Abstract
The opioid receptors, mu (μ), kappa (κ) and delta (δ), are widely distributed throughout the peripheral and central nervous system. When activated, the opioid receptors attenuate the transmission of pain signals to the spinal cord. Dynorphin A, an endogenous agonist at κ receptors, shares a common N-terminal “message” sequence (Tyr-Gly-Gly-Phe) with most mammalian opioid peptides and has a unique C-terrninal “address” sequence [1]. The “message” sequence has been reported to be important for k activation, while the “address” sequence is designated as the potency-enhancing domain [1].