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SAP97 Is Associated with the α-Amino-3-hydroxy-5-methylisoxazole-4-propionic Acid Receptor GluR1 Subunit*
TLDR
The findings suggest that SAP97 may be involved in localizing AMPA receptors at postsynaptic sites through its interaction with the GluR1 subunit.
Interaction with the NMDA receptor locks CaMKII in an active conformation
TLDR
It is shown that regulated CaMKII interaction with two sites on the NMDA receptor subunit NR2B provides a mechanism for the glutamate-induced translocation of the kinase to the synapse in hippocampal neurons.
Extracellular acidosis increases neuronal cell calcium by activating acid-sensing ion channel 1a.
TLDR
It is found that extracellular acidosis opened ASIC1a channels, which provided a pathway for Ca(2+) entry and elevated [Ca(2+)](c) in wild-type, but not ASIC1(-/-), hippocampal neurons, and this results indicate that ASIC 1a provides a non-voltage-gated pathway to enter neurons.
Calcium/calmodulin-dependent protein kinase II is associated with the N-methyl-D-aspartate receptor.
TLDR
It is shown that CaMKII directly binds to the NMDA receptor subunits NR1 and NR2B, which fills a critical gap in the understanding of LTP because Ca MKII-mediated phosphorylation of AMPA receptors is an important step during LTP.
Cyclic AMP-dependent Protein Kinase and Protein Kinase C Phosphorylate N-Methyl-d-aspartate Receptors at Different Sites*
TLDR
The results strongly suggest that NMDA receptor functions such as control of neuronal development or expression of synaptic plasticity are modulated by PKA- and PKC-mediated phosphorylation of NMDA receptors.
Regulation of Calcium/Calmodulin-dependent Protein Kinase II Docking toN-Methyl-d-aspartate Receptors by Calcium/Calmodulin and α-Actinin*
TLDR
The NR1 C0 region is a key site for recruiting CaMKII to the postsynaptic site, where it may act in concert with calmodulin to modulate the stimulatory role of α-actinin interaction with the NMDA receptor.
Motion-induced blindness in normal observers
TLDR
Honeybee navigation en route to the goal: visual ̄ight control and odometry, and three dimensional path integration in the house mouse.
Overexpression of acid-sensing ion channel 1a in transgenic mice increases acquired fear-related behavior.
TLDR
The amygdala showed prominent expression, and overexpressing ASIC1a enhanced fear conditioning, an animal model of acquired anxiety, raising the possibility that ASIC1A and H(+)-gated currents may contribute to the development of abnormal fear and to anxiety disorders in humans.
cAMP-dependent protein kinase phosphorylation of the acid-sensing ion channel-1 regulates its binding to the protein interacting with C-kinase-1
TLDR
The acid-sensing ion channel-1 (ASIC1) contributes to synaptic plasticity and may influence the response to cerebral ischemia and acidosis and regulation of this interaction by phosphorylation provides a mechanism to control the cellular localization of ASIC1.
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