Calmodulin Mediates Calcium-Dependent Inactivation of N-Methyl-D-Aspartate Receptors

نویسندگان
چکیده

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Calmodulin Mediates Calcium-Dependent Inactivation of N-Methyl-D-Aspartate Receptors

Ca2+ influx through N-methyl-D-aspartate (NMDA) receptors activates signal transduction pathways critical for many forms of synaptic plasticity in the brain. NMDA receptor-mediated Ca2+ influx also downregulates the gating of NMDA channels through a process called Ca2+-dependent inactivation (CDI). Recent studies have demonstrated that the calcium binding protein calmodulin directly interacts w...

متن کامل

Intracellular domains of NR2 alter calcium-dependent inactivation of N-methyl-D-aspartate receptors.

At central excitatory synapses, the transient elevation of intracellular calcium reduces N-methyl-D-aspartate (NMDA) receptor activity. Such 'calcium-dependent inactivation' is mediated by interactions of calcium/calmodulin and alpha-actinin with the C terminus of NMDA receptor 1 (NR1) subunit. However, inactivation is also NR2-subunit specific, because it occurs in NR2A- but not NR2C-containin...

متن کامل

Calcium/calmodulin-dependent protein kinase II is associated with the N-methyl-D-aspartate receptor.

The molecular basis of long-term potentiation (LTP), a long-lasting change in synaptic transmission, is of fundamental interest because of its implication in learning. Usually LTP depends on Ca2+ influx through postsynaptic N-methyl-D-aspartate (NMDA)-type glutamate receptors and subsequent activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). For a molecular understanding of LTP ...

متن کامل

Identification of a Ca2+/calmodulin-dependent protein kinase II regulatory phosphorylation site in non-N-methyl-D-aspartate glutamate receptors.

Glutamate receptor ion channels are colocalized in postsynaptic densities with Ca2+/calmodulin-dependent protein kinase II (CaM-kinase II), which can phosphorylate and strongly enhance non-N-methyl-D-aspartate (NMDA) glutamate receptor current. In this study, CaM-kinase II enhanced kainate currents of expressed glutamate receptor 6 in 293 cells and of wild-type glutamate receptor 1, but not the...

متن کامل

Nitric oxide mediates vasodilatation in response to activation of N-methyl-D-aspartate receptors in brain.

Neurons release nitric oxide (NO) in response to activation of receptors for the excitatory amino acid N-methyl-D-aspartate (NMDA). We examined the hypothesis that activation of receptors for NMDA produces dilatation of the cerebral microcirculation that is mediated by NO. Diameters of cerebral arterioles were measured using a closed cranial window in anesthetized rabbits. Under control conditi...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Neuron

سال: 1998

ISSN: 0896-6273

DOI: 10.1016/s0896-6273(00)80553-x