The Experts below are selected from a list of 104922 Experts worldwide ranked by ideXlab platform
Helmut Kettenmann - One of the best experts on this subject based on the ideXlab platform.
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the principal neurons of the medial nucleus of the trapezoid body and ng2 Glial cells receive coordinated excitatory synaptic input
The Journal of General Physiology, 2009Co-Authors: Jochen Müller, Daniel Reyesharo, Tatjyana Pivneva, Joachim Lubke, Christiane Nolte, Roland Schaette, Helmut KettenmannAbstract:Glial cell processes are part of the synaptic structure and sense spillover of transmitter, while some Glial cells can even receive direct synaptic input. Here, we report that a defined type of Glial cell in the medial nucleus of the trapezoid body (MNTB) receives excitatory glutamatergic synaptic input from the calyx of Held (CoH). This giant glutamatergic terminal forms an axosomatic synapse with a single principal neuron located in the MNTB. The NG2 Glia, as postsynaptic principal neurons, establish synapse-like structures with the CoH terminal. In contrast to the principal neurons, which are known to receive excitatory as well as inhibitory inputs, the NG2 Glia receive mostly, if not exclusively, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor–mediated evoked and spontaneous synaptic input. Simultaneous recordings from neurons and NG2 Glia indicate that they partially receive synchronized spontaneous input. This shows that an NG2+ Glial cell and a postsynaptic neuron share presynaptic terminals.
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The principal neurons of the medial nucleus of the trapezoid body and NG2(+) Glial cells receive coordinated excitatory synaptic input.
The Journal of General Physiology, 2009Co-Authors: Jochen Müller, Tatjyana Pivneva, Joachim Lubke, Daniel Reyes-haro, Christiane Nolte, Roland Schaette, Helmut KettenmannAbstract:Glial cell processes are part of the synaptic structure and sense spillover of transmitter, while some Glial cells can even receive direct synaptic input. Here, we report that a defined type of Glial cell in the medial nucleus of the trapezoid body (MNTB) receives excitatory glutamatergic synaptic input from the calyx of Held (CoH). This giant glutamatergic terminal forms an axosomatic synapse with a single principal neuron located in the MNTB. The NG2 Glia, as postsynaptic principal neurons, establish synapse-like structures with the CoH terminal. In contrast to the principal neurons, which are known to receive excitatory as well as inhibitory inputs, the NG2 Glia receive mostly, if not exclusively, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor–mediated evoked and spontaneous synaptic input. Simultaneous recordings from neurons and NG2 Glia indicate that they partially receive synchronized spontaneous input. This shows that an NG2+ Glial cell and a postsynaptic neuron share presynaptic terminals.
Mirjana Maleticsavatic - One of the best experts on this subject based on the ideXlab platform.
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the Glia neuron lactate shuttle and elevated ros promote lipid synthesis in neurons and lipid droplet accumulation in Glia via apoe d
Cell Metabolism, 2017Co-Authors: Kevin R. Mackenzie, Mirjana Maleticsavatic, Nagireddy Putluri, Hugo Jozef BellenAbstract:Summary Elevated reactive oxygen species (ROS) induce the formation of lipids in neurons that are transferred to Glia, where they form lipid droplets (LDs). We show that Glial and neuronal monocarboxylate transporters (MCTs), fatty acid transport proteins (FATPs), and apolipoproteins are critical for Glial LD formation. MCTs enable Glia to secrete and neurons to absorb lactate, which is converted to pyruvate and acetyl-CoA in neurons. Lactate metabolites provide a substrate for synthesis of fatty acids, which are processed and transferred to Glia by FATP and apolipoproteins. In the presence of high ROS, inhibiting lactate transfer or lowering FATP or apolipoprotein levels decreases Glial LD accumulation in flies and in primary mouse Glial-neuronal cultures. We show that human APOE can substitute for a fly Glial apolipoprotein and that APOE4, an Alzheimer's disease susceptibility allele, is impaired in lipid transport and promotes neurodegeneration, providing insights into disease mechanisms.
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the Glia neuron lactate shuttle and elevated ros promote lipid synthesis in neurons and lipid droplet accumulation in Glia via apoe d
Cell Metabolism, 2017Co-Authors: Kevin R. Mackenzie, Mirjana Maleticsavatic, Nagireddy Putluri, Hugo J. BellenAbstract:Summary Elevated reactive oxygen species (ROS) induce the formation of lipids in neurons that are transferred to Glia, where they form lipid droplets (LDs). We show that Glial and neuronal monocarboxylate transporters (MCTs), fatty acid transport proteins (FATPs), and apolipoproteins are critical for Glial LD formation. MCTs enable Glia to secrete and neurons to absorb lactate, which is converted to pyruvate and acetyl-CoA in neurons. Lactate metabolites provide a substrate for synthesis of fatty acids, which are processed and transferred to Glia by FATP and apolipoproteins. In the presence of high ROS, inhibiting lactate transfer or lowering FATP or apolipoprotein levels decreases Glial LD accumulation in flies and in primary mouse Glial-neuronal cultures. We show that human APOE can substitute for a fly Glial apolipoprotein and that APOE4, an Alzheimer's disease susceptibility allele, is impaired in lipid transport and promotes neurodegeneration, providing insights into disease mechanisms.
Kevin R. Mackenzie - One of the best experts on this subject based on the ideXlab platform.
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the Glia neuron lactate shuttle and elevated ros promote lipid synthesis in neurons and lipid droplet accumulation in Glia via apoe d
Cell Metabolism, 2017Co-Authors: Kevin R. Mackenzie, Mirjana Maleticsavatic, Nagireddy Putluri, Hugo Jozef BellenAbstract:Summary Elevated reactive oxygen species (ROS) induce the formation of lipids in neurons that are transferred to Glia, where they form lipid droplets (LDs). We show that Glial and neuronal monocarboxylate transporters (MCTs), fatty acid transport proteins (FATPs), and apolipoproteins are critical for Glial LD formation. MCTs enable Glia to secrete and neurons to absorb lactate, which is converted to pyruvate and acetyl-CoA in neurons. Lactate metabolites provide a substrate for synthesis of fatty acids, which are processed and transferred to Glia by FATP and apolipoproteins. In the presence of high ROS, inhibiting lactate transfer or lowering FATP or apolipoprotein levels decreases Glial LD accumulation in flies and in primary mouse Glial-neuronal cultures. We show that human APOE can substitute for a fly Glial apolipoprotein and that APOE4, an Alzheimer's disease susceptibility allele, is impaired in lipid transport and promotes neurodegeneration, providing insights into disease mechanisms.
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the Glia neuron lactate shuttle and elevated ros promote lipid synthesis in neurons and lipid droplet accumulation in Glia via apoe d
Cell Metabolism, 2017Co-Authors: Kevin R. Mackenzie, Mirjana Maleticsavatic, Nagireddy Putluri, Hugo J. BellenAbstract:Summary Elevated reactive oxygen species (ROS) induce the formation of lipids in neurons that are transferred to Glia, where they form lipid droplets (LDs). We show that Glial and neuronal monocarboxylate transporters (MCTs), fatty acid transport proteins (FATPs), and apolipoproteins are critical for Glial LD formation. MCTs enable Glia to secrete and neurons to absorb lactate, which is converted to pyruvate and acetyl-CoA in neurons. Lactate metabolites provide a substrate for synthesis of fatty acids, which are processed and transferred to Glia by FATP and apolipoproteins. In the presence of high ROS, inhibiting lactate transfer or lowering FATP or apolipoprotein levels decreases Glial LD accumulation in flies and in primary mouse Glial-neuronal cultures. We show that human APOE can substitute for a fly Glial apolipoprotein and that APOE4, an Alzheimer's disease susceptibility allele, is impaired in lipid transport and promotes neurodegeneration, providing insights into disease mechanisms.
Jochen Müller - One of the best experts on this subject based on the ideXlab platform.
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the principal neurons of the medial nucleus of the trapezoid body and ng2 Glial cells receive coordinated excitatory synaptic input
The Journal of General Physiology, 2009Co-Authors: Jochen Müller, Daniel Reyesharo, Tatjyana Pivneva, Joachim Lubke, Christiane Nolte, Roland Schaette, Helmut KettenmannAbstract:Glial cell processes are part of the synaptic structure and sense spillover of transmitter, while some Glial cells can even receive direct synaptic input. Here, we report that a defined type of Glial cell in the medial nucleus of the trapezoid body (MNTB) receives excitatory glutamatergic synaptic input from the calyx of Held (CoH). This giant glutamatergic terminal forms an axosomatic synapse with a single principal neuron located in the MNTB. The NG2 Glia, as postsynaptic principal neurons, establish synapse-like structures with the CoH terminal. In contrast to the principal neurons, which are known to receive excitatory as well as inhibitory inputs, the NG2 Glia receive mostly, if not exclusively, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor–mediated evoked and spontaneous synaptic input. Simultaneous recordings from neurons and NG2 Glia indicate that they partially receive synchronized spontaneous input. This shows that an NG2+ Glial cell and a postsynaptic neuron share presynaptic terminals.
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The principal neurons of the medial nucleus of the trapezoid body and NG2(+) Glial cells receive coordinated excitatory synaptic input.
The Journal of General Physiology, 2009Co-Authors: Jochen Müller, Tatjyana Pivneva, Joachim Lubke, Daniel Reyes-haro, Christiane Nolte, Roland Schaette, Helmut KettenmannAbstract:Glial cell processes are part of the synaptic structure and sense spillover of transmitter, while some Glial cells can even receive direct synaptic input. Here, we report that a defined type of Glial cell in the medial nucleus of the trapezoid body (MNTB) receives excitatory glutamatergic synaptic input from the calyx of Held (CoH). This giant glutamatergic terminal forms an axosomatic synapse with a single principal neuron located in the MNTB. The NG2 Glia, as postsynaptic principal neurons, establish synapse-like structures with the CoH terminal. In contrast to the principal neurons, which are known to receive excitatory as well as inhibitory inputs, the NG2 Glia receive mostly, if not exclusively, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor–mediated evoked and spontaneous synaptic input. Simultaneous recordings from neurons and NG2 Glia indicate that they partially receive synchronized spontaneous input. This shows that an NG2+ Glial cell and a postsynaptic neuron share presynaptic terminals.
Frank Pfrieger - One of the best experts on this subject based on the ideXlab platform.
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Glial cells promote dendrite formation and the reception of synaptic input in Purkinje cells from postnatal mice.
Glia, 2009Co-Authors: Isabelle Buard, Celine C Steinmetz, Thomas Claudepierre, Frank PfriegerAbstract:Previous studies suggest that Glial cells contribute to synaptogenesis in specific neurons from the postnatal CNS. Here, we studied whether this is true for Purkinje cells (PCs), which represent a unique neuronal cell type due to their large size, massive synaptic input, and high vulnerability. Using new Glia-free cultures enriched in PCs from postnatal mice we show that these neurons survived and grew, but displayed only low levels of excitatory and inhibitory synaptic activity. Coculture with Glial cells strongly enhanced the frequency and size of spontaneous and miniature excitatory synaptic currents as well as neurite growth and branching. Immunocytochemical staining for microtubule-associated protein 2- (MAP2-) positive neurites revealed impaired dendrite formation in PCs under Glia-free conditions, which can explain the absence of synaptic activity. Glial signals strongly enhanced dendritogenesis in PCs and thus their ability to receive excitatory synaptic input from granule cells (GCs). The enhancement of dendrite formation was mimicked by Glia-conditioned medium (GCM), whereas the increase in synaptic activity required physical presence of Glia. This indicated that dendrite development is necessary but not sufficient for PCs to receive excitatory synaptic input and that synaptogenesis requires additional signals. The level of inhibitory synaptic activity was low even in cocultures due to a low incidence of inhibitory interneurons. Taken together, our results reinforce the idea that Glial cells promote synaptogenesis in specific neuronal cell types.