lateral of the lesion, using laser scanning photostimulation (LSPS)/glutamate uncaging. Excitatory input from deep and supragranular layers to layer 5 pyramidal cells was greater in FL cortex, while no significant differences were seen in layer 2/3 cells. The increased input was due to a greater number of LSPS-evoked excitatory postsynaptic currents (EPSCs), without differences in amplitude or kinetics. Inhibitory input was increased in a region-specific manner in pyramidal cells in FL cortex, due to an increased inhibitory postsynaptic current (IPSC) amplitude. Connectivity within layer 5, parts of which are destroyed during lesioning, was more severely affected than connectivity in layer 2/3. Thus, we observed 2 distinct mechanisms of altered synaptic input: 1) increased EPSC frequency suggesting an increased number of excitatory synapses and 2) higher IPSC amplitude, suggesting an increased strength of inhibitory synapses. These increases in both excitatory and inhibitory connectivity may limit the extent of circuit hyperexcitability.

Tianying Wang - One of the best experts on this subject based on the ideXlab platform.

  • Accumulation of GABAergic Neurons, Causing a Focal Ambient GABA Gradient, and Downregulation of KCC2 Are Induced During Microgyrus Formation in a Mouse Model
    2016
    Co-Authors: Of Polymicrogyria, Tianying Wang, Tatsuro Kumada, Toshitaka Morishima, Satomi Iwata, Takeshi Kaneko, Yuchio Yanagawa, Sachiko Yoshida, Atsuo Fukuda
    Abstract:

    Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration under-lying such malformations. A focal freeze-lesion (FFL) of the post-natal day zero (P0) glutamic acid decarboxylase–green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered micro-gyrus at P7. GABAergic interneurons accumulated around the necro-sis including the superficial region during Microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 Microgyrus. GABA imaging showed that an extracellular GABA level temporally in-creased in the GABAergic neuron-positive area, including the necro-tic center, at P4. The expression of the Cl – transporter KCC2 wa

  • accumulation of gabaergic neurons causing a focal ambient gaba gradient and downregulation of kcc2 are induced during Microgyrus formation in a mouse model of polymicrogyria
    Cerebral Cortex, 2014
    Co-Authors: Tianying Wang, Tatsuro Kumada, Toshitaka Morishima, Satomi Iwata, Takeshi Kaneko, Yuchio Yanagawa, Sachiko Yoshida, Atsuo Fukuda
    Abstract:

    Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration underlying such malformations. A focal freeze-lesion (FFL) of the postnatal day zero (P0) glutamic acid decarboxylase–green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered Microgyrus at P7. GABAergic interneurons accumulated around the necrosis including the superficial region during Microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 Microgyrus. GABA imaging showed that an extracellular GABA level temporally increased in the GABAergic neuron-positive area, including the necrotic center, at P4. The expression of the Cl – transporter KCC2 was downregulated in the Microgyrus-forming GABAergic and E17.5born glutamatergic neurons at P4; these cells may need a high intracellular Cl – concentration to induce depolarizing GABA effects. Bicuculline decreased the frequency of spontaneous Ca 2+ oscillations in these Microgyrus-forming cells. Thus, neonatal FFL causes specific neuronal accumulation, preceded by an increase in ambient GABA during Microgyrus formation. This GABA increase induces GABAA receptor-mediated Ca 2+ oscillation in KCC2-downregulated Microgyrus-forming cells, as seen in migrating cells during early neocortical development.

Julia Brill - One of the best experts on this subject based on the ideXlab platform.

  • Advance Access publication March 25, 2010 Enhanced Infragranular and Supragranular Synaptic Input onto Layer 5 Pyramidal Neurons in a Rat Model of Cortical Dysplasia
    2016
    Co-Authors: Julia Brill, John R Huguenard
    Abstract:

    Cortical dysplasias frequently underlie neurodevelopmental disorders and epilepsy. Rats with a neonatally induced cortical Microgyrus [freeze-lesion (FL)], a model of human polymicrogyria, display epileptiform discharges in vitro. We probed excitatory and inhibitory connectivity onto neocortical pyramidal neurons in layers 2/3 and 5 of postnatal day 16--22 rats, approximately 1--2 mm lateral of the lesion, using laser scanning photostimulation (LSPS)/glutamate uncaging. Excitatory input from deep and supragranular layers to layer 5 pyramidal cells was greater in FL cortex, while no significant differences were seen in layer 2/3 cells. The increased input was due to a greater number of LSPS-evoked excitatory postsynaptic currents (EPSCs), without differences in amplitude or kinetics. Inhibitory input was increased in a region-specific manner in pyramidal cells in FL cortex, due to an increased inhibitory postsynaptic current (IPSC) amplitude. Connectivity within layer 5, parts of which are destroyed during lesioning, was more severely affected than connectivity in layer 2/3. Thus, we observed 2 distinct mechanisms of altered synaptic input: 1) increased EPSC frequency suggesting an increased number of excitatory synapses and 2) higher IPSC amplitude, suggesting an increased strength of inhibitory synapses. These increases in both excitatory and inhibitory connectivity may limit the extent of circuit hyperexcitability

  • Cerebral Cortex doi:10.1093/cercor/bhq040 Enhanced Infragranular and Supragranular Synaptic Input onto Layer 5 Pyramidal Neurons in a Rat Model of Cortical Dysplasia
    2016
    Co-Authors: Julia Brill, John R Huguenard
    Abstract:

    Cortical dysplasias frequently underlie neurodevelopmental disorders and epilepsy. Rats with a neonatally induced cortical Microgyrus [freeze-lesion (FL)], a model of human polymicrogyria, display epileptiform discharges in vitro. We probed excitatory and inhibitory connectivity onto neocortical pyramidal neurons in layers 2/3 and 5 of postnatal day 16--22 rats, approximately 1--2 mm lateral of the lesion, using laser scanning photostimulation (LSPS)/glutamate uncaging. Excitatory input from deep and supragranular layers to layer 5 pyramidal cells was greater in FL cortex, while no significant differences were seen in layer 2/3 cells. The increased input was due to a greater number of LSPS-evoked excitatory postsynaptic currents (EPSCs), without differences in amplitude or kinetics. Inhibitory input was increased in a region-specific manner in pyramidal cells in FL cortex, due to an increased inhibitory postsynaptic current (IPSC) amplitude. Connectivity within layer 5, parts of which are destroyed during lesioning, was more severely affected than connectivity in layer 2/3. Thus, we observed 2 distinct mechanisms of altered synaptic input: 1) increased EPSC frequency suggesting an increased number of excitatory synapses and 2) higher IPSC amplitude, suggesting an increased strength of inhibitory synapses. These increases in both excitatory and inhibitory connectivity may limit the extent of circuit hyperexcitability

  • enhanced infragranular and supragranular synaptic input onto layer 5 pyramidal neurons in a rat model of cortical dysplasia
    Cerebral Cortex, 2010
    Co-Authors: Julia Brill, John R Huguenard
    Abstract:

    Cortical dysplasias frequently underlie neurodevelopmental disorders and epilepsy. Rats with a neonatally induced cortical Microgyrus [freeze-lesion (FL)], a model of human polymicrogyria, display epileptiform discharges in vitro. We probed excitatory and inhibitory connectivity onto neocortical pyramidal neurons in layers 2/3 and 5 of postnatal day 16-22 rats, approximately 1-2 mm lateral of the lesion, using laser scanning photostimulation (LSPS)/glutamate uncaging. Excitatory input from deep and supragranular layers to layer 5 pyramidal cells was greater in FL cortex, while no significant differences were seen in layer 2/3 cells. The increased input was due to a greater number of LSPS-evoked excitatory postsynaptic currents (EPSCs), without differences in amplitude or kinetics. Inhibitory input was increased in a region-specific manner in pyramidal cells in FL cortex, due to an increased inhibitory postsynaptic current (IPSC) amplitude. Connectivity within layer 5, parts of which are destroyed during lesioning, was more severely affected than connectivity in layer 2/3. Thus, we observed 2 distinct mechanisms of altered synaptic input: 1) increased EPSC frequency suggesting an increased number of excitatory synapses and 2) higher IPSC amplitude, suggesting an increased strength of inhibitory synapses. These increases in both excitatory and inhibitory connectivity may limit the extent of circuit hyperexcitability.

Sachiko Yoshida - One of the best experts on this subject based on the ideXlab platform.

  • Accumulation of GABAergic Neurons, Causing a Focal Ambient GABA Gradient, and Downregulation of KCC2 Are Induced During Microgyrus Formation in a Mouse Model
    2016
    Co-Authors: Of Polymicrogyria, Tianying Wang, Tatsuro Kumada, Toshitaka Morishima, Satomi Iwata, Takeshi Kaneko, Yuchio Yanagawa, Sachiko Yoshida, Atsuo Fukuda
    Abstract:

    Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration under-lying such malformations. A focal freeze-lesion (FFL) of the post-natal day zero (P0) glutamic acid decarboxylase–green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered micro-gyrus at P7. GABAergic interneurons accumulated around the necro-sis including the superficial region during Microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 Microgyrus. GABA imaging showed that an extracellular GABA level temporally in-creased in the GABAergic neuron-positive area, including the necro-tic center, at P4. The expression of the Cl – transporter KCC2 wa

  • accumulation of gabaergic neurons causing a focal ambient gaba gradient and downregulation of kcc2 are induced during Microgyrus formation in a mouse model of polymicrogyria
    Cerebral Cortex, 2014
    Co-Authors: Tianying Wang, Tatsuro Kumada, Toshitaka Morishima, Satomi Iwata, Takeshi Kaneko, Yuchio Yanagawa, Sachiko Yoshida, Atsuo Fukuda
    Abstract:

    Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration underlying such malformations. A focal freeze-lesion (FFL) of the postnatal day zero (P0) glutamic acid decarboxylase–green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered Microgyrus at P7. GABAergic interneurons accumulated around the necrosis including the superficial region during Microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 Microgyrus. GABA imaging showed that an extracellular GABA level temporally increased in the GABAergic neuron-positive area, including the necrotic center, at P4. The expression of the Cl – transporter KCC2 was downregulated in the Microgyrus-forming GABAergic and E17.5born glutamatergic neurons at P4; these cells may need a high intracellular Cl – concentration to induce depolarizing GABA effects. Bicuculline decreased the frequency of spontaneous Ca 2+ oscillations in these Microgyrus-forming cells. Thus, neonatal FFL causes specific neuronal accumulation, preceded by an increase in ambient GABA during Microgyrus formation. This GABA increase induces GABAA receptor-mediated Ca 2+ oscillation in KCC2-downregulated Microgyrus-forming cells, as seen in migrating cells during early neocortical development.