c-Jun N terminal kinase signaling pathways mediate cannabinoid tolerance in an agonist-specific manner

Henderson-Redmond, Angela N.; Nealon, Caitlin M.; Davis, Brian J.; Yuill, Matthew B.; Sepulveda, Diana E.; Blanton, Henry L.; Piscura, Mary K; Zee, Michael L.; Haskins, Chris; Marcus, David J.; Guindon, Josée; Morgan, Daniel J.

doi:10.1016/j.neuropharm.2019.107847

Cited by 21 publications

(21 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, one limitation of this study when extrapolating the results habitual cannabis users is the use of WIN55,212-2 rather than 9 -THC since desensitization, internalization, recycling, and tolerance are highly agonistspecific (Hsieh et al, 1999;Wu et al, 2008;Martini et al, 2007;Morgan et al, 2014;Nealon et al, 2019). Indeed, a recent study reported that 9 -THC-but not WIN55,212-2mediated tolerance is dependent on c-Jun N-terminal Kinase (JNK) signaling (Henderson-Redmond et al, 2020).…”

Section: G Protein-coupled Receptor Associated Protein 1 (Gasp1)mentioning

confidence: 97%

Protein Interactors and Trafficking Pathways That Regulate the Cannabinoid Type 1 Receptor (CB1R)

Fletcher‐Jones

Hildick

Evans

et al. 2020

Front. Mol. Neurosci.

View full text Add to dashboard Cite

The endocannabinoid system (ECS) acts as a negative feedback mechanism to suppress synaptic transmission and plays a major role in a diverse range of brain functions including, for example, the regulation of mood, energy balance, and learning and memory. The function and dysfunction of the ECS are strongly implicated in multiple psychiatric, neurological, and neurodegenerative diseases. Cannabinoid type 1 receptor (CB1R) is the most abundant G protein-coupled receptor (GPCR) expressed in the brain and, as for any synaptic receptor, CB1R needs to be in the right place at the right time to respond appropriately to changing synaptic circumstances. While CB1R is found intracellularly throughout neurons, its surface expression is highly polarized to the axonal membrane, consistent with its functional expression at presynaptic sites. Surprisingly, despite the importance of CB1R, the interacting proteins and molecular mechanisms that regulate the highly polarized distribution and function of CB1R remain relatively poorly understood. Here we set out what is currently known about the trafficking pathways and protein interactions that underpin the surface expression and axonal polarity of CB1R, and highlight key questions that still need to be addressed.

show abstract

Section: G Protein-coupled Receptor Associated Protein 1 (Gasp1)mentioning

confidence: 97%

Protein Interactors and Trafficking Pathways That Regulate the Cannabinoid Type 1 Receptor (CB1R)

Fletcher‐Jones

Hildick

Evans

et al. 2020

Front. Mol. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Indeed, inhibition of PKA in cerebellum can block precipitated withdrawal signs in mouse, while PKA activation mimics precipitated withdrawal (Tzavara et al, 2000). Phosphorylation of CB1 mediated by the c-Jun terminal kinase has also been implicated in THC-induced tolerance (Henderson-Redmond et al, 2020).…”

Section: Ac Camp and Pkamentioning

confidence: 99%

Cannabis use, abuse, and withdrawal: Cannabinergic mechanisms, clinical, and preclinical findings

Kesner

Lovinger

2021

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…Is atypical regulation a broader phenomenon observed with other GPCRs? While not conclusively resolved, evidence suggests that D2 dopamine receptor, CB1 cannabinoid receptor, and 7A serotonin receptor may undergo analogous types of regulation 113–116 . Another intriguing example involves kappa opioid receptor (KOR).…”

Section: Regulation Of Gpcr Signalingmentioning

confidence: 99%

A cellular perspective of bias at G protein‐coupled receptors

2020

View full text Add to dashboard Cite

G protein-coupled receptors (GPCRs) modulate cell function over short-and long-term timescales. GPCR signaling depends on biochemical parameters that define the what, when, and where of receptor function: what proteins mediate and regulate receptor signaling, where within the cell these interactions occur,and how long these interactions persist. These parameters can vary significantly depending on the activating ligand. Collectivity, differential agonist activity at a GPCR is called bias or functional selectivity. Here we review agonist bias at GPCRs with a focus on ligands that show dramatically different cellular responses from their unbiased counterparts.

show abstract

c-Jun N terminal kinase signaling pathways mediate cannabinoid tolerance in an agonist-specific manner

Cited by 21 publications

References 54 publications

Protein Interactors and Trafficking Pathways That Regulate the Cannabinoid Type 1 Receptor (CB1R)

Protein Interactors and Trafficking Pathways That Regulate the Cannabinoid Type 1 Receptor (CB1R)

Cannabis use, abuse, and withdrawal: Cannabinergic mechanisms, clinical, and preclinical findings

A cellular perspective of bias at G protein‐coupled receptors

Contact Info

Product

Resources

About