Acute Tramadol Administration Induces the Expression of pERK1/2 in Different Limbic and Pain Processing Structures

International audienceTramadol is a painkiller with some abuse potentials. The current study aimed to investigate rat cerebral structures that were activated by acute intraperitoneal administration of tramadol (10 mg/kg). The expression of pERK1/2 was used as a molecular tool for tramadol-induced

Reinforcing effect of tramadol in the rat

International audienceTramadol is one of the most commonly prescribed analgesic opioids in various pharmacopeias. Tramadol has been linked to abuse in recent clinical investigations. However, the behavioral effects and neural substrates of the drug have not been well characterized in preclinical studies. As a result, the present study investigated the effects of tramadol on behavioral sensitizations in rats. Its impacts on cellular and molecular alterations in the brain were also investigated. In conditioned place preference (CPP) paradigm, tramadol induced behavioral as well as motor sensitizations. These effects were dramatically reduced by intraperitoneal administration of naltrexone, an opioid receptor antagonist. Tramadol caused changes in several molecular markers (pERK1/2, Δ-FosB, PKCγ, PKMζ GAD67) in the anterior cingulate cortex, which could indicate an increase in excitation within this structure. Tramadol is demonstrated in the present study to be a reinforcing drug in rats, as it increased both behavioral and motor sensitizations. Tramadol’s effects are most likely due to the high levels of excitation it causes in the brain, which is mostly caused by the activation of opioid receptors

The Neuroprotective Effect of Clove Essential Oil Against 6-Ohda-Induced Cell Death in Sh-Sy5y and A Rat Model of Parkinson's Disease

International audienceParkinson's Disease (PD) is the second most prevalent neurological disorder. Natural therapies are becoming more popular for preventing disease onset. Clove Essential Oil (CEO), a potent antioxidant derived from Syzygium aromaticum buds, was tested in vitro (SH-SY5Y) and in vivo (PD rat model) for its ability to protect against 6-OHDA-induced cell death. Twenty-four hours of SH-SY5Y cells' exposure to 6-OHDA (100µM) drastically decreased cell viability. At doses lesser than 20µg/ml, CEO and its main component Eugenol (EG) had no cytotoxic effect on SH-SY5Y. CEO and EG at doses of 2.5-20µg/ml provided significant neuroprotection against 6-OH-DA-induced cell death. A PD rat model was generated by injecting 6-OHDA (21µg/animal) unilaterally into the striatum. An assessment of motor performance can predict neuronal cell loss in the Substancia Nigra Compacta (SNc). Compared to 6-OHDA-lesioned, CEO-treated (10mg/Kg) rats' locomotor performance (actimetry and cylinder tests) improved significantly one and two weeks after 6-OHDA-lesion. Tyrosine Hydroxylase (TH) cell count showed a significant decrease in cell death in ipsilateral SNc in both CEOtreated and 6-OHDA-lesioned rats when compared to contralateral. In contrast to the 6-OHDA-lesioned group, the ipsilateral SNc of the CEO-treated group showed a significant high TH cell number. In the present study, the neuroprotective effect of CEO was demonstrated both in vitro and in vivo against 6-OHDA cytotoxicity. Therefore, CEO could be used as a food supplement for PD prevention