Where it comes from
- Made in
- The nucleus incertus of the brainstem, a small group of neurons that project across the forebrain
- Sent out by
- Stress (through CRH) and the brain’s arousal rhythms
- Acts on
- Hippocampus (theta rhythm)
- Hypothalamus (feeding, stress hormones)
- Septum and amygdala
What it does
In medicine
- No approved medicine and no clinical test; relaxin-3 is not measured in people
- A systematic review of the human evidence in depression and anxiety found it thin: post-mortem and genetic hints, and no trial of anything 3
Beyond the body’s own use
- Agonists and blockers at RXFP3 are rodent tools so far. Blocking the receptor reduces alcohol seeking in rats 4, and activating it reduces anxious behaviour in rats and mice
- The peptide is awkward to turn into a drug: an analogue has to prefer RXFP3 over RXFP1 and has to reach the brain, which is why none has entered human trials
Sources
- McGowan et al., Central relaxin-3 administration causes hyperphagia in male Wistar rats, Endocrinology 2005
- Ma et al., Modulation of hippocampal theta oscillations and spatial memory by relaxin-3 neurons, Learning and Memory 2009
- Wong et al., The relaxin-3/RXFP3 system in clinical depression and anxiety, Neuroscience and Biobehavioral Reviews 2021
- Ryan et al., Relaxin-3/RXFP3 system regulates alcohol-seeking, Proceedings of the National Academy of Sciences 2013
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.