Help Any possible negative effects between Buspirone, Metoclopramide, and SN?

[Kalista]

I've been taking buspirone everyday and want to make sure there will be no negative effects between metoclopramide and SN.

Does anyone know if there are any?

 

[DepressedChemMajor]

The risk or severity of sedation can be increased when Metoclopramide is combined with Buspirone. Source: Drugbank

 

[Kalista]

Doesn't entirely sound like a bad thing, then. I don't feel drowsy taking buspirone anymore. Before it was mainly dizziness and nausea which has passed.

 

[penguinl0v3s]

No negative effects. Looking at the NIH library, this is notable about it.

Buspirone is classified in the azapirone drug class. It has a strong affinity for serotonin 5HT1a receptors, where it acts as a partial agonist, which some researchers believe produces the preponderance of clinical effects. It also has a weak affinity for serotonin 5HT2 receptors and acts as a weak antagonist on dopamine D2 autoreceptors. There is no effect on benzodiazepine GABA receptors. The underlying mechanism behind how the partial 5HT1a agonism translates into clinical results remains largely unknown. It is proposed from increased serotonergic activity in the amygdala and other parts of the brain's anxiety/fear circuitry. Due to the delayed anxiolytic effects seen clinically, buspirone likely provides relief through adaptations in 5HT1a receptors.[3]

This may or may not be important depending on if it's a competitive antagonist or not, because metoclopramide binds to some of the same receptors.

Metoclopramide works by antagonizing central and peripheral dopamine-two receptors (D2) in the medullary chemoreceptor trigger zone in the area postrema, usually stimulated by levodopa or apomorphine. It achieves this by decreasing the sensitivity of visceral afferent nerves that transmit from the gastrointestinal system to the vomiting center in the area postrema in the chemoreceptor trigger zone.[13] In addition to antagonizing dopamine receptors, metoclopramide is an antagonist at 5HT3 (type 3 serotonin receptors) and an agonist at 5HT4 receptors.[14][15] Metoclopramide also blocks the antiperistaltic effects of apomorphine, allowing metoclopramide to slow apomorphine's inhibition of gastric emptying, thereby accelerating gastric emptying by increasing the amplitude and duration of esophageal contractions. Consequently, it increases the resting tone of the lower esophageal sphincter while simultaneously relaxing the duodenal bulb and pyloric sphincter, thereby increasing the peristalsis of the duodenum and jejunum.[16][17]

The notable receptor here is the D2 receptor, because this is the one that prevents vomiting. Seeing that it's only a weak antagonist on D2, it probably isn't important, but I don't have much knowledge.