The endomorphins are a group of endogenous opioid peptides consisting of endomorphin-1 (Tyr-Pro-Trp-Phe-NH2) and endomorphin-2 (Tyr-Pro-Phe-Phe-NH2). They are tetrapeptides with the highest known affinity and selectivity for the μ-opioid receptor. Endomorphin-1 is found in the nucleus of the solitary tract, the periventricular hypothalamus, and the dorsomedial hypothalamus, where it is found within histaminergic neurons and may regulate sedative and arousal behaviors.[1] It is assumed that endomorphins are the cleavage products of a larger precursor, but this polypeptide or protein has not yet been identified.[2]

Experimental results

In rats similarly potent dosages of synthetic endomorphin and morphine produced comparable amounts of pain relief. However, motor skills and breathing were significantly impaired in those receiving morphine, while the endomorphin rats did not.[3][4]

The morphine rats spent more time in the compartment where they had received morphine, while the endomorphin rats did not. Only the morphine rats made efforts to secure further doses of the drug.[3]

Endomorphin did not activate spinal glial cells, an established morphine effect that helps to build tolerance of the drug.[3]

See also


  1. Greco, MA; Fuller, PM; Jhou, TC; Martin-Schild, S; Zadina, JE; Hu, Z; Shiromani, P; Lu, J (2008). "Opioidergic projections to sleep-active neurons in the ventrolateral preoptic nucleus". Brain Research. 1245: 96–107. doi:10.1016/j.brainres.2008.09.043. PMC 2753822Freely accessible. PMID 18840417.
  2. Stefan Offermanns; Walter Rosenthal (14 August 2008). Encyclopedia of Molecular Pharmacology. Springer Science & Business Media. pp. 904–. ISBN 978-3-540-38916-3.
  3. 1 2 3 Lavars, Nick (January 28, 2016). "New pain-relief drug shapes as less addictive alternative to morphine". www.gizmag.com. Retrieved 2016-01-30.
  4. Zadina, James E.; Nilges, Mark R.; Morgenweck, Jenny; Zhang, Xing; Hackler, Laszlo; Fasold, Melita B. (2016-06-01). "Endomorphin analog analgesics with reduced abuse liability, respiratory depression, motor impairment, tolerance, and glial activation relative to morphine". Neuropharmacology. 105: 215–227. doi:10.1016/j.neuropharm.2015.12.024.

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