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Attn: Linkadge(?) Can you elaborate on this study?

Posted by PeterMartin on May 20, 2021, at 12:10:50

Linkadge (or anyone else w/ scientific knowledge):

I'm taking a relatively new medicine called Rybelsus (aka Semaglutide/Ozempic) for weight loss. It's a GLP-1 (glucose like protein) receptor agonist. This class of medication is relatively new (post-2010). Per some research it seems like there are GLP-1 receptors in the brain and the medication does cross the BBB.

I'm also taking methylphenidate and Marplan. I found this study that shows GLP-1 receptors can alter the way dopamine works in regards to Cocaine (stimulant).

I'm curious if based on this paper you think Semaglutide may change the way Methylphenidate works in the brain? Could it potentially make it more effective/less addictive?

Basically I'm hoping someone can read this and see if there may be a beneficial interaction between Ritalin & GLP-1 agonists like the one I'm taking. Thanks!!


Cocaine-evoked increases in dopamine signaling are greater in the NAc shell vs core.

Central GLP-1R activation suppresses phasic dopamine signaling in the NAc core.

GLP-1R effects are not due to alterations in dopamine reuptake.

Drugs of abuse increase the frequency and magnitude of brief (13 s), high concentration (phasic) dopamine release events in terminal regions. These are thought to be a critical part of drug reinforcement and ultimately the development of addiction. Recently, metabolic regulatory peptides, including the satiety signal glucagon-like peptide-1 (GLP-1), have been shown to modulate cocaine reward-driven behavior and sustained dopamine levels after cocaine administration. Here, we use fast-scan cyclic voltammetry (FSCV) to explore GLP-1 receptor (GLP-1R) modulation of dynamic dopamine release in the nucleus accumbens (NAc) during cocaine administration. We analyzed dopamine release events in both the NAc shell and core, as these two subregions are differentially affected by cocaine and uniquely contribute to motivated behavior. We found that central delivery of the GLP-1R agonist Exendin-4 suppressed the induction of phasic dopamine release events by intravenous cocaine. This effect was selective for dopamine signaling in the NAc core. Suppression of phasic signaling in the core by Exendin-4 could not be attributed to interference with cocaine binding to one of its major substrates, the dopamine transporter, as cocaine-induced increases in reuptake were unaffected. The results suggest that GLP-1R activation, instead, exerts its suppressive effects by altering dopamine release possibly by suppressing the excitability of dopamine neurons. Given the role of NAc core dopamine in the generation of conditioned responses based on associative learning, suppression of cocaine-induced dopamine signaling in this subregion by GLP-1R agonism may decrease the reinforcing properties of cocaine. Thus, GLP-1Rs remain viable targets for the treatment and prevention of cocaine seeking, taking and relapse.




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