nmda receptors are located in nerve cells in the brain.
nmda receptors are located in nerve cells in the brain.
where are nmda receptors located in the brain?
in nerve cells
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the earliest proposed mechanism for plastic activity is based around glutamate receptors and their ability to change in number and strength based on synapse activity. glutamate binds two main receptor types: ampa receptors (ampars) and nmda receptors (nmdars). these are named after drugs that bind to the receptors: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (ampa) and n-methyl-d-aspartate (nmda), respectively, but they both bind glutamate. when a glutamatergic synapse releases glutamate it binds to any ampa and the nmda receptors present in the postsynaptic membrane. the ampa receptors are ionotropic receptors that are responsible for fast synaptic transmission. in a nutshell the nmda receptors evoke a response in the cell only when sufficient glutamate has been transmitted to cause that cell to depolarize enough to unblock the nmda receptor. sufficient depolarization in the membrane will cause the magnesium cation blockade in the nmda receptors to vacate, thus allowing calcium influx into the cell. nmda receptors are "coincidence detectors". they determine when the presynaptic and postsynaptic neuron are linked in time via activity. when this occurs, nmda receptors become the control mechanism that dictates how the ampa and nmda receptors are to be rearranged. the rearrangement of ampa and nmda receptors has become the central focus of current studies of metaplasticity as it directly determines ltp and ltd thresholds. however, some evidence indicates that g protein-coupled receptors (gpcrs) are responsible for controlling nmda receptor activity, which suggests that nmdar-mediated changes in synaptic strength are modulated by the activity of gpcrs. there is large amounts of research focused on finding the specific enzymes and intracellular pathways involved in the nmdar-mediated modulation of membrane ampa receptors. recent biochemical research has shown that a deficiency in the protein tenascin-r (tnr) leads to a metaplastic increase in the threshold for ltp induction. tnr is an extracellular-matrix protein expressed by oligodendrocytes during myelination.
metaplasticity