Description:Synaptic plasticity, the cellular correlate for learning and memory, involves a number of molecules that reside in the dendritic spine. For example, long-term potentiation (LTP) of the excitatory postsynaptic current (EPSC) is induced by postsynaptic NMDA receptor and Ca 2+ /calmodulin-dependent kinase II (CaMKII) activity. Intrigued by recent findings that dendritic spines also harbor the metabotropic GABA B receptor for the major inhibitory transmitter GABA, as well as its downstream effector the G protein-activated inwardly rectifying K + (GIRK) channel, we wondered whether pairing glutamate release with postsynaptic depolarization would affect the slow inhibitory postsynaptic current (sIPSC) mediated by GABA B receptors and GIRK channels. Remarkably, we found that the same signaling pathway for inducing LTP of the EPSC also potentiated the sIPSC. Moreover, in mice lacking Nova-2, which is targeted in paraneoplastic opsoclonus myoclonus ataxia (POMA) patients and binds RNAs for synaptic proteins, the hippocampal CA1 neurons exhibited no LTP of slow synaptic inhibition.We have made it easy for you to find a PDF Ebooks without any digging. And by having access to our ebooks online or by storing it on your computer, you have convenient answers with NMDA Receptor-dependent Long-term Potentiation of Slow Synaptic Inhibition in Hippocampus. To get started finding NMDA Receptor-dependent Long-term Potentiation of Slow Synaptic Inhibition in Hippocampus, you are right to find our website which has a comprehensive collection of manuals listed. Our library is the biggest of these that have literally hundreds of thousands of different products represented.
Pages
280
Format
PDF, EPUB & Kindle Edition
Publisher
—
Release
2005
ISBN
1792002173
NMDA Receptor-dependent Long-term Potentiation of Slow Synaptic Inhibition in Hippocampus
Description: Synaptic plasticity, the cellular correlate for learning and memory, involves a number of molecules that reside in the dendritic spine. For example, long-term potentiation (LTP) of the excitatory postsynaptic current (EPSC) is induced by postsynaptic NMDA receptor and Ca 2+ /calmodulin-dependent kinase II (CaMKII) activity. Intrigued by recent findings that dendritic spines also harbor the metabotropic GABA B receptor for the major inhibitory transmitter GABA, as well as its downstream effector the G protein-activated inwardly rectifying K + (GIRK) channel, we wondered whether pairing glutamate release with postsynaptic depolarization would affect the slow inhibitory postsynaptic current (sIPSC) mediated by GABA B receptors and GIRK channels. Remarkably, we found that the same signaling pathway for inducing LTP of the EPSC also potentiated the sIPSC. Moreover, in mice lacking Nova-2, which is targeted in paraneoplastic opsoclonus myoclonus ataxia (POMA) patients and binds RNAs for synaptic proteins, the hippocampal CA1 neurons exhibited no LTP of slow synaptic inhibition.We have made it easy for you to find a PDF Ebooks without any digging. And by having access to our ebooks online or by storing it on your computer, you have convenient answers with NMDA Receptor-dependent Long-term Potentiation of Slow Synaptic Inhibition in Hippocampus. To get started finding NMDA Receptor-dependent Long-term Potentiation of Slow Synaptic Inhibition in Hippocampus, you are right to find our website which has a comprehensive collection of manuals listed. Our library is the biggest of these that have literally hundreds of thousands of different products represented.