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

Noor Azuin Suliman,Mohamad Aris Mohd Moklas,Zulkhairi Amom,Rusliza Basir,Mohamad Taufik Hidayat Baharuldin,Che Norma Mat Taib,Mohd Ilham Adenan

doi:10.1155/2016/3517209

Abstract

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.

Highlights

Chronic exposure to opiates, for example, morphine, causes the progress of plasticity in the brain, expressed by dependence and addictive symptoms
The present study provides new insight into neurobiological and molecular changes associated with chronic morphine exposure in the cell line, which may help in developing a new pharmacotherapy derived from E. cuneatum
Chronic treatment of morphine was proved to cause dependence symptoms observed in the cell line

Summary

Introduction

For example, morphine, causes the progress of plasticity in the brain, expressed by dependence and addictive symptoms. The core features of addiction to opioid drugs are listing the tolerance, the withdrawal symptoms, and uncontrollable use of the drugs [3]. Biochemical trafficking among cellular compartment is facilitated by membrane carriers, usually vesicle. Classical synaptic neurotransmitter release is facilitated by the synaptic vesicle exocytosis [5]. The monoaminergic neurotransmitters are released by exocytosis of the small dense-core vesicle from the axonal varicosities [5]. Most neurotransmitter release is mediated by the same fundamental mechanism that involves four classes of proteins, namely, SNARE proteins, Rab-proteins, SM-proteins, and Rab-effectors [6]. The SNARE proteins and SM-proteins are responsible for catalysing the fusion reaction taking place on the presynaptic membrane, while Rab-proteins and Rabeffectors are taking role during docking and fusion reaction between the synaptic vesicle and presynaptic membrane [6]

Methods

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Discussion

Conclusion