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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 .
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.
The common dopamine and glutamate models proposed are not mutually exclusive; each is seen to have a role in the neurobiology of schizophrenia. [128] The most common model put forward was the dopamine hypothesis of schizophrenia, which attributes psychosis to the mind's faulty interpretation of the misfiring of dopaminergic neurons. [129]
In 1999, Moghaddam and her colleagues tested the compound LY354740, a metabotropic glutamate receptor agonist, which they found to suppress aberrant glutamate release, reduced behavioral disruptions in animals given PCP, and overall have less side effects than typical benzodiazepines used to treat certain symptoms of schizophrenia. [1]
Glutamate is the most prominent neurotransmitter in the body, and is the main excitatory neurotransmitter, being present in over 50% of nervous tissue. [2] [3] Glutamate was initially discovered to be a neurotransmitter in insect studies in the early 1960s.
A neurotransmitter is a signaling molecule ... Common neurotransmitters include glutamate, GABA ... drugs used to treat patients with schizophrenia such as ...
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