Posted by JackD on December 11, 2004, at 22:37:52
In reply to opiates for depression, posted by lew on December 11, 2004, at 16:50:22
Awesome, that's great you've found something that works. I just recently found "the right" combination as well and what I've been writing could pertain to you. Check out my previous posts. I just did a quick search for info about Tramadol and found that it is actually structurally similar to Effexor. That is soooo amazing. It's another peice to the jigsaw puzzle. Go to www.pubmed.com to look for more abstracts. Oh, so anyway, Namenda (Memantine HCL) prevents and even reverses opiate tolerance (in theory) so maybe you should ask your doctor if you can try it with the tramadol. Oh and be careful with Tramadol regarding serotonin syndrome!!!
Hot damn I'm soooooo psyched that I read your post... this is the second time in the past few weeks that I've just happened onto something like this. Someone should seriously start looking into all this. Effexor, Pain, Depression, Opioid System, Tolerance, Bipolar II, Memantine... and now Tramadol. Go, GO! Go out and tell the world!!!!
Oh I almost forgot, here:
"Effects of Chronic Tramadol on Pre- and Post-Synaptic Measures of Monoamine Function
by Hopwood SE, Owesson CA, Callado LF, McLaughlin DP, Stamford JA.
Academic Department of Anaesthesia and Intensive Care, St Bartholomew's and The Royal London School of Medicine and Dentistry,
Royal London Hospital, Whitechapel, UK.
J Psychopharmacol 2001 Sep;15(3):147-53ABSTRACT
The atypical analgesic tramadol has strong structural similarities to the antidepressant venlafaxine and is a mixed noradrenaline (NA) and serotonin (5-HT) uptake inhibitor. Because tramadol has been found active in the forced swim test, a common predictor of antidepressant efficacy, we therefore examined the effects of chronic tramadol on various pre- and post-synaptic monoamine measures. Male Wistar rats (150-200 g) received tramadol (20 mg/kg i.p.) or vehicle for 21 days and were sacrificed 24 h after the last dose. Quantitative autoradiography revealed that specific frontocortical [3H]dihydroalprenolol and [3H]ketanserin binding was lower in the chronic tramadol group than controls (beta: 37+/-8 and 217+/-56 fmol/mg; 5-HT2A: 23+/-3 and 44+/-7 fmol/mg, respectively, p < 0.05). Chronic tramadol had no effect on the magnitude of electrically stimulated noradrenaline (NA) efflux or uptake in locus coeruleus (LC) slices. Although dexmedetomidine (10 nM) decreased LC NA efflux equally (by approximately 60%) in chronic tramadol and vehicle groups, desipramine (50 nM) increased LC NA efflux more in vehicle (to 164+/-7%) than tramadol-treated rats (144+/-6%; p < 0.05). Chronic tramadol had no effect on dorsal raphe (DRN) or median raphe (MRN) 5-HT efflux. However, 5-HT uptake in tramadol-treated rats was slower (p < 0.05) in MRN and nearly so (p = 0.055) in DRN. The selective 5-HT1A agonist 8-OH-DPAT reduced 5-HT efflux in both DRN and MRN. Its effect in DRN was greater in rats given chronic tramadol than in vehicle controls (54+/-2 versus 32+/-6% reduction in 5-HT efflux, respectively). In conclusion, we suggest that tramadol has many of the pre- and postsynaptic neurochemical features of a conventional antidepressant, as might be predicted from its pharmacology. "
poster:JackD
thread:427838
URL: http://www.dr-bob.org/babble/20041211/msgs/428043.html