Posted by Joel on February 11, 2002, at 15:24:24
In reply to Re: please be civil » Joel » Jason911, posted by Dr. Bob on February 10, 2002, at 15:46:01
> > > practically everything you said was pasted directly out of biopsychiatry.com
> >
> > NOTHING I said was pasted from ANYWHERE but my paper. The studies and facts are probably quite similar to what is from biopsychiatry.com. Don't accuse me of anything.
>
> That's right, no false accusations, here, please.
>
> > > Oh also wellbutrin increases dopamine production and decreases release.
> >
> > Duh. Have you read any of my posts???
>
> But no sarcasm, either, OK?
>
> BobOk I was wrong about one thing, it wasnt listed in biophyschiatry.com. That was my fault, I knew I had read an acticle about that somewhere that looked identical and I ASSUMED it was from there and for that Im terribly sorry. But I checked and found the acticle and yes, you did paste things or copy them word for word. The article can be found elsewhere.
Ill show you some examples of OBVIOUS copy pasting.
This is what you said:
"It wasn't until the 1990s that Knoll's deprenyl research took a new direction. Working with rat brain stems, rabbit pulmonary and ear arteries, frog hearts and rats in shuttle boxes, Knoll discovered a new mode of action of deprenyl that he believes explains its widespread clinical utility. Knoll discovered that deprenyl [selegiline] (and it's cousin, PEA) are "catecholamine enhancers". Catecholamines refers to the inter-related neurotransmitters dopamine, noradrenaline, and adrenaline. Catecholamines are the transmitters for key activating brain circuits - the mesolimbic-cortical circuit and the locus coeruleus. The neurons from these two brain circuits project from the brain stem, through the mid-brain, to the cerebral cortex. They help to maintain focus, concentration, alertness and effortful attention."This is what the report on the website said:
"During the 1990s Knoll’s deprenyl research took a new direction. Working with rat brain stems, rabbit pulmonary and ear arteries, frog hearts and rats in shuttle boxes, Knoll discovered a new mode of action of deprenyl that he believes explains its widespread clinical utility. (2,16) Knoll discovered that deprenyl (and its “cousin”, PEA) are “catecholamine activity enhancers”.Catecholamines refers to the inter-related neurotransmitters dopamine, noradrenalin, and adrenalin. Catecholamines are the transmitters for key activating brain circuits - the mesolimbic-cortical circuit and the locus coeruleus. The neurons of the mesolimbic-cortical circuit and locus coeruleus project from the brain stem, through the mid-brain, to the cerebral cortex. They help to maintain focus, concentration, alertness and effortful attention. (17)"
Again, you said:
"Here's how it works: when an electrical impulse travels down the length of a neuron - from the recieving dendrite, through the cell body, and down the transmitting axon - it triggers the release of packets of nerotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron , causing yet another transmitter release. What Knoll and colleagues discovered through their highly technical experiments is that deprenyl and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release. In other words, deprenyl (and PEA) cause a larger release of transmitters in response to a given electrical impulse. It's like "turning up the volume" on catecholamine nerve cell activity. And this may be clinically very useful in depression where there may be under-activity of both dopamine and noradrenalin neurons."The report said:
"When an electrical impulse travels down the length of a neuron - from the receiving dendrite, through the cell body, and down the transmitting axon - it triggers the release of packets of neurotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron, causing yet another transmitter release. What Knoll and colleagues discovered through their highly technical experiments is that deprenyl and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release. (2,16)In other words, deprenyl (and PEA) cause a larger release of transmitters in response to a given electrical impulse. It’s like “turning up the volume” on catecholamine nerve cell activity. And this may be clinically very useful in various contexts - such as Parkinson’s disease and Alzheimer’s disease, where the nigrostriatal tract and mesolimbic-cortical circuits under-function (1,17), as well as in depression, where they may be under-activity of both dopamine and noradrenalin neurons. (18,19)"
Last time, You said:
"Even deprenyl in itself has shown in autopsy studies to not only increase dopamine levels by 40-70% in Parkinson patients but increase PEA levels 1300-3500%! You see, PEA is the preferred substrate for MAO-B, the MAO that deprenyl inhibits. PEA has an extremely rapid turnover due to its rapid and continuous breakdown by MAO-B. Thus deprenyl's catecholamine activity enhancer has a dual mode of action. At MAO-B inhibiting doses, deprenyl has a huge catecholamine enhancing effects due to the major increases in PEA levels. Many authors have pointed out the probable dopamine neuron activity enhancing effect of PEA in Parkinson patients taking deprenyl. Knoll's discovery of PEA's catecholamine activity enhancer effect now explains this PEA dopamine-enhancing effect."And the report said...:
"Autopsy studies have shown that while deprenyl increases dopamine levels in Parkinson patient brains by only 40-70%, deprenyl increases PEA levels 1300 - 3500%! (14,22) PEA is the preferred substrate for MAO-B, the MAO that deprenyl inhibits. Paterson and colleagues have shown that PEA has an extremely rapid turnover due to its rapid and continuous breakdown by MAO-B. (21) Thus deprenyl's catecholamine activity enhancer activity has a dual mode of action. At low, non-MAO-B inhibiting doses, deprenyl has a direct catecholamine activity enhancer activity.At higher, MAO-B inhibiting doses, deprenyl creates an additional catecholamine activity enhancer effect, due to the huge increases in brain PEA levels that deprenyl causes, PEA also being a catecholamine activity enhancer substance. Many authors have pointed out the probable dopamine neuron activity enhancing effect of PEA in Parkinson patients taking deprenyl. (14, 15, 22)
Knoll’s discovery of PEA’s catecholamine activity enhancer effect now explains this PEA dopamine-enhancing effect."
Amazingly, a lot of these "papers" look the same to me."NOTHING I said was pasted from ANYWHERE but my paper. The studies and facts are probably quite similar to what is from biopsychiatry.com. Don't accuse me of anything."
Oh really? See I take offence to that. You made it sound like you had done tons of information on deprenyl, but really most of your paper was about your troubles and other copied postings from other acticles. In actuallity, youve never tried deprenyl. People like me who have, know that its VERY mild in comparison to other anti-depressants. Now in some cases that may be a good thing, but it is not a miracle drug by any means.
Also that website you got most of that information from actually SELLS deprenyl overseas, theyll say whatever they can to convince you to buy it. Anyways just think about what I said, Im not accusing you I hope you understand that we all know quite a bit about anti depressants too, and it seems rather foolish to expect us to believe you when you dont believe us.
poster:Joel
thread:93294
URL: http://www.dr-bob.org/babble/20020208/msgs/93772.html