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Evidence-Based Complementary and Alternative Medicine
Volume 2016, Article ID 3517209, 9 pages
Research Article

Morphine Antidependence of Erythroxylum cuneatum (Miq.) Kurz in Neurotransmission Processes In Vitro

1Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 Serdang, Selangor Darul Ehsan, Malaysia
2Atta-ur-Rahman Institute for Natural Product Discovery, Aras 9 Bangunan FF3, UiTM Puncak Alam, Bandar Baru Puncak Alam, 42300 Selangor Darul Ehsan, Malaysia
3Faculty of Health Sciences, Universiti Teknologi MARA, Kampus Puncak Alam, 42300 Puncak Alam, Selangor Darul Ehsan, Malaysia

Received 1 August 2016; Revised 11 October 2016; Accepted 23 October 2016

Academic Editor: Ki-Wan Oh

Copyright © 2016 Noor Azuin Suliman et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Opiate abuse has been studied to cause adaptive changes observed in the presynaptic release and the mediated-synaptic plasticity proteins. The involvement of neuronal SNARE proteins reveals the role of the neurotransmitter release in expressing the opioid actions. The present study was designed to determine the effect of the alkaloid extract of Erythroxylum cuneatum (E. cuneatum) against chronic morphine and the influences of E. cuneatum on neurotransmission processes observed in vitro. The human neuroblastoma cell line, SK-N-SH, was treated with the morphine, methadone, or E. cuneatum. The cell lysates were collected and tested for α-synuclein, calmodulin, vesicle-associated membrane protein 2 (VAMP 2), and synaptotagmin 1. The extract of E. cuneatum was observed to upregulate the decreased expression of dependence proteins, namely, α-synuclein and calmodulin. The effects were comparable to methadone and control. The expressions of VAMP 2 and synaptotagmin 1 were normalised by the plant and methadone. The extract of E. cuneatum was postulated to treat dependence symptoms after chronic morphine and improve the soluble N-ethylmaleimide-sensitive factor activating protein receptor (SNARE) protein involved in synaptic vesicle after.