Hydrogen sulphide induces micro opioid receptor-dependent analgesia in a rodent model of visceral pain.

ABSTRACT:

Background

Hydrogen sulphide (H2S) is a gaseous neuro-mediator that exerts analgesic effects in rodent models of visceral pain by activating KATP channels. A body of evidence support the notion that KATP channels interact with endogenous opioids. Whether H2S-induced analgesia involves opioid receptors is unknown.

Methods

The perception of painful sensation induced by colorectal distension (CRD) in conscious rats was measured by assessing the abdominal withdrawal reflex. The contribution of opioid receptors to H2S-induced analgesia was investigated by administering rats with selective mu, kappa and delta opioid receptor antagonists and antisenses. To investigate whether H2S causes mu opioid receptor (MOR) transactivation, the neuronal like cells SKNMCs were challenged with H2

SUBMITTER: Distrutti E 

PROVIDER: S-EPMC2908066 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature