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Nikas, S. P.

Publications and source records attributed to Nikas, S. P..

2 recordsLinked to original sources

Efficacy profiling of structurally diverse cannabinoid receptor ligands across transducer-coupling assays

The full efficacy range of ligands at CB1 and CB2 (i.e., inverse agonists, neutral agonists, partial agonists, full agonists, and high-efficacy agonists) has been reported collectively across numerous laboratories and assay platforms. Canonical Gi/o and {beta}-arrestin signaling have each been suggested to shape physiological effects differently via different classes of cannabinoid ligands. These prior efficacy classifications, however, were obtained in multiple assay systems, often using indirect, amplified readouts and different reference agonists, making them difficult to compare across ligands. Here we profiled a structurally diverse panel of 22 cannabinoid ligands: synthetic cannabinoid receptor agonists (SCRAs), {Delta}-tetrahydrocannabinol ({Delta}-THC) analogues, endocannabinoid analogues, and antagonists/inverse agonists at CB1 and CB2 receptors using bioluminescence resonance energy transfer (BRET) assays, measuring Gi1 engagement and {beta}-arrestin 2 recruitment and normalizing every response to the reference full agonist CP55,940. At CB1, SCRAs and {Delta}-THC analogues acted as high-efficacy agonists. At CB1, these high-efficacy agonists were also highly efficacious in {beta}-arrestin 2 recruitment. Across the panel, the most consistent trend was a loss of agonist efficacy from CB1 to CB2. Among antagonists, inverse agonists suppressed constitutive CB1 activity more than neutral antagonists. Together, these CP55,940-normalized measurements provide a common efficacy scale and a framework for interpreting pharmacodynamics of CB1 and CB2 cannabinoid receptors.

pharmacology and toxicology↗

Modulation of cannabinoid receptor signaling by endocannabinoids

Endocannabinoids (eCBs) are endogenous lipid molecules that activate the cannabinoid receptor 1 (CB1), a G protein coupled receptor (GPCR) that signals primarily through the Gi/o family of G proteins to regulate neurotransmitter release. Consequently, CB1 is an important therapeutic target for several neurological disorders. How eCBs interact with CB1 is not known and the downstream signaling they activate is not well understood. In this study we show that eCBs do not activate Gi1 as much as synthetic cannabinoids. To characterize activation of CB1 by eCB, we formed an eCB analogue-bound (AMG315) CB1-Gi signaling complex for structural studies. The structure reveals differences in the orthosteric ligand binding pocket not seen in the previous CB1 structures, providing insights into the structural determinants of ligand efficacy. In combination with signaling and simulation data, this study provides mechanistic insights into CB1 activation by different classes of ligands, and sheds light on the G protein preferences between endogenous and exogenous ligands.

biochemistry↗