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The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors .
These data suggest that mGlu2/3 receptor agonists have antipsychotic properties and may provide a new alternative for the treatment of schizophrenia. [5] Other NMDA receptor modulators are being studied and this modality of treatment may once approved as antipsychotic medications gradually replace the current (dopaminergic) antipsychotics.
The metabotropic glutamate receptors, or mGluRs, are a type of glutamate receptor that are active through an indirect metabotropic process. They are members of the group C family of G-protein-coupled receptors, or GPCRs. [1] Like all glutamate receptors, mGluRs bind with glutamate, an amino acid that functions as an excitatory neurotransmitter.
These glutamate receptors are suggested to play a role in modulating gene expression in glial cells, both during the proliferation and differentiation of glial precursor cells in brain development and in mature glial cells. [12] Glutamate receptors serve to facilitate the impact of the neurotransmitter glutamate in the central nervous system.
The causes of schizophrenia that underlie the development of schizophrenia, a psychiatric disorder, are complex and not clearly understood.A number of hypotheses including the dopamine hypothesis, and the glutamate hypothesis have been put forward in an attempt to explain the link between altered brain function and the symptoms and development of schizophrenia.
Metabotropic glutamate receptor 3 (mGluR3) is an inhibitory G i /G 0-coupled G-protein coupled receptor (GPCR) [4] generally localized to presynaptic sites of neurons in classical circuits. [5] However, in higher cortical circuits in primates, mGluR3 are localized post-synaptically, where they strengthen rather than weaken synaptic connectivity ...
Stylized depiction of an activated NMDAR. Glutamate is in the glutamate-binding site and glycine is in the glycine-binding site. The allosteric site, which modulates receptor function when bound to a ligand, is not occupied. NMDARs require the binding of two molecules of glutamate or aspartate and two of glycine [1] [2]
It has been proposed that schizophrenia may be due to an increase or a decrease in glutamate signaling, leading to abnormal excitatory signaling in the prefrontal cortex region of the brain. [15] Glutamate release by astrocytes has been linked to the synchrony of neurons in the hippocampus and cortex. A decrease in system Xc- activity may ...
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