Posted by scott-d-o on December 13, 2003, at 16:31:41
In reply to Re: Ritalin Boosts serotonin !?, posted by zeugma on December 13, 2003, at 14:35:52
> If Ritalin's primary effect in terms of ADD symtomology is by blocking 5-HT reuptake, why have SSRI's been shown to be clinically useless in treating ADD? And why would TCA's, and Strattera, which affect norepinephrine, relieve ADD symptoms?
Is this post intended for me? If so, I think you need to re-read what I posted. I never said that norepinephrine, or dopamine for that matter, do not play a role in attention and focus. In fact, I think NE plays the greatest role of all the monoamines in these problems. I also never said that SSRI's are useful in this regard.
I am saying, however, that it is very probable that Ritalin's "calming effect" is associated with it's effect as a very potent 5-HT reuptake inhibitor. I think hyperactivity and attention deficit symptoms have been grouped together too closely under the umbrella of the disorder "ADHD". It seems to me that this has inevitiably led to a lot of misdiagnosis as far as assuming a child has ADD just because he has a lot of energy, doesn't like to sit still for long periods, has difficulty focusing in school, etc. Most children have these types of problems. I wonder how many parents have taken their children into a psychiatrist thinking their child may have ADHD, and were told after the session, "nope, he doesn't have ADHD, sorry.." Probably not a likely occurence, I'm sure the majority just pull out the prescription pad and send them on their way.
I have never seen any clinical trials testing the efficacy of SSRI's in ADHD. I think if a SSRI was administered to a "hyperactive" child it may have a very similar calming effect but perhaps it may not do anything for attention and focus. However, can you imagine what it would do to the medical community if trials did show that a SSRI was just as effective as methylphenidate in treating ADHD in children? I am sure there are not very many people willing to conduct such a study whose outcome might demonstrate that we have been giving an analog of nature's most powerful stimulant to our children for decades and for no particular reason.
I have seen just as many children with attentional difficulties that are not hyperactive at all. They may be very quiet during school and do nothing but stare off into space all day. Sadly, these children are almost never diagnosed. I have seen studies that have shown that methylphenidate is relatively ineffective in treating adult ADD compared to ADD in children. Why do you think this is?
>
> By the way, cocaine's primary effect is not on 5-HT either. It is much more powerful as a dopamine and norepinephrine reuptake inhibitor.Much more powerful? That's kind of a relative term. It is more selective than the *SSRI's* are at blocking dopamine and norepinephrine reuptake, however it is actually a very powerful reuptake inhibitor of all the monoamines including serotonin, where it has an impact on the serotonin transporter much greater than any SSRI. I have read many articles stating the actual percentage increase of extracellular 5-HT is actually greater than that of DA, and it is more selective for DA then NE. I don't feel like looking for the article right now, but this should at least demonstrate that cocaine/methylphenidate's affects on serotonin should not to be ignored.
Serotonin transporters upregulate with chronic cocaine use.
Mash DC, Staley JK, Izenwasser S, Basile M, Ruttenber AJ.
Department of Neurology, School of Medicine, University of Miami, Miami, FL 33136, USA. dmash@newssun.med.miami.edu
Cocaine potently inhibits serotonin (5-HT) reuptake in cell bodies and at nerve terminals and 5-HT has been implicated as a modulator of dopaminergic neurotransmission. Chronic use of cocaine may lead to a "serotonin-deficit" form of 5-HT dysregulation. We have examined the status of the 5-HT transporter (SERT) using ligand binding and autoradiographic methods in subgroups of cocaine overdose deaths. Quantitative autoradiography of [125I]RTI-55 was used to map and measure the effect of chronic cocaine use on SERT densities in the striatum, substantia nigra, amygdala, and adjacent paralimbic cortical areas of cocaine overdose (CO) victims with and without preterminal evidence of excited delirium (ED). SERT densities were elevated in the nucleus accumbens and throughout the anterior and posterior sectors of striatum in CO victims compared with age-matched and drug-free control subjects. In contrast, SERT densities were increased significantly in the anterior striatum, but not the posterior sectors in ED victims. Significant elevations in SERT were measured in the orbitofrontal gyrus (Brodmann area 11), the anterior portion of the insular cortex and the cingulate gyrus (Brodmann area 24) in CO and ED victims. Saturation binding site analysis demonstrated an increase in the density of RTI-55 binding sites with no change in the affinity of the radioligand for the SERT. Chronic cocaine exposure upregulated SERT densities in the substantia nigra of the CO, but not ED victims. The lack of SERT upregulation in the substania nigra and posterior striatum suggests the possibility of a distinct phenotype for fatal ED victims that exhibited an acute onset of bizarre and violent behavior prior to death. Adaptive changes in the SERT densities may contribute to depressed mood and drug craving associated with acute cocaine abstinence.
PMID: 11207425 [PubMed - indexed for MEDLINE]
poster:scott-d-o
thread:288926
URL: http://www.dr-bob.org/babble/20031213/msgs/289436.html