Modulation of extracellular signal-regulated kinases cascade by chronic delta 9-tetrahydrocannabinol treatment.
Tiziana Rubino, Greta Forlani, Daniela Viganò, Renata Zippel, Daniela Parolaro
Molecular and cellular neurosciences March 2004 DOI: 10.1016/j.mcn.2003.11.003 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Preclinical experimental study Peer reviewed |
|---|---|
| Population | Mice, including Ras-GRF1 knockout mice |
| Intervention | Delta(9)-tetrahydrocannabinol (THC) |
| Topics | Cannabis |
| Key findings | Acute THC activated ERK signaling mainly in the caudate putamen and cerebellum, an effect that adapted after chronic treatment, while chronic THC increased ERK cascade components in the prefrontal cortex and hippocampus. Ras-GRF1 knockout mice, which lack cannabinoid-induced ERK activation, did not develop tolerance to THC's analgesic and hypolocomotor effects, suggesting the ERK cascade is involved in synaptic plasticity from chronic cannabinoid exposure. |
Abstract
Acute Delta(9)-tetrahydrocannabinol (THC) injection increased ERK pathway (ERK, pCREB, and c-fos) mostly in the caudate putamen and cerebellum. This effect underwent to homeostatic adaptation after chronic treatment. Moreover, chronic THC exposure induced increases in the ERK cascade (ERK, pCREB, and Fos B) in the prefrontal cortex and hippocampus, suggesting that different neuronal circuits seem to be involved in the early phase and late phase of exposure. The involvement of ERK pathway in cannabinoid chronic exposure was also confirmed in Ras-GRF1 knock out mice, a useful model where cannabinoid-induced ERK activation is lost. In fact, Ras-GRF1 ko mice did not develop tolerance to THC analgesic and hypolocomotor effect. Our data suggest that ERK cascade could play a pivotal role in the induction of synaptic plasticity due to cannabinoid chronic exposure.
Comparable studies
Other preclinical and animal studies on cannabis, most cited first.
Citations in the library
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- Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol (THC): neuroprotection and ERK signaling. Experimental Brain Research September 2012
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