β-endorphin is an opioid peptide produced primarily in the anterior lobe of the pituitary gland [27]. Following release from its precursor protein, pro-opiomelanocortin (POMC), β-endorphin is circulated via the blood stream to interact with specific opioid receptors located throughout the body [28]. The peptide interacts primarily with the μ-opioid peptide (MOP) receptor, although it can also bind to and activate other opioid receptors, e.g. the delta receptor [29]. It produces analgesia by inhibiting the firing of peripheral somatosensory fibers. Stress-induced increases in the release of β-endorphin are positively correlated with the amelioration of pain, whereas administration of exogenous opioids, such as fentanyl, reduces plasma levels of the peptide [27]. In experimental animals, exogenous opioids such as morphine have been shown to down-regulate the expression of POMC and subsequently induce a decrease in the biosynthesis of β-endorphin [30]. It has been suggested that decreased β-endorphin concentrations may play a role in a variety of chronic pain disorders [27].
