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Neuronal Calcium Channels Blocker, Ziconotide (ɷ-Conotoxin Mviia), Reverses Morphine Withdrawal-Induced Memory Impairments Via Alteration in Hippocampal Nmda Receptor Expression in Rats Publisher



Bozorgi H1 ; Motaghi E2 ; Zamani M3 ; Ghavimi R4
Authors
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Authors Affiliations
  1. 1. Laboratory of Learning and Memory, Research Center of Physiology and Department of Pharmacology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran
  2. 2. Department of Pharmacology, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran
  3. 3. Department of Pharmacology, School of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
  4. 4. Department of Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Toxin Reviews Published:2020


Abstract

ɷ-Conotoxin MVIIA (ziconotide or SNX-111) is an atypical analgesic drug with the water-soluble formulation and routinely is injected into the brain and spinal regions in human and animal model studies. The aim of the current study was to investigate the neurobehavioral protection of this agent as a selective N-type calcium channels antagonist following spontaneous morphine withdrawal in rats. Male rats were administered morphine (10–50 mg/kg) intraperitoneal (IP) twice daily for 7 days. Ziconotide was injected intrathecal (IT) either in chronic form (0.1, 0.3 and 1 µg/rat) concurrent with daily doses of morphine or it was injected as a single dose (1 µg/rat) on the last day. Novel object recognition task (NOR) and radial arm maze (RAM) were used in order to evaluation of the recognition and spatial working/reference memory performances, respectively. The amount of N-methyl-D-aspartate (NMDA) receptor subunits including NR2A and NR2B in the hippocampus and prefrontal cortex were determined by western blotting. We observed that abrupt cessation after chronic exposure to morphine led to decrease in both recognition and working/reference memory performances (p <.01). Spontaneous withdrawal also significantly suppressed the amount of NR2A and NR2B. This impairment was attenuated by single and chronic doses of ziconotide (p <.05). Also, expression of NR2A and NR2B were significantly increased during both drug delivery protocols. Our findings suggest that ziconotide prevents morphine withdrawal-induced memory deficits through alteration in glutamatergic transmission and regulation of NMDA receptors (NMDARs). © 2018 Informa UK Limited, trading as Taylor & Francis Group.
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