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  1. #1
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    Default Bupropion: Generic vs. Brand

    The generic Bupropion XL manufactured by Par Pharmaceuticals is indistinguishable to me from the brand name. If your insurance switches you to generic I recommend you seek out a pharmacy that sells this brand. I've taken the Teva and Genpharma brands and they were both rough. Whatever Par Pharm is doing, they are doing it right.

    It also just struck me that it would be funny if Par Pharma was owned by Par Deus.

  2. Likes kassem23, Tussmann liked this post
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    PM coming your way bdog

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    Senior Member Tussmann's Avatar
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    http://news.priorsmart.com/biovail-l...ompanies-l3aA/

    For some reason it won't pull up the case for me. Does this ancedote say something to contradict your support for Par?

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    Senior Member Tussmann's Avatar
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    "Shortly after ConsumerLab.com’s report in October 2007 of potential problems with a generic version of the anti-depressant Wellbutrin XL, the FDA announced an investigation of the generic distributed by Teva Pharmaceuticals and manufactured by Impax Laboratories. The FDA has yet to disclose its results, but recent events corroborate ConsumerLab.com’s findings: A high-ranking FDA official, Dr. Robert Temple, noted in a radio interview that human bioequivalence tests showed the generic to release ingredient sooner than Wellbutrin XL. The United States Pharmacopeia (USP) published information indicating that this generic releases 25% to 50% of its active ingredient during the first two hours of dissolution while original Wellbutrin XL releases less than 20%. ConsumerLab.com notes that it recently learned that several lots of a twice-a-day generic bupropion were recalled by Teva in November for failing to dissolve properly."

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    Senior Member eclypz's Avatar
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    I've actually toyed with the idea of trying brand name wellbutrin, but I prefer the smaller dose of 150mg. All I have ever used is the generic indian pharm version and it does make me edgy. I wonder if a better dissolution would take the edge off?

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    Quote Originally Posted by Tussmann View Post
    http://news.priorsmart.com/biovail-l...ompanies-l3aA/

    For some reason it won't pull up the case for me. Does this ancedote say something to contradict your support for Par?
    Biovail bought the rights to Wellbutrin XL from Glaxo-Smith Kline in 2009. If they are suing Par then it may be because Par's release technology is similar enough to Glaxo's/Biovail's to warrant some kind of patent infringement. I couldn't find any lawsuits from Biovail to any of the other generic manufacturers, so this may have something to do with how effective Par's is compared to the other generics I've tried.

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    Quote Originally Posted by eclypz View Post
    I've actually toyed with the idea of trying brand name wellbutrin, but I prefer the smaller dose of 150mg. All I have ever used is the generic indian pharm version and it does make me edgy. I wonder if a better dissolution would take the edge off?
    In my experience it absolutely does.

    I was ready to shell out the 200+ dollars a month for the brand, but decided to give this generic a one month try from a pharmacy I just switched over to since it was <20 dollars a month. I went into the trial pretty pessismistic as a result of my other generic trials, so I don't think placebo is playing much of a role on this one. To say I am pleased would be an understatement. Now a I can get a years worth for the same price I would pay for a month and it is just as effective as far as I can tell.

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    Senior Member eclypz's Avatar
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    I think I've found a source for the brand name, I'll have to try it. It's about 30 dollars for a month supply, so not bad.

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    Bump, because I need a place to ask this question. Bupropion has very, very little NRI activity. It does however increase 5-HT firing in the DRN by 100% in rodents, an effect that was proved to be NE related through testing again with NE lesioned rats. So, the consensus is that the increased 5-HT activity is due to the NE releasing effect of Bupropion. Why is it that NE release excites 5-Ht activity, while inhibiting NE re-uptake does not? Both suppress adrenergic firing, I assume via negative feedback.

    Id also like to propose that because DA is stored in the same vesicles as NE within PFC neurons, then NE release would also release DA. Such an effect would increase DA and NE neurotransmission in the PFC similarly to true NRIs. The effects being ADHD friendly, right?

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    NRI's do it as well.

    http://www.ncbi.nlm.nih.gov/pubmed/14767716

    Present pharmacotherapy of major depression is, in principle, based on enhancement of central monoaminergic neurotransmission. Clinical studies utilizing depletion experiments indicate that antidepressants which primarily enhance serotonergic or noradrenergic central activity, i.e. serotonin or nor-adrenaline reuptake inhibitors, largely work by two separate neuronal pathways. However, experimental studies have shown that noradrenaline may regulate serotonergic neurotransmission both at the serotonin cell body and nerve-terminal level. We therefore investigated the effects of the selective NRI reboxetine on serotonergic neuronal activity and extracellular levels of transmitter in the nerve-terminal area. In vivo electrophysiological experiments showed that low doses of reboxetine significantly enhance the firing rate of serotonergic neurons in the dorsal raphe nucleus of anaesthetized rats. Also, in the medial prefrontal cortex reboxetine (3 mg/kg s.c.) enhanced, whereas citalopram (3 mg/kg s.c.) reduced, extracellular concentrations of serotonin measured by means of microdialysis in awake rats, using a low dose of citalopram (0,5 micro M) in the perfusion solution. Local administration of reboxetine only induced an increase in cortical serotonin levels at very high concentrations (1000 micro M). Hence, NRIs may cause a secondary enhancement of central serotonergic activity by a mechanism separate from 5-HT reuptake inhibition; an effect that may contribute to their clinical antidepressant efficacy.

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    Quote Originally Posted by bdog527 View Post
    NRI's do it as well.

    http://www.ncbi.nlm.nih.gov/pubmed/14767716

    Present pharmacotherapy of major depression is, in principle, based on enhancement of central monoaminergic neurotransmission. Clinical studies utilizing depletion experiments indicate that antidepressants which primarily enhance serotonergic or noradrenergic central activity, i.e. serotonin or nor-adrenaline reuptake inhibitors, largely work by two separate neuronal pathways. However, experimental studies have shown that noradrenaline may regulate serotonergic neurotransmission both at the serotonin cell body and nerve-terminal level. We therefore investigated the effects of the selective NRI reboxetine on serotonergic neuronal activity and extracellular levels of transmitter in the nerve-terminal area. In vivo electrophysiological experiments showed that low doses of reboxetine significantly enhance the firing rate of serotonergic neurons in the dorsal raphe nucleus of anaesthetized rats. Also, in the medial prefrontal cortex reboxetine (3 mg/kg s.c.) enhanced, whereas citalopram (3 mg/kg s.c.) reduced, extracellular concentrations of serotonin measured by means of microdialysis in awake rats, using a low dose of citalopram (0,5 micro M) in the perfusion solution. Local administration of reboxetine only induced an increase in cortical serotonin levels at very high concentrations (1000 micro M). Hence, NRIs may cause a secondary enhancement of central serotonergic activity by a mechanism separate from 5-HT reuptake inhibition; an effect that may contribute to their clinical antidepressant efficacy.
    I've seen that study. I think most others, including others with reboxetine, show that NRIs do not usually affect 5-HT firing. I've got to go to work so i can't look for stuff now.

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    IIRC a1-alpha adrenoreceptor agonists increase 5-HT firing while a2 agonists decrease it.

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    Reboxetine is a non-tricyclic antidepressant with selective noradrenergic (NA) reuptake-blocking effects. The effects of acute and sustained administration of reboxetine, on the firing activity of locus coeruleus NA neurons and dorsal raphe 5-HT neurons, were assessed using in vivo extracellular unitary recording in rats anaesthetized with chloral hydrate. Reboxetine (0.1-1.25 mg/kg, i.v.) dose-dependently decreased the firing activity of NA neurons (ED50 = 480 +/- 14 microg/kg). A 2-day treatment with reboxetine at 1.25, 2.5, 5, or 10 mg/kg per day (using osmotic minipumps implanted subcutaneously) produced significant decreases of 52%, 68%, 81%, and 83%, respectively, of NA firing activity. When the reboxetine treatment (2.5 mg/kg per day) duration was prolonged to 7 days, a 66% decrease in NA firing activity was observed which further decreased to 80% after 21 days of treatment. In contrast, 5-HT neuron firing rate remained unaltered following short- and long-term reboxetine treatments. The suppressant effect of the alpha2-adrenoceptor agonist clonidine on the firing activity of NA neurons was unchanged in long-term reboxetine-treated rats, but its effect on the firing activity of 5-HT neurons was blunted. The enhancement of NA firing activity by the 5-HT1A agonist 8-OH-DPAT was abolished in long-term reboxetine-treated rats, whereas, the inhibitory effect of the 5-HT2 agonist DOI was attenuated by about three-fold. In conclusion, sustained NA reuptake blockade by reboxetine lead to profound alterations in the function of NA neurons and of 5-HT receptors modulating their firing activity.
    The rat rostral raphé nuclei receive catecholaminergic innervation from the locus coeruleus and other areas. In the present study, we investigated noradrenergic modulation of 5-HT release in rat dorsal and median raphé nuclei (DRN and MRN) slices (350 μm thick) superfused with artificial cerebrospinal fluid (aCSF). The raphé was locally stimulated (0.1 ms pulses, 10 mA) and 5-HT release was monitored at carbon fibre microelectrodes using fast cyclic voltammetry. The selective noradrenaline reuptake inhibitor desipramine (50 nM) did not increase stimulated (20 pulses, 100 Hz) 5-HT release but significantly slowed 5-HT reuptake in both DRN and MRN. On short stimulus trains (10 pulses, 200 Hz), the α2-selective agonist dexmedetomidine (10 nM) decreased evoked 5-HT release in DRN and MRN (to 44±3 and 43±7% of pre-drug values, respectively, at minimum). In both nuclei, this response was antagonised by the selective α2A-antagonist BRL 44408 (1 μM: P<0.001 vs. dexmedetomidine) but not by the selective α2B/C-adrenoceptor antagonist ARC 239 (500 nM), the selective 5-HT1A antagonist WAY 100635 (100 nM) or the α1-selective antagonist prazosin (1 μM), suggesting that the effect of dexmedetomidine is wholly attributable to α2A-receptor activation. The α1-adrenoceptor agonist phenylephrine (5 μM) significantly decreased 5-HT release (to 49±7 and 41±4% of pre-drug values in DRN and MRN, respectively). The response was blocked by prazosin (P<0.001) and BRL 44408 (P<0.01) in DRN and by prazosin, BRL 44408 and WAY 100635 (all P<0.05) in MRN, suggesting that the effect of phenylephrine is, under these conditions, only partly mediated via α1-adrenoceptors. On long stimuli (30 pulses, 10 Hz), BRL 44408 (1 μM) increased evoked 5-HT efflux to 187±17 and 178±2% of pre-drug values in DRN and MRN, respectively (both P<0.001 vs. vehicle). Collectively, these data show that activation of both α1 and α2A-adrenoceptors can decrease stimulated 5-HT release in the rostral raphé nuclei. Since the effect of dexmedetomidine was not antagonised by prazosin, we suggest that its effect was mediated directly, possibly through α2A receptors located on 5-HT cell elements, and not transduced indirectly through α1-adrenoceptor activation, as previously suggested by others.
    Unexpectedly, however, the firing activity of 5-HT
    neurons was increased by 100% in the bupropiontreated
    animals. To study this phenomenon further,
    NE-lesioned rats were given bupropion to see how it
    affected serotonergic firing activity in the absence of
    NE neurons. Administration of bupropion was no
    longer associated with an increase in serotonergic
    firing activity. Because NRIs do not modify 5-HT
    neuronal firing, it was hypothesized that bupropion
    stimulates the release of NE.
    In that study they concluded that the 5-HT action must be be caused by NE release which confused me.

  15. #14
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    Hmm...perhaps it is via a nicotinic mechanism then? I posted a study not too long ago that showed bupropion elevated levels of DA in the VTA via Nicotinic Acetylcholinergic Receptors. Maybe something similar is occurring in the Raphe Nucleus.

    A quick search found this. I haven't read the full text.

    Presynaptic nicotinic receptors facilitate monoaminergic transmission.

    Li X, Rainnie DG, McCarley RW, Greene RW.
    Source

    Harvard Medical School and Brockton Veterans Administration Medical Center, Neuroscience Laboratory, Brockton, Massachusetts 02401, USA.

    http://www.ncbi.nlm.nih.gov/pubmed/9465015

    Abstract


    Nicotine is reported to increase arousal and attention and to elevate mood, effects that are most often associated with changes in the function of monoaminergic neuromodulatory systems (Feldman et al., 1997). Recent studies have shown a nicotinic receptor-mediated presynaptic enhancement of fast glutamatergic (McGehee et al., 1995; Gray et al., 1996) and GABAergic (Lena and Changeux, 1997) transmission. However, the mechanism of nicotinic effects on metabotropic-mediated transmission in general, and on monoaminergic transmission in particular, is less well understood. We have examined nicotinic effects on dorsal raphe neurons of rats using whole-cell current and voltage-clamp recording techniques in vitro. In the majority of these neurons, activation of presynaptic nicotinic receptors induced a depolarization mediated by norepinephrine acting on alpha1 receptors. Blockade of this response revealed a hyperpolarization mediated by serotonin acting on 5-HT1A receptors. Because the norepinephrine effect was sensitive to methyllycaconitine (100 nM), it is concluded that nicotinic receptors with an alpha7 subunit can facilitate release of norepinephrine to activate metabotropic receptors. In contrast, methyllycaconitine-insensitive nicotinic receptors can induce 5-HT release in the dorsal raphe nucleus.

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    Quote Originally Posted by bdog527 View Post
    Hmm...perhaps it is via a nicotinic mechanism then? I posted a study not too long ago that showed bupropion elevated levels of DA in the VTA via Nicotinic Acetylcholinergic Receptors. Maybe something similar is occurring in the Raphe Nucleus.

    A quick search found this. I haven't read the full text.

    Presynaptic nicotinic receptors facilitate monoaminergic transmission.

    Li X, Rainnie DG, McCarley RW, Greene RW.
    Source

    Harvard Medical School and Brockton Veterans Administration Medical Center, Neuroscience Laboratory, Brockton, Massachusetts 02401, USA.

    http://www.ncbi.nlm.nih.gov/pubmed/9465015

    Abstract


    Nicotine is reported to increase arousal and attention and to elevate mood, effects that are most often associated with changes in the function of monoaminergic neuromodulatory systems (Feldman et al., 1997). Recent studies have shown a nicotinic receptor-mediated presynaptic enhancement of fast glutamatergic (McGehee et al., 1995; Gray et al., 1996) and GABAergic (Lena and Changeux, 1997) transmission. However, the mechanism of nicotinic effects on metabotropic-mediated transmission in general, and on monoaminergic transmission in particular, is less well understood. We have examined nicotinic effects on dorsal raphe neurons of rats using whole-cell current and voltage-clamp recording techniques in vitro. In the majority of these neurons, activation of presynaptic nicotinic receptors induced a depolarization mediated by norepinephrine acting on alpha1 receptors. Blockade of this response revealed a hyperpolarization mediated by serotonin acting on 5-HT1A receptors. Because the norepinephrine effect was sensitive to methyllycaconitine (100 nM), it is concluded that nicotinic receptors with an alpha7 subunit can facilitate release of norepinephrine to activate metabotropic receptors. In contrast, methyllycaconitine-insensitive nicotinic receptors can induce 5-HT release in the dorsal raphe nucleus.
    Quite interesting, but it only deepened my confusion. Some key points from the study:

    1. nicotine's action on pre-synaptic nicotinic receptors casued NE release that activated post-synaptic a1 receptors causing depolarization of 5-HT neurons (increased excitability)
    2. a nicotinic antagonist prevented the depolarization (paradoxical to how Bupropion increases excitability)
    3. NRI in conjunction with nicotine prolonged the depolarization.

    This leads me to believe that nicotinic-antagonism by bupropion is independent of it's NE releasing property. Also, bupropion might activate post-synaptic a1 receptors more efficiently than NRIs, although I don't know how nicotinic antagonism fits in. Just speculation of course.

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