Effect of the analgesics dipyrone, tramadol, and meloxicam on the behavior of laboratory rats

Alemán-Laporte, Jilma; Alvarado, Gilbert; Antiovvrio, Ana Tada Fonseca Brasil; Trías, Jaime Fornaguera; Rojas-Carvajal, Mijail; Mori, Cláudia Madalena Cabrera

doi:10.1016/j.jveb.2022.08.001

Cited by 2 publications

(3 citation statements)

References 24 publications

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“…The present findings in the open field test are similar to those reported by Szkutnik-Fiedler et al (2012) and Ubale et al (2015). Although previous research showed inhibited locomotor activity after acute (Alemán-Laporte et al, 2022) or chronic tramadol administration to rats (Elsukary et al, 2022) in contrast to our observation of unaffected activity, it may be explained by the discrepancy of open The level of DA is known to be reduced after naloxone-induced withdrawal (Rada et al, 2004), which was observed in the present study. Synaptic plasticity is the main functional alteration of the brain that leads to adaptive behavior.…”

Section: Figsupporting

confidence: 87%

“…(2015). Although previous research showed inhibited locomotor activity after acute (Alemán-Laporte et al ., 2022) or chronic tramadol administration to rats (Elsukary et al ., 2022) in contrast to our observation of unaffected activity, it may be explained by the discrepancy of open field testing time relative to the tramadol time of last administration.…”

Section: Discussionmentioning

confidence: 90%

“…Alemán-Laporte et al . (2022) described increased open arm time and frequency after tramadol administration similar to our findings in naloxone-induced withdrawal treatment with oral or implanted tramadol.…”

Section: Discussionmentioning

confidence: 99%

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A novel tramadol–polycaprolactone implant could palliate heroin conditioned place preference and withdrawal in rats: behavioral and neurochemical study

Elshebiney,

Elgohary,

El-Shamarka

et al. 2024

Behavioural Pharmacology

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Drug dependence is a chronic brain disease characterized by craving and recurrent episodes of relapse. Tramadol HCl is a promising agent for withdrawal symptoms management, considering its relatively low abuse potential and safety. Oral administration, however, is not preferred in abstinence maintenance programs. Introducing an implantable, long-lasting formula is suggested to help outpatient abstinence programs achieve higher rates of treatment continuation. Tramadol implants (T350 and T650) were prepared on polycaprolactone polymer ribbons by the wet method. Male Wistar rats were adapted to heroin-conditioned place preference (CPP) at escalating doses (3–30 mg/kg, intraperitoneally, for 14 days). Implants were surgically implanted in the back skin of rats. After 14 days, the CPP score was recorded. Naloxone (1 mg/kg, intraperitoneally) was used to induce withdrawal on day 15, and symptoms were scored. Elevated plus maze and open field tests were performed for anxiety-related symptoms. Striata were analyzed for neurochemical changes reflected in dopamine, 3,4-dihydroxyphenyl acetic acid, gamma-aminobutyric acid, and serotonin levels. Brain oxidative changes including glutathione and lipid peroxides were assessed. The tramadol implants (T350 and T650) reduced heroin CPP and limited naloxone-induced withdrawal symptoms. The striata showed increased levels of 3,4-dihydroxyphenyl acetic acid, and serotonin and decreased levels of gamma-aminobutyric acid and dopamine after heroin withdrawal induction, which were reversed after implanting T350 and T650. Implants restore the brain oxidative state. Nonsignificant low naloxone-induced withdrawal score after the implant was used in naive subjects indicating low abuse potential of the implants. The presented tramadol implants were effective at diminishing heroin CPP and withdrawal in rats, suggesting further investigations for application in the management of opioid withdrawal.

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Section: Figsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 90%

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A novel tramadol–polycaprolactone implant could palliate heroin conditioned place preference and withdrawal in rats: behavioral and neurochemical study

Elshebiney,

Elgohary,

El-Shamarka

et al. 2024

Behavioural Pharmacology

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Role of apoptosis and autophagy in mediating tramadol-induced neurodegeneration in the rat hippocampus

et al. 2023

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BackgroundTramadol (TRA) is a pain killer, which its abuse is widely increased during recent years, but clear mechanism for induction of neurotoxicity remains unclear. The present study aims to investigate involvement of apoptosis and autophagy signaling pathways and also mitochondrial system on TRA induced neurotoxicity. Materials and MethodsSixthy adult male rats were randomly divided into ve groups that received standard saline and TRA in doses of 25, 50, 75, 100 and 150 mg/kg as intraperitoneal administration for 21 days, respectively. In 22th day, Open Field Test (OFT), as standard test for hippocampal cell damages was used. Also hippocampal level of JNK, Bcl-2, Beclin1 and Bax proteins as well as mitochondrial quadruple complex enzymes was measured ResultsTRA at doses 75,100 and 150 mg/kg causes dysfunction in OFT behavioral and also in mentioned high doses could increases level of both activated (total) and non-activated from of JNK and also increased Beclin-1 and Bax. TRA at doses of 75,100 and 150 mg/kg increased phosphorylated form of Bcl-2 level while decreased un-phosphorylated (total form) form of Bcl-2. ConclusionAccording to obtained data, TRA causes activation of apoptosis and or autophagy processes via modulation of TNF-α or IL-1β/JNK/Bcl-2/Beclin1 and Bcl-2/Bax signaling pathway and causes dysfunction of mitochondrial respiratory chain enzymes.

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Effect of the analgesics dipyrone, tramadol, and meloxicam on the behavior of laboratory rats

Cited by 2 publications

References 24 publications

A novel tramadol–polycaprolactone implant could palliate heroin conditioned place preference and withdrawal in rats: behavioral and neurochemical study

A novel tramadol–polycaprolactone implant could palliate heroin conditioned place preference and withdrawal in rats: behavioral and neurochemical study

Role of apoptosis and autophagy in mediating tramadol-induced neurodegeneration in the rat hippocampus

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