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Thread: prozac and 4-AP interaction?

  1. #1

    prozac and 4-AP interaction?

    I'm taking 4-AP and may start prozac because it could help nerve regeneration.

    Does anyone know if they can't mix?

  2. #2
    Super Moderator Sue Pendleton's Avatar
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    Jul 2001
    Wisconsin USA
    Quote Originally Posted by Sandi's Daughter
    I'm taking 4-AP and may start prozac because it could help nerve regeneration.

    Does anyone know if they can't mix?
    I can't get your link to work. Can you try a work around or, if short, just copy it. I want to know if Prozac regenerates! 4-aminopyridine is a potassium channel blocker. As far as I know the use of Prozac or other SSRIs does not appear to be a problem. It is always a good idea to have the prescribing doctor of one or both drugs check on concurrent use problems for each patient.
    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

    Disclaimer: Answers, suggestions, and/or comments do not constitute medical advice expressed or implied and are based solely on my experiences as a SCI patient. Please consult your attending physician for medical advise and treatment. In the event of a medical emergency please call 911.

  3. #3
    is it working?

    this was done on MS patients so beware...

  4. #4
    Hi, Sandi's daughter, it is not a good idea to double-post in the Cure forum and another forum. It splits up the discussion. Please post in one forum please. There are other responses in the thread that you started in the Cure Forum

    I have commented on the other thread that I didn't think that there was any evidence that serotonin uptake blockers had beneficial effects in spinal cord injury. Let me expand on that. Mostert, et al. (2006) found that fluoxetine increased cerebral white matter NAA/Cr (metabolism) ratios in patients with multiple sclerosis. Romani, et al. (2004) had reported the both 4-AP and fluoxetine reduced fatigue but one assumes that the latter is due to reducing depression rather than any regenerative effects. Engesser-Cesar, et al. (2007) recently reported that fluoxetine increased neurogenesis and neurotrophins in the hippocampus but not the spinal cord. Note that lithium also has been shown to increase neurogenesis in hippocampus (Chen, et al., 2000).

    In the study that you mentioned, it is a preliminary report from Czechoslovakia that seems to have "radiological effects" (as opposed presumably to functional effects), suggesting that fluoxetine improved the radiological appearance of the brains in people with multiple sclerosis. It is not clear what this means in terms of actual effects of fluoxetine on remyelination. It is also not clear whether this is a specific effect of fluoxetine or all serotonin-uptake blockers.


    Reference cited
    1. Mostert JP, Sijens PE, Oudkerk M and De Keyser J (2006). Fluoxetine increases cerebral white matter NAA/Cr ratio in patients with multiple sclerosis. Neurosci Lett. 402: 22-4. Department of Neurology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen 9713 GZ, The Netherlands. Axonal degeneration in multiple sclerosis (MS) may be caused by mitochondrial dysfunction and is associated with decreased levels of N-acetylaspartate (NAA) as measured with 1H-magnetic resonance spectroscopy (MRS). Fluoxetine stimulates astrocytic glycogenolysis, which serves as an energy source for axons. Eleven patients with MS received fluoxetine orally 20 mg a day during the first week, and 40 mg a day during the second week. The mean NAA/Creatine ratio in cerebral white matter of the MS patients increased from 1.77 at baseline to 1.84 at the end of the second week (p=0.007). These findings show evidence for a reversible axonal dysfunction in patients with MS and provide a rationale for investigating whether fluoxetine has neuroprotective effects in MS.
    2. Romani A, Bergamaschi R, Candeloro E, Alfonsi E, Callieco R and Cosi V (2004). Fatigue in multiple sclerosis: multidimensional assessment and response to symptomatic treatment. Mult Scler. 10: 462-8. Laboratorio Potenziali Evocati, Istituto Neurologico C. Mondino, Pavia, Italy. Sixty relapsing remitting multiple sclerosis (MS) patients were selected on the basis of their score on the Fatigue Severity Scale (FSS) and formed two groups: 40 patients (fatigued MS; MSf) scored above the 75th percentile of a previously assessed representative MS sample (100 patients), and 20 age- and sex-matched patients (nonfatigued MS patients; MSnf) scored below the 25th percentile. The patients underwent clinical evaluation (Expanded Disability Status Scale (EDSS)), further assessment of fatigue (Fatigue Impact Scale), scales evaluating depression (Hamilton Depression Rating Scale (HDRS) and Beck's Depression Inventory (BDI)) and neuropsychological tests. All patients were evaluated for muscle fatigability and central activation by means of a biomechanical test of sustained contraction; they also underwent somatosensory evoked potentials (SSEPs) and transcranial magnetic stimulation (TMS). The patients of the MSf subgroup were then randomized to one of the following two treatments: 4-aminopyridine (4-AP) 24 mg/day and fluoxetine (FLX) 20 mg/day. After a one-week titration this treatment proceeded for 8 weeks. At the end of the treatment, EDSS, fatigue and depression scores were further evaluated. At baseline, fatigue test scores consistently correlated with depression and cognitive test scores, but not with the fatigability test. Fatigue scores decreased in both treatment groups in a similar way. Due to the design of the study, this cannot be disjoined from a placebo effect. The changes of fatigue scores could not be predicted in the FLX group, whereas in the 4-AP group higher basal fatigability test scores were associated with greater reduction in fatigue scores.
    3. Engesser-Cesar C, Anderson AJ and Cotman CW (2007). Wheel running and fluoxetine antidepressant treatment have differential effects in the hippocampus and the spinal cord. Neuroscience. 144: 1033-44. Institute for Brain Aging and Dementia, University of California, Irvine, 1113 Gillespie NRF, Irvine, CA 92697-4540, USA. Exercise and antidepressants used independently have been shown to increase hippocampal brain-derived neurotrophic factor (BDNF) and neurogenesis. Despite the fact that patients with depression are often prescribed both, the effects of the exercise and fluoxetine antidepressant treatment used in combination are unknown. Using C57Bl/10 female mice, BDNF protein, insulin-like growth factor 1 (IGF-1) protein and neurogenesis were measured in the hippocampus after 21 days of wheel running, 21 days of fluoxetine antidepressant therapy (daily i.p. injections of 5 mg/kg, 10 mg/kg or 25 mg/kg) and the combination of the two. BDNF protein and cytogenesis/neurogenesis increased in the hippocampus with fluoxetine (high dose), but not wheel running. Hippocampal IGF-1 protein did not change with either treatment. There were no synergistic effects of combining exercise and fluoxetine treatment. Recent reports have also shown that exercise induces molecular mechanisms that benefit the spinal cord and can improve recovery after spinal cord injury (SCI); therefore, we repeated the assays in the spinal cord. Results showed that BDNF, IGF-1 and neurogenesis behave independently in the hippocampus and spinal cord. BDNF protein did not change in the spinal cord with either wheel running or fluoxetine treatment. Spinal cord IGF-1 protein did not change with wheel running, but it decreased with fluoxetine (high dose). Furthermore, spinal cord cytogenesis decreased with fluoxetine treatment. The combined wheel running and fluoxetine groups did not show synergistic results. Thus, the hippocampus and the spinal cord respond in distinct ways to wheel running and fluoxetine, and a prior induction of BDNF, IGF-1 or cytogenesis is unlikely to be the mechanism for wheel running providing a margin of protection against SCI.
    4. Chen G, Rajkowska G, Du F, Seraji-Bozorgzad N and Manji HK (2000). Enhancement of hippocampal neurogenesis by lithium. J Neurochem. 75: 1729-34. Laboratory of Molecular Pathophysiology, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. Increasing evidence suggests that mood disorders are associated with a reduction in regional CNS volume and neuronal and glial cell atrophy or loss. Lithium, a mainstay in the treatment of mood disorders, has recently been demonstrated to robustly increase the levels of the cytoprotective B-cell lymphoma protein-2 (bcl-2) in areas of rodent brain and in cultured cells. In view of bcl-2's antiapoptotic and neurotrophic effects, the present study was undertaken to determine if lithium affects neurogenesis in the adult rodent hippocampus. Mice were chronically treated with lithium, and 5-bromo-2-deoxyuridine (BrdU) labeling of dividing cells was conducted over 12 days. Immunohistochemical analysis was undertaken 1 day after the last injection, and three-dimensional stereological cell counting revealed that lithium produced a significant 25% increase in the BrdU-labeled cells in the dentate gyrus. Double-labeling immunofluorescence studies were undertaken to co-localize BrdU-positive cells with neuron-specific nuclear protein and showed that approximately 65% of the cells were double-labeled. These results add to the growing body of evidence suggesting that mood stabilizers and antidepressants exert neurotrophic effects and may therefore be of use in the long-term treatment of other neuropsychiatric disorders.

    Last edited by Wise Young; 11-12-2007 at 01:39 PM.

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