Receiver NMDA

receiving NMDA are receiving ionotropes activated by the Glutamate. They are specifically activated by N-methyl-D-ASPARTATe (NMDA). They are permeable with sodium, but also with potassium and calcium. Had with the permeability of sodium and potassium, the potential of reversion of the NMDAR is around 0mV. The calcium entry in the neuron via the NMDAR would be a mechanism of induction of synaptic plasticity. Receivers NMDA are blocked by an ion magnesium which occupies the entry of the pore, releasable in the event of inversion of electrochemical potential. The glycine is also necessary to the activation of receivers NMDA.

Structure

Receivers NMDA are tetramers, formed of two sub-units NR1 and two sub-units NR2 (NR2A, NR2B, NR2C or NR2D). Sub-units NR1 are obligatory, while sub-units NR2 specify the electrophysiological properties of receivers NMDA, such their sensitivity to glutamate, their permeability to calcium, the inhibition of magnesium. Sub-units NR2 also specify their interactions with intracellular proteins. The sites of connection of the glycine is localized on sub-units NR1, while the sites of connection of glutamate are located on sub-units NR2.

Expression

In embryo NR2D is expressed in first, then NR2B and NR2C are expressed. NR2A starts with is expressed around the birth. NR2D is mainly expressed in the germinal zones and the new neurons. NR2C is expressed almost that exclusively in the cerebellum. NR2A and NR2B are found in all the surfaces of the brain, particularly those implied in the training and the memory. One finds them in abundance in the hippocampus and the cortex. During the development one observes with the glutamatergic synapse a replacement of the receivers including/understanding sub-unit NR2B by those containing NR2A, the mechanism probably passes by a loss of localization of sub-units NR2B, following the change of composition of the molecules of scaffolding present on the one hand at the synapse and on the other hand in the extrasynaptic zones, the level of expression of NR2B being constant.

Role

Receivers NMDA are the receivers mainly post-synaptic persons in charge of the slow phase of the exiting post-synaptic potentials (PPSE). Receivers NMDA are regarded as detectors of coincidence at the time of the phenomena of summation of the post-synaptic potentials. Indeed, to open receivers NMDA must be stimulated by the arrival of presynaptic glutamate, but also by a post-synaptic depolarization (normally caused by the activation of receivers AMPA sensitive to glutamate and more rapids that NMDAR). The connection of glutamate forces a change conformational of the receiver which opens the pore, but that cannot be released from the magnesium which blocks it that if there is a depolarization which pushes back it. The calcium entry is also responsible for the induction of modifications of the intensity of the synaptic force of transmission, by name the synaptic Plasticité. In particular the activation of the CAMWOOD kinase 2 by calcium is necessary for the long-term potentiation. The enzymatic cascade of second messenger ERK/MAPK, person in charge of the activation of the synthesis of new proteins necessary to the function of the synapses during the induction of the long-term potentiation, is it also activated by receivers NMDA.

Drugs

Finally, certain drugs hallucinogens act directly on receivers NMDA, in particular the kétamine, an anesthetic which deteriorates the capacity of the neurons to summon the signals correctly that they receive since the NMDAR, persons in charge of this function, are disturbed. More detrimental still, the PCP activates open receivers NMDA directly by keeping them in a tonic way. Still there, the neurons are not able any more to integrate the signals normally only they receive, which causes the hallucination. The continual opening of receivers NMDA causes a calcium entry too much marked. However, calcium, although necessary to the induction of the phenomena of memory (synaptic plasticity), is also responsible for the self-destruction (apoptose) of the cells. In short, the PCP " brûle" neurons via its action on receivers NMDA.

See too

Receiving Receiving AMPA
kaïnate
Synapse

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