GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
In vivo characterization of the effects of ghrelin on the modulation of acute pain at the supraspinal level in mice.
Wei. Jie J; Zhi. Xing X; Wang. Xiao-Lang XL; Zeng. Ping P; Zou. Ting T; Yang. Bei B; Wang. Jing-Lei JL
Key Findings
- Central (i.c.v.) administration of ghrelin produced dose‑ and time‑dependent antinociception in mice.
- The pain‑relief effect of ghrelin was blocked by the opioid antagonist naloxone, indicating involvement of the opioid system.
- Blocking the ghrelin receptor with [d‑Lys3]‑GHRP‑6 also eliminated ghrelin’s antinociceptive effect, confirming the role of GHS‑R1a.
Practical Outcomes
- While the study shows ghrelin can act as a pain‑killer in the brain, the method (direct brain injection) isn’t feasible for personal use. It suggests that future drugs targeting the ghrelin system might help with pain, but current self‑experimenters have no actionable protocol from this research.
Summary
In mice, injecting the hormone ghrelin directly into the brain lowered pain responses in two standard pain tests. This pain‑relief effect disappeared when drugs that block opioid receptors or the ghrelin receptor were also given, showing that ghrelin works through both its own receptor and the body’s opioid system.
Abstract
Ghrelin, an acylated peptide produced in the stomach, increases food intake and growth hormone secretion, inhibits pro-inflammatory cascade, etc. Ghrelin and its receptor (GHS-R1a) mRNA were found in the area related to the regions for controlling pain transmission, such as the hypothalamus, the midbrain, the spinal cord, etc. Ghrelin has been shown to have antinociceptive activity and also anti-inflammatory properties in inflammatory pain and chronic neuropathic pain. Therefore, the aim of the present study was to investigate the effects of ghrelin for the first time in the acute pain modulation at the supraspinal level, using the tail withdrawal test and hot-plate test in mice. Intracerebroventricular (i.c.v.) administration of ghrelin (mouse, 0.1-3 nmol) produced a dose- and time-related antinociceptive effect in the tail withdrawal test and hot-plate test, respectively. Antinociceptive effect elicited by ghrelin (i.c.v., 1 nmol) was significantly antagonized by opioid receptor antagonist naloxone (i.c.v., 10 nmol co-injection or i.p., 10mg/kg, 10 min prior to ghrelin) in both tail withdrawal test and hot-plate test. At these doses, naloxone significantly antagonized the antinociceptive effect induced by morphine (i.c.v., 3 nmol). Ghrelin (i.c.v., 1 nmol)-induced antinociception was significantly antagonized by co-injection with 10 nmol [d-Lys3]-GHRP-6, the selective antagonist of GHS-R1a identified more recently, while [d-Lys3]-GHRP-6 (10 nmol) alone induced neither hyperalgesia nor antinociception. Overall this data indicate that ghrelin could produce antinociception through an interaction with GHS-R1a and with the central opioid system. Thus ghrelin may be a promising peptide for developing new analgesic drugs.
Study Information
pubmed
2013
2013-03-14T00:00:00.000Z
10.1016/j.peptides.2013.03.004
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