![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 24 of 24. This is the beginning of the thread.
Posted by SLS on April 9, 2009, at 7:24:21
Yes, I have heard for years that SSRIs cause dopamine depletion, and that this might be responsible for the induction of apathy or a loss of therapeutic effect ("poop-out"). However, where is there scientific evidence to support this notion? I would say that chronic SSRI usage might produce a change in the activity of neural pathways afferent to dopaminergic structures and circuits. However, to think that neurons actually run out of neurotransmitter seems unlikely to me. They probably are just not being stimulated to release dopamine.
What do you think? Is there any scientific evidence that demonstrates that an SSRI can produce dopamine depletion downstream?
- Scott
Posted by sowhysosad on April 9, 2009, at 18:20:31
In reply to Dopamine depletion: A myth?, posted by SLS on April 9, 2009, at 7:24:21
> Yes, I have heard for years that SSRIs cause dopamine depletion, and that this might be responsible for the induction of apathy or a loss of therapeutic effect ("poop-out"). However, where is there scientific evidence to support this notion? I would say that chronic SSRI usage might produce a change in the activity of neural pathways afferent to dopaminergic structures and circuits. However, to think that neurons actually run out of neurotransmitter seems unlikely to me. They probably are just not being stimulated to release dopamine.
>
> What do you think? Is there any scientific evidence that demonstrates that an SSRI can produce dopamine depletion downstream?
>
>
> - ScottInteresting theory Scott.
How would this tie in with anecdotal evidence from people whose SSRI "side efffects" have been seemingly alleviated by dopaminergic meds or supplements?
Would this suggest that the relevant neurons are still being stimulated to release dopamine, reversing the SSRI's effects, under these circumstances?
Posted by SLS on April 10, 2009, at 5:44:10
In reply to Re: Dopamine depletion: A myth? » SLS, posted by sowhysosad on April 9, 2009, at 18:20:31
> > Yes, I have heard for years that SSRIs cause dopamine depletion, and that this might be responsible for the induction of apathy or a loss of therapeutic effect ("poop-out"). However, where is there scientific evidence to support this notion? I would say that chronic SSRI usage might produce a change in the activity of neural pathways afferent to dopaminergic structures and circuits. However, to think that neurons actually run out of neurotransmitter seems unlikely to me. They probably are just not being stimulated to release dopamine.
> >
> > What do you think? Is there any scientific evidence that demonstrates that an SSRI can produce dopamine depletion downstream?
> >
> >
> > - Scott
>
> Interesting theory Scott.
>
> How would this tie in with anecdotal evidence from people whose SSRI "side efffects" have been seemingly alleviated by dopaminergic meds or supplements?
>
> Would this suggest that the relevant neurons are still being stimulated to release dopamine, reversing the SSRI's effects, under these circumstances?Yes.
I believe you are exactly right when it comes to using amphetamines in this fashion.
- Scott
Posted by sowhysosad on April 10, 2009, at 20:19:34
In reply to Re: Dopamine depletion: A myth? » sowhysosad, posted by SLS on April 10, 2009, at 5:44:10
And what about other types of meds that boost dopamine, like bupropion, NADH or selegiline? How would you explain the perceived relief some people get from "low dopamine" SE's with those?
I've heard that bupropion may increase dopamine firing rates, so that would tie in with your theory.
Fascinated to hear your informed view Scott as I may be going back on an SSRI and am terrified of dopamine-related issues.
> > How would this tie in with anecdotal evidence from people whose SSRI "side efffects" have been seemingly alleviated by dopaminergic meds or supplements?
> >
> > Would this suggest that the relevant neurons are still being stimulated to release dopamine, reversing the SSRI's effects, under these circumstances?
>
> Yes.
>
> I believe you are exactly right when it comes to using amphetamines in this fashion.
>
>
> - Scott
Posted by SLS on April 11, 2009, at 17:39:51
In reply to Re: Dopamine depletion: A myth?, posted by sowhysosad on April 10, 2009, at 20:19:34
Hi.
Although an SSRI might lead to reduced activity of DA pathways, at least it isn't as if the neurons there run out of neurotransmitter. If they did, there would be very little remediation for a hypodopaminergic condition. As it is, I believe, there is plenty of dopamine to go around. You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics. There might even be some viable herbal alternatives like Ginkgo biloba.
If you do experience what you believe to be a hypodopaminergic state (reduced libido, amotivation, anergy and fatigue, apathy, etc.), and the above remedies don't help, you can simply change drugs. Often, not all of the SSRIs will affect an individual the same way.
- Scott
Posted by sowhysosad on April 11, 2009, at 19:01:28
In reply to Re: Dopamine depletion: A myth? » sowhysosad, posted by SLS on April 11, 2009, at 17:39:51
You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics. There might even be some viable herbal alternatives like Ginkgo biloba.
Do you think Provigil would hit the spot?
Posted by SLS on April 12, 2009, at 7:19:27
In reply to Re: Dopamine depletion: A myth? » SLS, posted by sowhysosad on April 11, 2009, at 19:01:28
> You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics. There might even be some viable herbal alternatives like Ginkgo biloba.
>
> Do you think Provigil would hit the spot?I forgot about Provigil. Good thinking. Yes, I believe that it can increase the activity of certain DA pathways. Some believe that this drug is a DA reuptake inhibitor. I don't think this has been shown conclusively. However, even if it doesn't inhibit DA reuptake, the increase in glutamate (GLU) transmission Provigil produces in the thalamus very likely stimulates DA neurons downstream in the reward centers of the limbic system.
- Scott
Posted by SLS on April 12, 2009, at 7:25:31
In reply to Re: Dopamine depletion: A myth?, posted by SLS on April 12, 2009, at 7:19:27
> Some believe that this drug is a DA reuptake inhibitor. I don't think this has been shown conclusively.
Here is a very recent study that reports that Provigil does indeed inhibit the reuptake of dopamine by binding with the dopamine transporter (DAT). People are now looking at the possibility that Provigil is somewhat addictive, afterall.
- Scott
**********************************************
1: JAMA. 2009 Mar 18;301(11):1148-54.Click here to read Links
Effects of modafinil on dopamine and dopamine transporters in the male human brain: clinical implications.
Volkow ND, Fowler JS, Logan J, Alexoff D, Zhu W, Telang F, Wang GJ, Jayne M, Hooker JM, Wong C, Hubbard B, Carter P, Warner D, King P, Shea C, Xu Y, Muench L, Apelskog-Torres K.National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, USA. nvolkow@nida.nih.gov
CONTEXT: Modafinil, a wake-promoting drug used to treat narcolepsy, is increasingly being used as a cognitive enhancer. Although initially launched as distinct from stimulants that increase extracellular dopamine by targeting dopamine transporters, recent preclinical studies suggest otherwise. OBJECTIVE: To measure the acute effects of modafinil at doses used therapeutically (200 mg and 400 mg given orally) on extracellular dopamine and on dopamine transporters in the male human brain. DESIGN, SETTING, AND PARTICIPANTS: Positron emission tomography with [(11)C]raclopride (D(2)/D(3) radioligand sensitive to changes in endogenous dopamine) and [(11)C]cocaine (dopamine transporter radioligand) was used to measure the effects of modafinil on extracellular dopamine and on dopamine transporters in 10 healthy male participants. The study took place over an 8-month period (2007-2008) at Brookhaven National Laboratory. MAIN OUTCOME MEASURES: Primary outcomes were changes in dopamine D(2)/D(3) receptor and dopamine transporter availability (measured by changes in binding potential) after modafinil when compared with after placebo. RESULTS: Modafinil decreased mean (SD) [(11)C]raclopride binding potential in caudate (6.1% [6.5%]; 95% confidence interval [CI], 1.5% to 10.8%; P = .02), putamen (6.7% [4.9%]; 95% CI, 3.2% to 10.3%; P = .002), and nucleus accumbens (19.4% [20%]; 95% CI, 5% to 35%; P = .02), reflecting increases in extracellular dopamine. Modafinil also decreased [(11)C]cocaine binding potential in caudate (53.8% [13.8%]; 95% CI, 43.9% to 63.6%; P < .001), putamen (47.2% [11.4%]; 95% CI, 39.1% to 55.4%; P < .001), and nucleus accumbens (39.3% [10%]; 95% CI, 30% to 49%; P = .001), reflecting occupancy of dopamine transporters. CONCLUSIONS: In this pilot study, modafinil blocked dopamine transporters and increased dopamine in the human brain (including the nucleus accumbens). Because drugs that increase dopamine in the nucleus accumbens have the potential for abuse, and considering the increasing use of modafinil, these results highlight the need for heightened awareness for potential abuse of and dependence on modafinil in vulnerable populations.
PMID: 19293415 [PubMed - indexed for MEDLINE]
Posted by Amelia_in_StPaul on April 12, 2009, at 21:41:46
In reply to Re: Dopamine depletion: A myth? » SLS, posted by sowhysosad on April 11, 2009, at 19:01:28
I thought neuroleptics were dopamine antagonists. You're saying that they stimulate DA?
> You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics.
>
Posted by SLS on April 13, 2009, at 8:06:07
In reply to Re: Dopamine depletion: A myth? » sowhysosad, posted by Amelia_in_StPaul on April 12, 2009, at 21:41:46
> I thought neuroleptics were dopamine antagonists. You're saying that they stimulate DA?
>
> > You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics.Hi Amelia.
Some of the neuroleptics are known to stimulate the synthesis and release of DA through the selective blockage of presynaptic autoreceptors. Sulpiride and amisulpride are examples of this. Abilify (aripiprazole) accomplishes DA enhancement by acting as a partial agonist at DA postsynaptic receptors.
- Scott
Posted by Alexanderfromdenmark on April 13, 2009, at 9:22:03
In reply to Dopamine depletion: A myth?, posted by SLS on April 9, 2009, at 7:24:21
Posted by Amelia_in_StPaul on April 13, 2009, at 12:01:50
In reply to Re: Dopamine depletion: A myth?, posted by SLS on April 13, 2009, at 8:06:07
Hi Scott.
Woah, that's a surprise. I've always heard that the idea was to quash the dopamine, not enhance it.
That Abilify enhances DA--is that why, in the words of a infamous psychiatrist around here--"Abilify is sh*t for hallucinations."
What does Haldol do? Curious b/c my sister, who has schizophrenia, is on that. It is not the best thing ever, she still has manifold symptoms, but the doctor is loathe to destabilize her because she was misdiagnosed Bipolar for so many years (and not given antipsychotics), her psychosis took hold and is hard to shake. I disagree with him, but for various reasons my opinion doesn't really matter.
Finally, I've always been afraid to take any drugs that enhance dopamine. I do have ADD, but for instance Adderall did the job but too well--I felt pretty much like I was on acid, without the hallucinations. Wellbutrin gives me severe anxiety and anger, even at 75mg. Yet I am quite sure I have SSRI-induced apathy, blahness, etc.
So how does one parse out what the balance should be so that you have enough dopamine for antidepressant effects but not too much that you tip into psychosis? I'm sure this all has something to do with what parts of the brain the dopamine is being stimulated or downregulated.Ahhhh, a very long post full of queries. Sorry to have gone on and on. You strike me as someone that may have some answers about these questions I've had for a long, long time.
Thanks, Amelia
> > I thought neuroleptics were dopamine antagonists. You're saying that they stimulate DA?
> >
> > > You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics.
>
> Hi Amelia.
>
> Some of the neuroleptics are known to stimulate the synthesis and release of DA through the selective blockage of presynaptic autoreceptors. Sulpiride and amisulpride are examples of this. Abilify (aripiprazole) accomplishes DA enhancement by acting as a partial agonist at DA postsynaptic receptors.
>
>
> - Scott
>
>
Posted by SLS on April 13, 2009, at 14:52:34
In reply to enjoy this study, posted by Alexanderfromdenmark on April 13, 2009, at 9:22:03
> http://www.neuroassist.com/5-HTP-depletes-dopamine.pdf
Thanks!
I hope you don't mind if I pass this one along...
- Scott
Posted by desolationrower on April 14, 2009, at 11:51:35
In reply to Re: Dopamine depletion: A myth? » SLS, posted by Amelia_in_StPaul on April 13, 2009, at 12:01:50
> Hi Scott.
>
> Woah, that's a surprise. I've always heard that the idea was to quash the dopamine, not enhance it.
>
> That Abilify enhances DA--is that why, in the words of a infamous psychiatrist around here--"Abilify is sh*t for hallucinations."
>
> What does Haldol do? Curious b/c my sister, who has schizophrenia, is on that. It is not the best thing ever, she still has manifold symptoms, but the doctor is loathe to destabilize her because she was misdiagnosed Bipolar for so many years (and not given antipsychotics), her psychosis took hold and is hard to shake. I disagree with him, but for various reasons my opinion doesn't really matter.
>
> Finally, I've always been afraid to take any drugs that enhance dopamine. I do have ADD, but for instance Adderall did the job but too well--I felt pretty much like I was on acid, without the hallucinations. Wellbutrin gives me severe anxiety and anger, even at 75mg. Yet I am quite sure I have SSRI-induced apathy, blahness, etc.
> So how does one parse out what the balance should be so that you have enough dopamine for antidepressant effects but not too much that you tip into psychosis? I'm sure this all has something to do with what parts of the brain the dopamine is being stimulated or downregulated.
>
> Ahhhh, a very long post full of queries. Sorry to have gone on and on. You strike me as someone that may have some answers about these questions I've had for a long, long time.
>
> Thanks, Amelia
>
> > > I thought neuroleptics were dopamine antagonists. You're saying that they stimulate DA?
> > >
> > > > You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics.
> >
> > Hi Amelia.
> >
> > Some of the neuroleptics are known to stimulate the synthesis and release of DA through the selective blockage of presynaptic autoreceptors. Sulpiride and amisulpride are examples of this. Abilify (aripiprazole) accomplishes DA enhancement by acting as a partial agonist at DA postsynaptic receptors.
> >
> >
> > - Scott
> >
> >
>
>
Hi ameli.
Yes, too much or too little DA can be bad. Althouhg, even in schizophrenia, there is generally too little dopamine in the prefrontal cortex; it is the limbic system that has excess DA. and why neuroleptics can worsen the negative symptoms, which have more to do with the PFC. also, there are different ways dopamine can be used; if it comes in pulses, or just as a constant amount. and schizophrenia is associated with DA receptors that are too sensitive. anyway, have you ever tried protryptaline/desipramine? it might help with ADHD and they only effect DA in the pfc.i've made some posts in hte past on DA function you could probably search my name and find lots of stuff if you're interested. don't hesitate to ask anything.
-d/r
Posted by Amelia_in_StPaul on April 19, 2009, at 14:44:31
In reply to Re: Dopamine depletion: A myth?, posted by desolationrower on April 14, 2009, at 11:51:35
Hi d/r, thank you so much for that succinct but incredibly informative post. Yes, I will def. search your name for more. I have been afraid of dopamine b/c I haven't been sure as to what to shoot for and what I should avoid b/c of familial history. thanks so much!!! amelia
> > Hi Scott.
> >
> > Woah, that's a surprise. I've always heard that the idea was to quash the dopamine, not enhance it.
> >
> > That Abilify enhances DA--is that why, in the words of a infamous psychiatrist around here--"Abilify is sh*t for hallucinations."
> >
> > What does Haldol do? Curious b/c my sister, who has schizophrenia, is on that. It is not the best thing ever, she still has manifold symptoms, but the doctor is loathe to destabilize her because she was misdiagnosed Bipolar for so many years (and not given antipsychotics), her psychosis took hold and is hard to shake. I disagree with him, but for various reasons my opinion doesn't really matter.
> >
> > Finally, I've always been afraid to take any drugs that enhance dopamine. I do have ADD, but for instance Adderall did the job but too well--I felt pretty much like I was on acid, without the hallucinations. Wellbutrin gives me severe anxiety and anger, even at 75mg. Yet I am quite sure I have SSRI-induced apathy, blahness, etc.
> > So how does one parse out what the balance should be so that you have enough dopamine for antidepressant effects but not too much that you tip into psychosis? I'm sure this all has something to do with what parts of the brain the dopamine is being stimulated or downregulated.
> >
> > Ahhhh, a very long post full of queries. Sorry to have gone on and on. You strike me as someone that may have some answers about these questions I've had for a long, long time.
> >
> > Thanks, Amelia
> >
> > > > I thought neuroleptics were dopamine antagonists. You're saying that they stimulate DA?
> > > >
> > > > > You just need to stimulate the DA nerves to fire. This can be accomplished by using stimulants, Wellbutrin, and possibly atypical neuroleptics.
> > >
> > > Hi Amelia.
> > >
> > > Some of the neuroleptics are known to stimulate the synthesis and release of DA through the selective blockage of presynaptic autoreceptors. Sulpiride and amisulpride are examples of this. Abilify (aripiprazole) accomplishes DA enhancement by acting as a partial agonist at DA postsynaptic receptors.
> > >
> > >
> > > - Scott
> > >
> > >
> >
> >
> Hi ameli.
> Yes, too much or too little DA can be bad. Althouhg, even in schizophrenia, there is generally too little dopamine in the prefrontal cortex; it is the limbic system that has excess DA. and why neuroleptics can worsen the negative symptoms, which have more to do with the PFC. also, there are different ways dopamine can be used; if it comes in pulses, or just as a constant amount. and schizophrenia is associated with DA receptors that are too sensitive. anyway, have you ever tried protryptaline/desipramine? it might help with ADHD and they only effect DA in the pfc.
>
> i've made some posts in hte past on DA function you could probably search my name and find lots of stuff if you're interested. don't hesitate to ask anything.
>
> -d/r
Posted by brot on April 27, 2009, at 20:43:41
In reply to Dopamine depletion: A myth?, posted by SLS on April 9, 2009, at 7:24:21
The selective serotonin reuptake inhibitor citalopram induces the storage of serotonin in catecholaminergic terminals.
Suarez-Roca H, Cubeddu LX.Pharmacology Section, Instituto de Investigaciones Clinicas, School of Medicine, University of Zulia, Maracaibo, Venezuela.
We investigated whether selective inhibition of serotonin (5-hydroxytryptamine; 5-HT) transporter with citalopram leads to accumulation of 5-HT in catecholaminergic neurons. In the rabbit olfactory tubercle, citalopram (1-10 microM) inhibited [(3)H]5-HT uptake; however, the maximal degree of inhibition achieved was 70%. Addition of nomifensine (1-10 microM) was required for complete inhibition of [(3)H]5-HT uptake. In slices labeled with 0.1 microM [(3)H]5-HT, cold 5-HT (0.03-1 microM) induced a large increase in the efflux (release) of stored [(3)H]5-HT, an effect blocked by coperfusion with 1 microM citalopram. Similar concentrations (0.03-1 microM) of norepinephrine (NE) or dopamine (DA) failed to release [(3)H]5-HT. When labeling with 0.1 microM [(3)H]5-HT was carried out in the presence of citalopram, 1) low concentrations of 5-HT failed to release [(3)H]5-HT; 2) DA and NE were more potent and effective in releasing [(3)H]5-HT than in control slices; 3) coperfusion of NE, DA, or 5-HT with citalopram enhanced the release of [(3)H]5-HT induced by the catecholamines but not by 5-HT; and 4) coperfusion of NE or DA with nomifensine antagonized NE- and DA-evoked [(3)H]5-HT release, with a greater effect on NE than on DA. These results suggest that in the rabbit olfactory tubercle, where there is coexistence of 5-HT, NE, and DA neurons, inhibition of the 5-HT transporter led to accumulation of 5-HT in catecholaminergic terminals. Thus, during treatment with selective serotonin uptake inhibitors (SSRIs), 5-HT may be stored in catecholaminergic neurons acting as a false neurotransmitter and/or affecting the disposition of DA and/or NE. Transmitter relocation may be involved in the antidepressant action of SSRIs.
But i dont know if the drwan conclusions are correct....
Posted by SLS on April 28, 2009, at 7:38:15
In reply to Re: Dopamine depletion: A myth?, posted by brot on April 27, 2009, at 20:43:41
Hi.
Thanks for posting this.
This sounds like a reasonable mechanism by which dopamine depletion could occur. If 5-HT makes it past the outer cell membrane, it most likely will end up in the synaptic vesicles and displacing DA, as I believe the VAT2 is not selective for any one amine. It would be nice to see if there is an upregulation of dopamine receptors to compensate for this lack of dopamine. I think that would go a long way to supporting the dopamine depletion theory.
- Scott
*****************************************************
> http://www.ncbi.nlm.nih.gov/pubmed/12065714?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
>
> The selective serotonin reuptake inhibitor citalopram induces the storage of serotonin in catecholaminergic terminals.
> Suarez-Roca H, Cubeddu LX.
>
> Pharmacology Section, Instituto de Investigaciones Clinicas, School of Medicine, University of Zulia, Maracaibo, Venezuela.
>
> We investigated whether selective inhibition of serotonin (5-hydroxytryptamine; 5-HT) transporter with citalopram leads to accumulation of 5-HT in catecholaminergic neurons. In the rabbit olfactory tubercle, citalopram (1-10 microM) inhibited [(3)H]5-HT uptake; however, the maximal degree of inhibition achieved was 70%. Addition of nomifensine (1-10 microM) was required for complete inhibition of [(3)H]5-HT uptake. In slices labeled with 0.1 microM [(3)H]5-HT, cold 5-HT (0.03-1 microM) induced a large increase in the efflux (release) of stored [(3)H]5-HT, an effect blocked by coperfusion with 1 microM citalopram. Similar concentrations (0.03-1 microM) of norepinephrine (NE) or dopamine (DA) failed to release [(3)H]5-HT. When labeling with 0.1 microM [(3)H]5-HT was carried out in the presence of citalopram, 1) low concentrations of 5-HT failed to release [(3)H]5-HT; 2) DA and NE were more potent and effective in releasing [(3)H]5-HT than in control slices; 3) coperfusion of NE, DA, or 5-HT with citalopram enhanced the release of [(3)H]5-HT induced by the catecholamines but not by 5-HT; and 4) coperfusion of NE or DA with nomifensine antagonized NE- and DA-evoked [(3)H]5-HT release, with a greater effect on NE than on DA. These results suggest that in the rabbit olfactory tubercle, where there is coexistence of 5-HT, NE, and DA neurons, inhibition of the 5-HT transporter led to accumulation of 5-HT in catecholaminergic terminals. Thus, during treatment with selective serotonin uptake inhibitors (SSRIs), 5-HT may be stored in catecholaminergic neurons acting as a false neurotransmitter and/or affecting the disposition of DA and/or NE. Transmitter relocation may be involved in the antidepressant action of SSRIs.
Posted by Meltingpot on May 17, 2009, at 10:40:52
In reply to Dopamine depletion: A myth?, posted by SLS on April 9, 2009, at 7:24:21
Hi,
So if SSRIs do somehow decrease dopamine activity then can the same be said for tricyclics and SNRIs??
Denise
Posted by SLS on May 18, 2009, at 7:24:46
In reply to Re: Dopamine depletion: A myth? Tryciclics + SNRIs, posted by Meltingpot on May 17, 2009, at 10:40:52
> Hi,
>
> So if SSRIs do somehow decrease dopamine activity then can the same be said for tricyclics and SNRIs??
>
> DeniseI believe that this is more of an acute effect of these drugs rather than the result of chronic exposure. My guess is that the long-term effects of 5-HT reuptake inhibitors are to actually reset the balance of neurotransmission dynamics such that dopaminergic activity in certain critical dopaminergic pathways is INCREASED rather than decreased.
I do not believe that the apathy, amotivation, anorgasmia, and decrease libido that occurs during chronic use of a serotonin reuptake inhibitor has anything to do with some sort of global depletion of dopamine.
- Scott
Posted by desolationrower on May 19, 2009, at 0:24:22
In reply to Re: Dopamine depletion: A myth? Tryciclics + SNRIs, posted by SLS on May 18, 2009, at 7:24:46
ADs including ssris increase DA receptor sensitivity.
also nris increase DA in the pfc. there are some other interactions too, so i'd guess increase. there might be a rat study on this specifically.
-d/r
Posted by Meltingpot on May 21, 2009, at 11:43:43
In reply to Re: Dopamine depletion: A myth? Tryciclics + SNRIs, posted by SLS on May 18, 2009, at 7:24:46
Hi Scott,
If you don't believe that the apathy etc that ocurrs after long term SSRI use is because of dopamine deletion then do you have any theories on what causes it?
When I suddenly had success back in 2003 (how sad that sounds :-)) with Seroxat high dose, I had more energy, could stay up later, felt pleasure again and was much more sexual
When Seroxat seeemed to stop helping in 2005, although I did not feel as bad as I had done, I lost that sense of pleasure, started feeling tired and apathetic again and had an increase in anxiety. I'm just wondering what the hell happened at that point (as I guess many people do). I don't think I've felt really any good since sometime back in 2005 (although I have experienced different degrees of crapppiness)
Denise
Posted by Meltingpot on May 21, 2009, at 11:45:28
In reply to Re: Dopamine depletion: A myth? Tryciclics + SNRIs, posted by desolationrower on May 19, 2009, at 0:24:22
Hi again d/r,
Can you explain to me how SSRIs increase dopamine sensistivity as I've never quite understood how this happens.
Also, can you explain it to me as though I were a 10 year old child (that's about my level of understanding :-))?.
Posted by garnet71 on May 26, 2009, at 23:43:57
In reply to Re: Dopamine depletion: A myth? To d/r, posted by Meltingpot on May 21, 2009, at 11:45:28
Sorry, I'm not d/r, but i have been finding a lot of research that indicate SSRIS cause elevated prolactin, which somehow influences dopamine, or vice versa. Not that receptor sensitivity is not the case, but read some of the posts on the med board "prolactin" that I added; they are very easy to read. : )
Too lazy/tired to write it out for you or post links, sorry.
> Hi again d/r,
>
> Can you explain to me how SSRIs increase dopamine sensistivity as I've never quite understood how this happens.
>
> Also, can you explain it to me as though I were a 10 year old child (that's about my level of understanding :-))?.
>
>
Posted by metafunj on September 12, 2009, at 11:16:38
In reply to Re: Dopamine depletion: A myth? Tryciclics + SNRIs, posted by Meltingpot on May 17, 2009, at 10:40:52
Denise this study seems to indicate that SSRIs do decrease dopaminergic neurotransmittion. SSRIs decrease Serotonin transporters(SERT) and increase Dopamine transporters(DAT).
Decreased SERT means serotonin can hang around longer in the synapse and increased DAT means that dopamine gets taken out of the synapse faster. The abstract below shows that this occurs.
Abstract
Serotonin and dopamine transporter (SERT, DAT) availabilities have prospectively been investigated using [123I]β-CIT and single photon emission computed tomography in subjects with obsessive–compulsive disorder under treatment with the selective serotonin reuptake inhibitor citalopram. SERT availability decreased by a mean 36.5%, whereas DAT availability increased by about 40%. The data point at a citalopram induced modulation of both serotonergic and dopaminergic activity and support the notion of functional interactions of monoaminergic systems in the human brain.
Keywords: Serotonin and dopamine transporters; Single photon emission computed tomography; β-CIT; Serotonin reuptake inhibitor; Obsessive–compulsive disorder
This is the end of the thread.
Psycho-Babble Neurotransmitters | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.