Title : Changes in the expression of G protein-coupled receptor kinases and beta-arrestins in mouse brain during cannabinoid tolerance: a role for RAS-ERK cascade.

Pub. Date : 2006 Jun

PMID : 16954596






4 Functional Relationships(s)
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1 In the latter areas, ERK activation after chronic THC increased the transcription factors cyclic adenosine monophosphate response element-binding protein and Fos B as well as a downstream protein known as brainderived neurotrophic factor. Dronabinol mitogen-activated protein kinase 1 Mus musculus
2 As a whole, our data suggest that in the striatum and cerebellum, THC-induced ERK activation could represent a key signaling event to initiate homologous desensitization of CB1 receptor, accounting for the development of tolerance to THC-induced hypolocomotion. Dronabinol mitogen-activated protein kinase 1 Mus musculus
3 As a whole, our data suggest that in the striatum and cerebellum, THC-induced ERK activation could represent a key signaling event to initiate homologous desensitization of CB1 receptor, accounting for the development of tolerance to THC-induced hypolocomotion. Dronabinol mitogen-activated protein kinase 1 Mus musculus
4 In the prefrontal cortex and hippocampus, THC-induced alteration in GRKs and beta-arrestins primarily depends on other kinases, whereas ERK activation could be part of the molecular adaptations that underlie the complex behavioral phenotype that defines the addicted state. Dronabinol mitogen-activated protein kinase 1 Mus musculus