Using the latency for tail-flick after thermal stimulation we have assessed the effects of α-, γ1- and γ2-MSH on nociceptive threshold in the mice. Intracisternal injections of γ2-MSH induced a distinct analgesia, while γ1-MSH in the same doses gave only a minor analgesia. Intracisternal α-MSH instead gave a short-term hyperalgesia. The effect of γ2-MSH was not blocked by any of the MC4/MC3 receptor antagonist HS014, naloxone or by the prior intracisternal administrations of γ1-MSH. However, the γ2-MSH analgesic response was completely attenuated by treating animals with the GABAA antagonist bicuculline. The γ2-MSH analgesic effect was moreover additive to the analgesia afforded by muscimol and ethanol, but not to that afforded by diazepam. In addition both γ1- and γ2-MSH induced moderate catalepsy, but could at the same time attenuate haloperidol induced catalepsia. We conclude that γ2-MSH mediates a central analgesic effect via GABA-receptor dependent pathway that is distinct from melanocortic- and opioid-receptors. Moreover, the mechanism for γ2-MSH's analgesic effect appears to be distinct from that causing moderate catalepsia by γ-MSH's.
Field of Science*
- 3.2 Clinical medicine
- 1.1. Scientific article indexed in Web of Science and/or Scopus database