An analogue of growth hormone releasing factor (GRF), (Ac-Try1, D-Phe2)-GRF-(1-29), specifically antagonizes the facilitation of the flexor reflex induced by intrathecal vasoactive intestinal peptide in rat spinal cord.
Xu. X J XJ; Wiesenfeld-Hallin. Z Z
Key Findings
- The GRF‑1‑29 analogue antagonizes VIP‑induced facilitation of the nociceptive flexor reflex in rat spinal cord.
- It is about 15 times less potent than VIP itself, yet still effective at low picomolar concentrations.
- The antagonist does not interfere with reflex facilitation caused by other neuropeptides (substance P, somatostatin, CGRP, galanin) or normal C‑fiber activation.
Practical Outcomes
- For biohackers, this study is mainly a basic‑science finding in rats and does not provide dosage, safety, or efficacy data for humans. It suggests the peptide could be used experimentally to block VIP signaling, but there is no clear protocol or benefit for longevity, metabolism, or performance at this stage.
Summary
In rats, a modified growth‑hormone‑releasing‑factor peptide (Ac‑Try1, D‑Phe2‑GRF‑1‑29) blocks the pain‑enhancing effects of vasoactive intestinal peptide (VIP) in the spinal cord, showing it works as a specific VIP antagonist but doesn’t affect other pain‑related signals.
Abstract
The effect of intrathecal (i.t.) vasoactive intestinal peptide (VIP) and an analogue of growth hormone releasing factor (GRF) with putative VIP antagonistic property, (Ac-Try1, D-Phe2)-GRF-(1-29), on the nociceptive flexor reflex was studied in decerebrate, spinalized, unanesthetized rats. VIP (10 pM) facilitated the flexor reflex for several minutes. A similar facilitation was induced by the VIP antagonist applied i.t. with a potency 15 times less than that of VIP. Pre-administration of the VIP antagonist dose-dependently antagonized the reflex facilitation by i.t. VIP. In contrast, the reflex facilitation induced by i.t. substance P, somatostatin, calcitonin gene-related peptide and galanin was not influenced by the VIP-antagonist. The VIP antagonist by itself did not depress the flexor reflex over the dose range of 3 pM-3 nM and neither did it block the facilitation of the flexor reflex induced by a brief conditioning electrical stimulus train that activated the C-afferents in skin innervated by the sural nerve. The present results indicate that this GRF analogue is an effective and specific VIP antagonist in the rat spinal cord. Furthermore, it is suggested that VIP may not be involved in the transmission of cutaneous nociceptive information under normal conditions.
Study Information
pubmed
1991
10.1016/0143-4179(91)90104-q