μ-Opioid receptor in the CA1 involves in tramadol and morphine cross state-dependent memory

Niknamfar, Saba; Zadeh-Tehrani, Setareh Nouri; Sadat‐Shirazi, Mitra‐Sadat; Akbarabadi, Ardeshir; Rahimi-Movaghar, Afarin; Zarrindast, Mohammad‐Reza

doi:10.1016/j.neulet.2019.04.054

Cited by 7 publications

(6 citation statements)

References 40 publications

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“…The results obtained in the present study are consistent with those previously reported, although in models other than pain, in which naltrexone significantly decreases the response of discriminatory behavior to tramadol [16], the inhibition in memory recovery [17]. However, It should be noted that the effect of opioid antagonists, in the antinociception of tramadol, has only been reported in a model of cerebral ischemia pain, in which the effect of the opioid was significantly cancelled by β-funaltrexamine (MOR selective opioid receptor antagonist), but not naltrindole or nor-binaltorphimine [18].…”

Section: Discussionsupporting

confidence: 93%

Pharmacological approach to mechanism of action of tramadol in murine nociception and inflammation assays

F¹,

Noriega²,

Sierralta³

et al. 2020

World J. Adv. Res. Rev.

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The analgesic activity of tramadol has been recognized both in man and in several animal models of pain. However an extensive characterization of the opioid mechanism of action of tramadol of pain has not been reported. The objective of the present study was to evaluate the antinociceptive and anti-inflammatory activity of tramadol in different animal pain models and to determine the effect of the selective opioid antagonist: naltrexone, naltrindole and norbinaltorphimine. The i.p. administration of tramadol induced a dose-dependent with the following order of potency: formalin hind paw, phase II > formalin hind paw, phase I> acetic acid writhing > tail flick > hot plate. Pretreatment of the mice with naltrexone (1 mg/kg i.p.) antagonized tramadol activity in the acetic acid writhing test, in the hot plate and the tail flick assays, however lack of effect in the formalin hind paw assays. Naltrindole (1 mg/kg i.p.) did not induce a significant change in all the murine assays. However, the mice pretreated with nor-binaltorphimine (1 mg/kg, i.p.) did not modified the tramadol antinociception in the acetic acid writhing and in the hot plate assays. Besides, norbinaltorphimine pretreatment reversed significantly the tramadol effect in the tail flick and in the formalin hind paw assays. This findings suggests that tramadol effect is mediated by MOR and KOR rather DOR receptors.

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Section: Discussionsupporting

confidence: 93%

Pharmacological approach to mechanism of action of tramadol in murine nociception and inflammation assays

F¹,

Noriega²,

Sierralta³

et al. 2020

World J. Adv. Res. Rev.

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“…Also, amnesia-induced by Intra-CA1 administration of tramadol improved by pre-test injection of either tramadol or morphine. It seems that tramadol is capable of produced state-dependent memory and also, it has a cross state-dependent memory with morphine in the CA1 areas of the hippocampus, done possibly via a µ-opioid receptor (Niknamfar et al, 2019[ 46 ]).…”

Section: Induction Of Exogenous State-dependent Memory By Systemic Inmentioning

confidence: 99%

State-dependent memory and its modulation by different brain areas and neurotransmitters

Zarrindast

Khakpai

2020

EXCLI Journal; 19:Doc1081; ISSN 1611-2156

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“…Chronic exposure of morphine in animals impairs hippocampal long‐term memory retention (Bortolotto & Grilli, 2017; Dellarole et al, 2014; Mutso et al, 2012). Some reports also indicated that tramadol administration reduces memory function in experimental models by activating hippocampal μ‐opioid receptors (Baghishani et al, 2018; Hosseini‐Sharifabad et al, 2016; Niknamfar et al, 2019; Yan et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Effect of tramadol on apoptosis and synaptogenesis in hippocampal neurons: The possible role of µ‐opioid receptor

Hosseindoost

Akbarabadi

Sadat‐Shirazi

et al. 2022

Drug Development Research

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Tramadol is a synthetic opioid with centrally acting analgesic activity that alleviates moderate to severe pain and treats withdrawal symptoms of the other opioids. Like other opioid drugs, tramadol abuse has adverse effects on central nervous system components. Chronic administration of tramadol induces maladaptive plasticity in brain structures responsible for cognitive function, such as the hippocampus. However, the mechanisms by which tramadol induces these alternations are not entirely understood. Here, we examine the effect of tramadol on apoptosis and synaptogenesis of hippocampal neuronal in vitro. First, the primary culture of hippocampal neurons from neonatal rats was established, and the purity of the neuronal cells was verified by immunofluorescent staining. To evaluate the effect of tramadol on neuronal cell viability MTT assay was carried out. The western blot analysis technique was performed for the assessment of apoptosis and synaptogenesis markers. Results show that chronic exposure to tramadol reduces cell viability of neuronal cells and naloxone reverses this effect. Also, the level of caspase‐3 significantly increased in tramadol‐exposed hippocampal neurons. Moreover, tramadol downregulates protein levels of synaptophysin and stathmin as synaptogenesis markers. Interestingly, the effects of tramadol were abrogated by naloxone treatment. These findings suggest that tramadol can induce neurotoxicity in hippocampal neuronal cells, and this effect was partly mediated through opioid receptors.

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μ-Opioid receptor in the CA1 involves in tramadol and morphine cross state-dependent memory

Cited by 7 publications

References 40 publications

Pharmacological approach to mechanism of action of tramadol in murine nociception and inflammation assays

Pharmacological approach to mechanism of action of tramadol in murine nociception and inflammation assays

State-dependent memory and its modulation by different brain areas and neurotransmitters

Effect of tramadol on apoptosis and synaptogenesis in hippocampal neurons: The possible role of µ‐opioid receptor

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