Glutamate-induced excitatory transmission

**Glutamate-induced excitatory transmission** describes the fundamental neurophysiological process by which the neurotransmitter glutamate mediates fast synaptic excitation in the central nervous system. Upon neuronal activation, glutamate is released into the synaptic cleft and binds primarily to ionotropic receptors—such as NMDA, AMPA, and kainate receptors—on postsynaptic neurons[1][5]. This leads to depolarization and propagation of electrical signals. Metabotropic glutamate receptors (mGluRs), which are G protein-coupled receptors found pre-, post-synaptically and on glial cells, modulate neuronal excitability via second messenger cascades[1][3]. The termination of signal occurs through rapid reuptake by high-affinity sodium-dependent transporters known as EAATs located on neurons and glia[1][3]. Dysregulation or excessive activation of these pathways can result in **excitotoxicity**, contributing to cell death in conditions such as stroke or neurodegenerative diseases[4][5]. However, "glutamate-induced excitatory transmission" itself is a physiological event/process—not an individual druggable target molecule. > In summary: “Glutamate-induced excitatory transmission” refers broadly to synaptic processes involving multiple molecular entities—including various ionotropic/metabotropic glutamate receptors and transporters—but does not denote a single canonical therapeutic target[1][3][5].

Other names

Glutamate-induced excitatory transmission

null (Mechanisms of action pertain to drugs targeting specific molecules like NMDA receptors or EAATs, not this process directly)[2][4].