t st tantra Posted August 19, 2009 heard most of this on the weekend,enjoyed it,covered a few subjects including mention of d2 and psychosis....something i presume has relevance for me...... next week is on the portugese decriminalisation situation! Research into addiction The definitions of addiction have changed over the years, according to Barry Everitt, Professor of Neuroscience at the University of Cambridge. He and his colleagues have done research into addiction, identifying the kind of person who is more likely than others to become addicted to substances, and they have looked at new ways to help people overcome their addictions. http://www.abc.net.au/rn/healthreport/default.htm above for download below for transcript http://www.abc.net.au/rn/healthreport/stor....htm#transcript t s t . Share this post Link to post Share on other sites
t st tantra Posted August 19, 2009 Barry Everitt: If you do a metabolic study this was actually a dopamine receptor ligand that we used. Norman Swan: Dopamine is one of the key transmitters, message transmitters in the brain? Barry Everitt: And one that has long been implicated in mediating the positive effects of addictive drugs and it turned out that these impulsive animals had very low levels of dopamine D2 and D3. Or you can't really differentiate them so a sub type of dopamine receptor D2/D3 specifically in the ventral parts of the striatum, now the striatum is that area that receives the biggest dopaminergic innervation in the brain. Norman Swan: Where about is it? Barry Everitt: It's sub-cortical. Norman Swan: Under the surface. Barry Everitt: Under the surface and above the brain stem and we know about the striatum and dopamine because that's the locus of the pathology in Parkinson's Disease for example but that's the dorsal part of the striatum. This was the ventral striatum, an area known as the nucleus accumbens, which for the last 30 years has been regarded as the hot spot where addictive drugs act to bring about their positive reinforcing or rewarding effects. Norman Swan: So the roads are leading in the same direction? Barry Everitt: So the roads are all leading in the same direction but a different take, not just you know dopamine and positive reinforcement but the fact that these animals have low levels of dopamine receptors and take more drug. So you could think that actually one of the things that such individuals might be doing is kind of medicating, self-medicating a dopamine deficit. Norman Swan: And isn't the D3 receptor the one implicated in schizophrenia? Barry Everitt: Well no, the mechanism of action of anti-psychotic drugs is generally attributed to the D2 receptor and D2 receptors, again in this part of the brain, actually in the ventral part of the striatum - Norman Swan: I mean you know where I'm coming from; this could be the link with psychosis induced by things like cocaine and cannabis. Barry Everitt: And that's really where the dopamine hypothesis of schizophrenia comes from, it's the psychosis induced by amphetamine particularly which provides a mechanistic link through dopamine. And there is a tremendous co-morbidity between schizophrenia and drug abuse so there is undoubtedly a link to be made there. restless leg syndrome is often treated with d2 agonists and i want to know how it ties into this? cant word what i want,later...... t s t . Share this post Link to post Share on other sites
Alchemica Posted August 20, 2009 Nice topic, thanks for the link. As for the question: http://www.mdvu.org/library/disease/rls/rls_mpath.asp "a clear understanding of any defect in the metabolism or signaling in the dopamine system remains elusive..." I'll try and put in my (basic) understanding, but don't quote me on this: Have to consider that there are quite a few different dopamine pathways. Psychotic symptoms are generally attributed to the mesolimbic pathway - Blocking postsynaptic D2 receptors by a D2 antagonist acting in the mesolimbic dopamine pathway is one method that antipsychotics might act. The activity in the mesocortical dopamine pathway is attributed to negative symptoms etc. When D2 receptors are blocked (or not functioning as they should) in the nigrostriatal dopamine pathway, it can produce disorders of movement - the link above suggests that the "diencephalospinal A11" pathway is possibly a disturbed pathway at night in RLS. Then the other neurotransmitters also come into play - also having effects on dopamine signalling pathways. Dopamine suppresses acetylcholine activity, Serotonin inhibits dopamine release (via 5-HT2a) etc. The newer RLS treatments seem to be targeting D3 over D2 (still, both can have some wacky side effects). Share this post Link to post Share on other sites
t st tantra Posted August 20, 2009 thanx 4 the link. been offered pramipexole by my doctor but seems to have little to offer me except some crazy side effects and augmentation! i still suspect my life experience seems so different to most that the rls must be involved somehow and also feel i experience somewhat altered states when rls is active..... t s t . Share this post Link to post Share on other sites
FancyPants Posted August 21, 2009 I'm simplifying a bit, but I have to leave soon... I dont' understand how my RLS can be seemingly worsened when I'm smoking more ganja than usual. I've hardly had any over the last month or so and my RLS has lessened considerably. I thought it would be the other way around? Maybe I'm just missing something really really obvious Share this post Link to post Share on other sites
