CDPPB may be used in mGluR5-mediated cell signaling studies.
Biochem/physiol Actions
Activation of metabotropic glutamate 5 receptor by CDPPB enhances the function of NMDA receptor and markers of neuronal plasticity. This improves recognition memory and cognition deficits in schizophrenia.[1][2]
CDPPB is a glutamate metabotropic mGluR5 positive allosteric modulator.
In the search for strategies to treat schizophrenia, attention has focused on enhancing NMDA receptor function. In vitro experiments show that metabotropic glutamate 5 receptor (mGluR5) activation enhances NMDA receptor activity, and in vivo experiments indicate that mGluR5 positive allosteric
Cocaine use disorder (CUD) remains difficult to treat with no FDA-approved medications to reduce relapse. Antagonism of metabotropic glutamate receptor 5 (mGlu5) has been demonstrated to decrease cocaine-seeking but may also further compromise cognitive function in long-term cocaine users. Here we
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British journal of pharmacology, 169(4), 909-921 (2013-03-16)
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a polyglutamine expansion in the huntingtin protein. We have previously demonstrated that the cell signalling of the metabotropic glutamate receptor 5 (mGluR5) is altered in a mouse model of
Fragile X syndrome is caused by FMR1 gene silencing and loss of the encoded fragile X mental retardation protein (FMRP), which binds to mRNA and regulates translation. Studies in the Fmr1-/y mouse model of fragile X syndrome indicate that aberrant
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