scholarly journals The Metabotropic Glutamate Receptor Activates the Lipid Kinase PI3K in Drosophila Motor Neurons Through the Calcium/Calmodulin-Dependent Protein Kinase II and the Nonreceptor Tyrosine Protein Kinase DFak

Genetics ◽  
2011 ◽  
Vol 188 (3) ◽  
pp. 601-613 ◽  
Author(s):  
Curtis Chun-Jen Lin ◽  
James B. Summerville ◽  
Eric Howlett ◽  
Michael Stern
Keyword(s):  
Protein Kinase ◽  
Glutamate Receptor ◽  
Motor Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Dependent Protein Kinase ◽  
Lipid Kinase ◽  
Metabotropic Glutamate ◽  
Calcium Calmodulin Dependent ◽  
Tyrosine Protein Kinase ◽  
Dependent Protein

Mechanisms Underlying Dedepression of Synaptic NMDA Receptors in the Hippocampus

2008 ◽  
Vol 99 (1) ◽  
pp. 254-263 ◽  
Author(s):  
Wade Morishita ◽  
Robert C. Malenka
Keyword(s):  
Protein Kinase ◽  
Metabotropic Glutamate Receptors ◽  
Pyramidal Cells ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Protein Kinase ◽  
Metabotropic Glutamate ◽  
Calcium Calmodulin Dependent ◽  
Ca1 Region ◽  
Dependent Protein ◽  
Synaptic Responses

N-Methyl-d-aspartate receptor (NMDAR)–mediated synaptic responses in hippocampal CA1 pyramidal cells are depressed during NMDAR-dependent long-term depression (LTD) due to mechanisms, in part, distinct from those underlying LTD of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)–mediated synaptic responses. The mechanisms underlying dedepression of synaptic NMDARs, however, are not known. We find that dedepression of NMDAR-mediated synaptic responses in the CA1 region of the rat hippocampus is input specific and does not require synaptic stimulation to be maintained. The induction of dedepression does not require activation of metabotropic glutamate receptors, L-type Ca2+ channels, or release of Ca2+ from intracellular stores. It does, however, rely on activation of NMDARs. In contrast to the dedepression of AMPAR-mediated synaptic responses, dedepression of NMDAR-mediated synaptic responses does not depend on activation of calcium/calmodulin-dependent protein kinase II, protein kinase C, cAMP-dependent protein kinase, or Src kinases. However, dedepression of synaptic NMDARs is significantly impaired by inhibitors of mitogen-activated protein kinase signaling. Specifically, inhibitors of extracellular signal-regulated kinase 1/2 prevented normal dedepression of synaptic NMDARs by a mechanism that did not require protein synthesis. These results provide further evidence that synaptic NMDARs can be bidirectionally modified by activity but by mechanisms distinct from those responsible for the activity-dependent, bidirectional modulation of synaptic AMPARs.

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