Abstract:
INTRODUCTION:The present study was designed to investigate the rewarding effects induced by tramadol and its active metabolite O-desmethyltramadol (M1) under a neuropathic pain-like state. RESULTS:In opioid receptor binding and G protein activation, we confirmed that M1, but not tramadol, showed mu-opioid receptor (MOR) agonistic activity. Furthermore, we found that the subcutaneous (s.c.) injection of tramadol and M1 each produced a significant place preference in mice, and these effects were significantly suppressed by pretreatment with the MOR antagonist beta-funaltrexamine. The dopamine level in the mouse nucleus accumbens was significantly increased by s.c. injection of either tramadol or M1. Mice with sciatic nerve ligation exhibited a marked decrease in the latency of paw withdrawal in response to a thermal stimulus only on the ipsilateral side. Under these neuropathic pain-like conditions, the rewarding effect induced by s.c. injection of either tramadol or M1 was dramatically inhibited after sciatic nerve ligation. Furthermore, the M1-induced G protein activation in the lower midbrain area was suppressed after sciatic nerve ligation. DISCUSSION:Our present data support the notion that the rewarding effect induced by tramadol is mediated mainly through metabolism to its active metabolite M1 via MOR. Furthermore, the suppression of the M1-induced G protein activation in the lower midbrain area caused by sciatic nerve ligation may be responsible for inhibiting the rewarding effects induced by s.c. injection of tramadol and M1 under a neuropathic pain-like state.
journal_name
Psychopharmacology (Berl)journal_title
Psychopharmacologyauthors
Nakamura A,Narita M,Miyoshi K,Shindo K,Okutsu D,Suzuki M,Higashiyama K,Suzuki Tdoi
10.1007/s00213-008-1180-1subject
Has Abstractpub_date
2008-10-01 00:00:00pages
307-16issue
3eissn
0033-3158issn
1432-2072journal_volume
200pub_type
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