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Tramadol‐Induced Seizurogenic Effect: A Possible Role of Opioid‐Dependent γ‐Aminobutyric Acid Inhibitory Pathway
Author(s) -
Rehni Ashish K.,
Singh Inderbir,
Kumar Manoj
Publication year - 2008
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00276.x
Subject(s) - tramadol , (+) naloxone , gabapentin , pharmacology , opioid , chemistry , inhibitory postsynaptic potential , opioid receptor , aminobutyric acid , endocrinology , medicine , receptor , analgesic , alternative medicine , pathology
The present study has been designed to pharmacologically investigate the role of opioid and γ‐aminobutyric acid receptors on the seizurogenic effect of tramadol. A single injection of pentylenetetrazole (80 mg/kg) was used to elicit seizure activity in mice. Seizures were assessed in terms of the time latency of the onset of Straub's tail phenomenon, onset of jerky movements of whole body, convulsions and death. Tramadol administration (50 mg/kg) caused a marked increase in seizurogenic activity of pentylenetetrazole as measured in terms of a significant decrease in the time latency of the onset of Straub's tail phenomenon, jerky movements of whole body, convulsions and death. Moreover, prior administration of naloxone (2 mg/kg) and gabapentin (25 mg/kg), respectively, attenuated the seizurogenic activity that tramadol exerted on pentylenetetrazole‐treated mice. Furthermore, prior administration of naloxone (2 mg/kg) and gabapentin (25 mg/kg), respectively, also attenuated the seizurogenic activity exerted by tramadol per se . Therefore, it is suggested that tramadol exerts a seizurogenic effect on mice possibly via an opioid‐dependent γ‐aminobutyric acid inhibitory pathway.