NMDA receptor

From: 'NMDA receptor' <a href="https://en.wikipedia.org/wiki/NMDA_receptor">https://en.wikipedia.org/wiki/NMDA_receptor</a>

The N-methyl-D-aspartate receptor (also known as the NMDA receptor or NMDAR), is a <a title="Glutamate receptor" href="https://en.wikipedia.org/wiki/Glutamate_receptor">glutamate receptor</a> and <a title="Ion channel" href="https://en.wikipedia.org/wiki/Ion_channel">ion channel</a> <a title="Protein" href="https://en.wikipedia.org/wiki/Protein">protein</a> found in <a title="Nerve" href="https://en.wikipedia.org/wiki/Nerve">nerve cells</a>. The NMDA receptor is an ionotropic receptor. It is activated when <a class="mw-redirect" title="Glutamate" href="https://en.wikipedia.org/wiki/Glutamate">glutamate</a> and <a title="Glycine" href="https://en.wikipedia.org/wiki/Glycine">glycine</a> (or <a class="mw-redirect" title="D-serine" href="https://en.wikipedia.org/wiki/D-serine">D-serine</a>) bind to it, and when activated it allows <a class="mw-redirect" title="Cation" href="https://en.wikipedia.org/wiki/Cation">positively charged ions</a> to flow through the <a title="Cell membrane" href="https://en.wikipedia.org/wiki/Cell_membrane">cell membrane</a>.<a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-2">[2]</a> The NMDA receptor is very important for controlling <a title="Synaptic plasticity" href="https://en.wikipedia.org/wiki/Synaptic_plasticity">synaptic plasticity</a> and <a title="Memory" href="https://en.wikipedia.org/wiki/Memory">memory</a>function.<a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid19605837-3">[3]</a>
The NMDAR is a specific type of <a class="mw-redirect" title="Ionotropic" href="https://en.wikipedia.org/wiki/Ionotropic">ionotropic</a> <a title="Glutamate receptor" href="https://en.wikipedia.org/wiki/Glutamate_receptor">glutamate receptor</a>.<a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid1834949-4">[4]</a> The NMDA receptor is so named because the <a title="Agonist" href="https://en.wikipedia.org/wiki/Agonist">agonist</a> molecule <a class="mw-redirect" title="N-methyl-D-aspartate" href="https://en.wikipedia.org/wiki/N-methyl-D-aspartate">N</a><a class="mw-redirect" title="N-methyl-D-aspartate" href="https://en.wikipedia.org/wiki/N-methyl-D-aspartate">-methyl-D-aspartate</a>(NMDA) binds selectively to it, and not to other glutamate receptors. Activation of NMDA receptors results in the opening of an <a title="Ion channel" href="https://en.wikipedia.org/wiki/Ion_channel">ion channel</a> that is nonselective to <a title="Ion" href="https://en.wikipedia.org/wiki/Ion">cations</a>, with a combined <a title="Reversal potential" href="https://en.wikipedia.org/wiki/Reversal_potential">reversal potential</a> near 0 mV. While the opening and closing of the ion channel is primarily gated by <a title="Ligand (biochemistry)" href="https://en.wikipedia.org/wiki/Ligand_(biochemistry)">ligand</a>binding, the current flow through the ion channel is voltage dependent. Extracellular magnesium (Mg2+) and zinc (Zn2+) ions can bind to specific sites on the receptor, blocking the passage of other cations through the open ion channel. Depolarization of the cell dislodges and repels the Mg2+ and Zn2+ ions from the pore, thus allowing a voltage-dependent flow of sodium (Na+) and small amounts of calcium (Ca2+) ions into the cell and potassium (K+) out of the cell.<a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid10049997-5">[5]</a><a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid11775847-6">[6]</a><a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid11399431-7">[7]</a><a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid17088105-8">[8]</a>

Ca2+ flux through NMDARs is thought to be critical in <a title="Synaptic plasticity" href="https://en.wikipedia.org/wiki/Synaptic_plasticity">synaptic plasticity</a>, a cellular mechanism for <a title="Learning" href="https://en.wikipedia.org/wiki/Learning">learning</a> and <a title="Memory" href="https://en.wikipedia.org/wiki/Memory">memory</a>. The opening and closing (gating) of the NMDA receptor is complex. While it is primarily a ligand-gated channel, it does display weaker voltage-dependence modulation of the ligand-dependent gating. The ligand gating requires co-activation by two ligands: <a class="mw-redirect" title="Glutamate" href="https://en.wikipedia.org/wiki/Glutamate">glutamate</a> and either <a class="mw-redirect" title="D-serine" href="https://en.wikipedia.org/wiki/D-serine">D-serine</a> or <a title="Glycine" href="https://en.wikipedia.org/wiki/Glycine">glycine</a>.<a href="https://en.wikipedia.org/wiki/NMDA_receptor#cite_note-pmid2841759-9">[9]</a> The voltage-dependence of current through the channel is mainly due to binding of Mg2+ or Zn2+ ions to the protein as described above.

The activity of the NMDA receptor is affected by many <a class="mw-redirect" title="Psychoactive" href="https://en.wikipedia.org/wiki/Psychoactive">psychoactive</a> drugs such as <a title="Phencyclidine" href="https://en.wikipedia.org/wiki/Phencyclidine">phencyclidine</a> (PCP), <a class="mw-redirect" title="Alcoholic beverage" href="https://en.wikipedia.org/wiki/Alcoholic_beverage">alcohol</a> (<a title="Ethanol" href="https://en.wikipedia.org/wiki/Ethanol">ethanol</a>) and <a title="Dextromethorphan" href="https://en.wikipedia.org/wiki/Dextromethorphan">dextromethorphan</a> (DXM). The <a class="mw-redirect" title="Anaesthetic" href="https://en.wikipedia.org/wiki/Anaesthetic">anaesthetic</a> and <a title="Analgesic" href="https://en.wikipedia.org/wiki/Analgesic">analgesic</a> effects of the drugs <a title="Ketamine" href="https://en.wikipedia.org/wiki/Ketamine">ketamine</a> and <a title="Nitrous oxide" href="https://en.wikipedia.org/wiki/Nitrous_oxide">nitrous oxide</a> are partially because of their effects on NMDA receptor activity.