[Teacake]

What have you heard?

I was doing fine on Adderall, but It was making PTSD worse, and I got very depressed so I added Prozac. I got too much Prozac and took ot down, and now I'm pretty happy with the antidepressant effect, but apathetic and unable to focus.

My dx is major depression and PTSD. Probably also ADHD, although let's be real clear that ADHD is that which improves with Adderall, or a general low dopamine condition.

Anyway,when Prozac put me in bed for July, meaning I really didn't care if I got out of bed in the morning, I began to wonder if I was still on too high a dose. Then o wondered if Proac just changed the effectiive dose of Adderall. So I googled that and came across something that suggested Prozac prevents Amphetamine from working consistently.

Now I'm confused. Because I lack dopamine? What do you know or what have you hears about Prozac and adderall?
Adderall worked just fine without Prozac. And Prozac feels pretty good but for the los dopamine confusión. .

[krisakira]

Since starting Prozac I have also had to increase the dose of my Adderall (10 to 15 mg) and I did not think it had to do with being on Prozac, but who knows. All I know is that around the same time I started taking Prozac (switched from celexa) I have felt the need to go up on my adderall. I thought it was a manufacturer thing though.

[metamorphosis12]

When you are dealing with either adderall or dexedrine. You are dealing with amphetamine salts. you are dealing with meds. that can basically over power any other meds affecting your dopamine and norepinephrine. They not only hijack the DAT and NET systems. They basically exert so much control over the cells presynaptic neurons. The VMAT receives the NT's and the proton pump shuttles NT's into the synaptic vesicle. there the neurotransmitters can be stored for future neurotransmission.

That is how it is supposed to work. To clarify one thing, adderall has more of an affinity for NET. While dexedrine prefers to bind to the DAT system. But both are equal opportunity drugs. What happens next, i compare to a driver ant colony that is on the march in the amazon. When they come upon a house, the occupants have already left for the scouts come first. When the colony takes the house every living creature is killed for food. the occupants, who once had a vermin problem no longer have a single living thing to bother with in their home.

When an amphetamine enters the brain, it immediately binds to all of the DAT and NET transporters available. These run in a circle on presynaptic neurons. these travel in a circle path from the outside of the cell into the inside to dump off the DA or NR monoamines. as explained before a proton pump in the battery that runs the VMAT and the NT's into synaptic vesicles for later use.

Once the amphetamine hijacks the DAT. now unlike the other DA binding meds that use a much gentler form of action by allosterically blocking DAT. Amphetamine is a competitive inhibitor of dopamine. It acts directly at the DA substrate binding sites. So, now that it has attached itself to DAT or NET and the NE or DA NT. It is ready to go directly into the cell

By this point the transports have basically been rendered useless in any type of normal functioning and soon. at this point the amphetamine now inside the cell, competitively inhibits DA at the VMAT as well. And the drug is now transported even farther into the cell where the stored DA's are stored in the synaptic vesicles.

This is now the time that a complete malfunction of all the DA and NE cell units fall to pieces. The disruption in the vesicles creates a giant avalanche of events to the point that the cell will have to create a new ion channel for DA release.Two things happen next.And when taken together, it is one of those overwhelming feats in psychopharmacology and demonstrates how powerful these drugs are.

Massive amounts of intercellular dopamine are now available.The high concentration of intercellular DA cause channels to open and release the DA into the synapse.Now the high concentrations of DA in the cell also causes a complete 180 reversible of DAT functioning.So the DAT is now steadily pumping dopamine out of the neuron instead of into it.

The end result is a massive flooding of active DA into the synapse. Now ready to be utilized in the various regions of the brain. The end result is a complete cellular depletion of NE and DA neurotransmitters. These actions are what can make amphetamines so addicting. Tolerance builds at an alarming rate also.

Let me point out that this is a what happens when instant release amp is used at a high dose. That will lead to neurotoxicity. But it also follows the same mode of action on a less smaller scale with substantially less damage to the brain over time.

Also, both meds. come in a xr spanule form. Which is much easier on the cells; as the drug is released at a slow pace and the impact on the cells is at a slow steady pace.

Also check out wikipedias page on Adderall. They did a good job.
Adderall - Wikipedia, the free encyclopedia
You can also use pubmed, medline and other sites that concentrate on studies and papers on medications/drugs.

[Teacake]

Originally Posted by krisakira

Since starting Prozac I have also had to increase the dose of my Adderall (10 to 15 mg) and I did not think it had to do with being on Prozac, but who knows. All I know is that around the same time I started taking Prozac (switched from celexa) I have felt the need to go up on my adderall. I thought it was a manufacturer thing though.

Is the increased dose effective? Do you get the dame clarity you did on Adderall alone?

[Teacake]

Originally Posted by metamorphosis12

When you are dealing with either adderall or dexedrine. You are dealing with amphetamine salts. you are dealing with meds. that can basically over power any other meds affecting your dopamine and norepinephrine. They not only hijack the DAT and NET systems. They basically exert so much control over the cells presynaptic neurons. The VMAT receives the NT's and the proton pump shuttles NT's into the synaptic vesicle. there the neurotransmitters can be stored for future neurotransmission.

That is how it is supposed to work. To clarify one thing, adderall has more of an affinity for NET. While dexedrine prefers to bind to the DAT system. But both are equal opportunity drugs. What happens next, i compare to a driver ant colony that is on the march in the amazon. When they come upon a house, the occupants have already left for the scouts come first. When the colony takes the house every living creature is killed for food. the occupants, who once had a vermin problem no longer have a single living thing to bother with in their jo home.

When an amphetamine enters the brain, it immediately binds to all of the DAT and NET transporters available. These run in a circle on presynaptic neurons. these travel in a circle path from the outside of the cell into the inside to dump off the DA or NR monoamines. as explained before a proton pump in the battery that runs the VMAT and the NT's into synaptic vesicles for later use.

Once the amphetamine hijacks the DAT. now unlike the other DA binding meds that use a much gentler form of action by allosterically blocking DAT. Amphetamine is a competitive inhibitor of dopamine. It acts directly at the DA substrate binding sites. So, now that it has attached itself to DAT or NET and the NE or DA NT. It is ready to go directly into the cell

By this point the transports have basically been rendered useless in any type of normal functioning and soon. at this point the amphetamine now inside the cell, competitively inhibits DA at the VMAT as well. And the drug is now transported even farther into the cell where the stored DA's are stored in the synaptic vesicles.

This is now the time that a complete malfunction of all the DA and NE cell units fall to pieces. The disruption in the vesicles creates a giant avalanche of events to the point that the cell will have to create a new ion channel for DA release.Two things happen next.And when taken together, it is one of those overwhelming feats in psychopharmacology and demonstrates how powerful these drugs are.

Massive amounts of intercellular dopamine are now available.The high concentration of intercellular DA cause channels to open and release the DA into the synapse.Now the high concentrations of DA in the cell also causes a complete 180 reversible of DAT functioning.So the DAT is now steadily pumping dopamine out of the neuron instead of into it.

The end result is a massive flooding of active DA into the synapse. Now ready to be utilized in the various regions of the brain. The end result is a complete cellular depletion of NE and DA neurotransmitters. These actions are what can make amphetamines so addicting. Tolerance builds at an alarming rate also.

Let me point out that this is a what happens when instant release amp is used at a high dose. That will lead to neurotoxicity. But it also follows the same mode of action on a less smaller scale with substantially less damage to the brain over time.

Also, both meds. come in a xr spanule form. Which is much easier on the cells; as the drug is released at a slow pace and the impact on the cells is at a slow steady pace.

Also check out wikipedias page on Adderall. They did a good job.
Adderall - Wikipedia, the free encyclopedia
You can also use pubmed, medline and other sites that concentrate on studies and papers on medications/drugs.

No more amphetamine for you! Unless you need It to please tell me what all those acronyms mean.

[metamorphosis12]

Teacake, I sent you a pm that covers the acronyms and more.
DAT- Dopamine transporter
NET- Norepinephrine transporter
Your specific question, starts at page 105.
The chapters above also talks of what these acronyms mean and show it with
pictures .

[Teacake]

Originally Posted by metamorphosis12

Teacake, I sent you a pm that covers the acronyms and more.
DAT- Dopamine transporter
NET- Norepinephrine transporter
Your specific question, starts at page 105.
The chapters above also talks of what these acronyms mean and show it with
pictures .

Thank you, Metamorphosis! That was really above and beyond.

[metamorphosis12]

Originally Posted by Teacake

Thank you, Metamorphosis! That was really above and beyond.

No problem!

[kiwi33]

Negative interactions between Prozac (and other SSRIs/SNRIs) and amphetamines are classified as "Major".

To quote:

"In general, amphetamines and other sympathomimetic appetite suppressants should not be combined with selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs)."

This quote is from the "Professional" part of the "Interactions Checker" bit of http://www.drugs.com/

This site is a helpful resource.

[metamorphosis12]

Kiwi33 Thanks for the link, it looks informative!

This is a paper I did on amphetamines and the brain. There are two parts. Unfortunately some of the links are dead now.

amphetamines and modafinil/armodafinil, their effectiveness and effects on the brain

Pt. 1)
A great research paper with 220 references. This report, with a ton of links, can take you down many different avenues of the role on various stimulants!

An analysis of the effects of stimulant drugs ( amphetamine, modafinil/armorfinil, nicotine, caffeine, histamine (H3) receptor antagonists, and sedative/hypnotics and sleep promoting drugs
Assessment in 4 key areas:wakefulness; biology of sleep/wake and cognition; targets of wake promoting and/or cognition enhancing drugs; and ongoing clinical trials.

Approaches to Measuring the Effects of Wake-Promoting Drugs: A Focus on Cognitive Function
Christopher J. Edgar,1 Edward F. Pace-Schott,2 and Keith A. Wesnes3

Abstract
Quote:
Objectives-
In clinical drug development, wakefulness and wake-promotion maybe assessed by a large number of scales and questionnaires. Objective assessment of wakefulness is most commonly made using sleep latency/maintenance of wakefulness tests, polysomnography and/or behavioral measures. The purpose of the present review is to highlight the degree of overlap in the assessment of wakefulness and cognition, with consideration of assessment techniques and the underlying neurobiology of both concepts.
Design-
Reviews of four key areas were conducted: commonly used techniques in the assessment of wakefulness; neurobiology of sleep/wake and cognition; targets of wake promoting and/or cognition enhancing drugs; and ongoing clinical trials investigating wake promoting effects.
Results-
There is clear overlap between the assessment of wakefulness and cognition. There are common techniques which may be used to assess both concepts; aspects of the neurobiology of both concepts may be closely related; and wake promoting drugs may have nootropic properties (and vice-versa). Clinical trials of wake promoting drugs often, though not routinely, assess aspects of cognition.
Conclusions-
Routine and broad assessment of cognition in the development of wake promoting drugs may reveal important nootropic effects, which are not secondary to alertness/wakefulness, whilst existing cognitive enhancers may have under explored or unknown wake promoting properties.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747813/

Modafinil is used everyday or is often cycled to keep it's effectiveness up and tolerance down. 200mg is the most common dose. Studies have shown no benefit with an increase.
Other drugs can be directly influenced by modafinil and their elimination time may be prolonged due to modafinil's effect on the cytochrome-p450 family of enzymes.
Drugs that are largely eliminated via CYP2C19 metabolism, such as diazepam, propranolol, phenytoin (also via CYP2C9 or it's substrate) may have prolonged elimination upon use in conjunction with modafinil because of modafinils potential to inhibit the CYP2C19 and suppress CYP2C9, also to induce CYP3A4, CYP2B6, and CYP1A2.
http://www.ingentaconnect.com/conten...00002/art00002
http://www.ingentaconnect.com/conten...00013/art00003

Mechanism of Action: (as a stimulant and possible use in bi-polar and uni-polar depression)
Quote:
Modafinil is a unique wakefulness-promoting pharmaceutical
whose exact biochemical mechanism of action
is not known. However, it has been shown to increase
the levels of serotonin, histamine, and dopamine in the
brain [4–6]. Studies done on the wakefulness-promoting
mechanism of modafinil have proposed specific activation
of the tuberomammillary, a cluster of magnocellular cells in the posterior hypothalamus. Which is the main source of neuronal histamine in the brain.
Also it produces activation on orexin (a neurotransmitter that regulates arousal, wakefulness, and appetite containing neurons in the perifornical
area, although not in other areas involved in the
sleep–wake cycle (eg, the supraoptic nucleus) [7]. Histamine
and orexin have been implicated in the regulation
of wakefulness [8,9].

Modafinil administration into rat
nucleus accumbens resulted in a weak dopamine release
secondary to its ability to reduce local γ-aminobutyric
acidergic transmission [4]. By contrast, amphetamine
strongly elevated dopamine levels in the nucleus accumbens
and striatum. The difference in addiction potential
between modafinil and amphetamine is postulated and explained by this difference in dopaminergic activity.
Modafinil is also known to decrease GABA release from the
hypothalamus[10]. Modafinil appears to be distinct from
other psychostimulants (eg, amphetamine) by being
highly selective for specific areas in the central nervous
system (nuclei of the hypothalamus and amygdala) rather
than widespread brain activation and has little effect on
dopaminergic activity in the striatum.
http://www.springerlink.com/content/l2611pg1734228j1/

The effective elimination half-life of modafinil after multiple doses is about 15 hours. Apparent steady states of total modafinil are reached after 2-4 days of dosing. Absorption of modafinil is quick, with peak plasma concentrations occurring at 2-4 hours after ingestion. Food seems to have no affect on the bioavailibity, except possibly a delay in absorption around one hour.

[metamorphosis12]

This quote is from the "Professional" part of the "Interactions Checker" bit of Drugs.com | Pr

Originally Posted by kiwi33

Negative interactions between Prozac (and other SSRIs/SNRIs) and amphetamines are classified as "Major".

To quote:

"In general, amphetamines and other sympathomimetic appetite suppressants should not be combined with selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs)."
escription Drug Information, Interactions & Side Effects

Originally Posted by kiwi33

This site is a helpful resource.

Thanks for the link to that site. It looks very helpful.
I did a research paper on amphetamines and the brain. It has two parts. Unfortunately some of the links have died out. I think many of them still work.

1.) amphetamines-modafinil/armodafinil, their effectiveness and effects on the brain
Pt. 1)

This is a great research paper with 220 references. This report, with a ton of links, can take you down many different avenues of the role on various stimulants!

An analysis of the effects of stimulant drugs ( amphetamine, modafinil/armodafinil, nicotine, caffeine, histamine (H3) receptor antagonists, and sedative/hypnotics and sleep promoting drugs
Assessment in 4 key areas:wakefulness; biology of sleep/wake and cognition; targets of wake promoting and/or cognition enhancing drugs; and ongoing clinical trials.

Approaches to Measuring the Effects of Wake-Promoting Drugs: A Focus on Cognitive Function
Christopher J. Edgar,1 Edward F. Pace-Schott,2 and Keith A. Wesnes3

Abstract
Quote:
Objectives-
In clinical drug development, wakefulness and wake-promotion maybe assessed by a large number of scales and questionnaires. Objective assessment of wakefulness is most commonly made using sleep latency/maintenance of wakefulness tests, polysomnography and/or behavioral measures. The purpose of the present review is to highlight the degree of overlap in the assessment of wakefulness and cognition, with consideration of assessment techniques and the underlying neurobiology of both concepts.
Design-
Reviews of four key areas were conducted: commonly used techniques in the assessment of wakefulness; neurobiology of sleep/wake and cognition; targets of wake promoting and/or cognition enhancing drugs; and ongoing clinical trials investigating wake promoting effects.
Results-
There is clear overlap between the assessment of wakefulness and cognition. There are common techniques which may be used to assess both concepts; aspects of the neurobiology of both concepts may be closely related; and wake promoting drugs may have nootropic properties (and vice-versa). Clinical trials of wake promoting drugs often, though not routinely, assess aspects of cognition.
Conclusions-
Routine and broad assessment of cognition in the development of wake promoting drugs may reveal important nootropic effects, which are not secondary to alertness/wakefulness, whilst existing cognitive enhancers may have under explored or unknown wake promoting properties.
Approaches to Measuring the Effects of Wake-Promoting Drugs: A Focus on Cognitive Function

Modafinil is used everyday or is often cycled to keep it's effectiveness up and tolerance down. 200mg is the most common dose. Studies have shown no benefit with an increase. The effective elimination half-life of modafinil after multiple doses is about 15 hours. Apparent steady states of total modafinil are reached after 2-4 days of dosing. Absorption of modafinil is quick, with peak plasma concentrations occurring at 2-4 hours after ingestion. Food seems to have no affect on the bioavailibity, except possibly a delay in absorption around one hour.
Other drugs can be directly influenced by modafinil and their elimination time may be prolonged due to modafinil's effect on the cytochrome-p450 family of enzymes.
Drugs that are largely eliminated via CYP2C19 metabolism, such as diazepam, propranolol, phenytoin (also via CYP2C9 or it's substrate) may have prolonged elimination upon use in conjunction with modafinil because of modafinils potential to inhibit the CYP2C19 and suppress CYP2C9, also to induce CYP3A4, CYP2B6, and CYP1A2.
http://www.ingentaconnect.com/conten...00002/art00002
http://www.ingentaconnect.com/conten...00013/art00003

Mechanism of Action: (as a stimulant and possible use in bi-polar and uni-polar depression)
Quote:
Modafinil is a unique wakefulness-promoting pharmaceutical
whose exact biochemical mechanism of action
is not known. However, it has been shown to increase
the levels of serotonin, histamine, and dopamine in the
brain [4–6]. Studies done on the wakefulness-promoting
mechanism of modafinil have proposed specific activation
of the tuberomammillary, a cluster of magnocellular cells in the posterior hypothalamus. Which is the main source of neuronal histamine in the brain.
Also it produces activation on orexin (a neurotransmitter that regulates arousal, wakefulness, and appetite containing neurons in the perifornical
area, although not in other areas involved in the
sleep–wake cycle (eg, the supraoptic nucleus) [7]. Histamine
and orexin have been implicated in the regulation
of wakefulness [8,9].


Modafinil administration into rat
nucleus accumbens resulted in a weak dopamine release
secondary to its ability to reduce local γ-aminobutyric
acidergic transmission [4]. By contrast, amphetamine
strongly elevated dopamine levels in the nucleus accumbens
and striatum. The difference in addiction potential
between modafinil and amphetamine is postulated and explained by this difference in dopaminergic activity.
Modafinil is also known to decrease GABA release from the
hypothalamus[10]. Modafinil appears to be distinct from
other psychostimulants (eg, amphetamine) by being
highly selective for specific areas in the central nervous
system (nuclei of the hypothalamus and amygdala) rather
than widespread brain activation and has little effect on
dopaminergic activity in the striatum.
Abstract-
Adjunctive use of modafinil in bipolar patients: just another stimulant or not? - Springer
Full text-
Home -
Springer


Brain Explorer
A great website on the brain, covering neurological aspects (maps, brain disorders, glossary, neurotransmission and more!)
http://www.brainexplorer.org/brain_a...as_index.shtml

[metamorphosis12]

2.) amphetamines-modafinil/armodafinil, their effectiveness and effects on the brain

pt.2)

Modafinil, like other stimulants, increases the release of monoamines – specifically, the catecholamines norepinephrine and dopamine – from the synaptic terminals. However, modafinil also elevates histamine levels. Which is one of the differences between it and amphetamines. Modafinil has also been the target of studies, identifying effects on dopamine in the striatum and nucleus accumbens, noradrenaline in the hypothalamus and serotonin in the amygdala and frontal cortex.


Your Brain and What It Does
---AMYGDALA: Lying deep in the center of the limbic emotional brain, this powerful structure, the size and shape of an almond, is constantly alert to the needs of basic survival including sex, emotional reactions such as anger and fear. Consequently it inspires aversive cues, such as sweaty palms, and has recently been associated with a range of mental conditions including depression to even autism. It is larger in male brains, often enlarged in the brains of sociopaths and it shrinks in the elderly.
-BRAIN STEM: The part of the brain that connects to the spinal cord. The brain stem controls functions basic to the survival of all animals, such as heart rate, breathing, digesting foods, and sleeping. It is the lowest, most primitive area of the human brain.
CEREBELLUM: Two peach-size mounds of folded tissue located at the top of the brain stem, the cerebellum is the guru of skilled, coordinated movement (e.g., returning a tennis serve or throwing a slider down and in) and is involved in some learning pathways.
-CEREBRUM: This is the largest brain structure in humans and accounts for about two-thirds of the brain’s mass. It is divided into two sides — the left and right hemispheres—that are separated by a deep groove down the center from the back of the brain to the forehead. These two halves are connected by long neuron branches called the corpus callosum which is relatively larger in women’s brains than in men’s. The cerebrum is positioned over and around most other brain structures, and its four lobes are specialized by function but are richly connected. The outer 3 millimeters of “gray matter” is the cerebral cortex which consists of closely packed neurons that control most of our body functions, including the mysterious state of consciousness, the senses, the body’s motor skills, reasoning and language.

-The Frontal Lobe: is the most recently-evolved part of the brain and the last to develop in young adulthood. It’s dorso-lateral prefrontal circuit is the brain’s top executive. It organizes responses to complex problems, plans steps to an objective, searches memory for relevant experience, adapts strategies to accommodate new data, guides behavior with verbal skills and houses working memory. Its orbitofrontal circuit manages emotional impulses in socially appropriate ways for productive behaviors including empathy, altruism, interpretation of facial expressions. Stroke in this area typically releases foul language and fatuous behavior patterns.
-The Temporal Lobe controls memory storage area, emotion, hearing, and, on the left side, language.
-The Parietal Lobe receives and processes sensory information from the body including calculating location and speed of objects.
The Occipital Lobe processes visual data and routes it to other parts of the brain for identification and storage.
-HIPPOCAMPUS: located deep within the brain, it processes new memories for long-term storage. If you didn't have it, you couldn't live in the present, you'd be stuck in the past of old memories. It is among the first functions to falter in Alzheimer's.
-HYPOTHALAMUS: Located at the base of the brain where signals from the brain and the body’s hormonal system interact, the hypothalamus maintains the body’s status quo. It monitors numerous bodily functions such as blood pressure and body temperature, as well as controlling body weight and appetite.
-THALAMUS: Located at the top of the brain stem, the thalamus acts as a two-way relay station, sorting, processing, and directing signals from the spinal cord and mid-brain structures up to the cerebrum, and, conversely, from the cerebrum down the spinal cord to the nervous system. The Brain - Diagram and Explanation "Recently, modafinil was screened at a large panel of receptors and transporters in an attempt to elucidate its pharmacology.[26] Of the sites tested, it was found to significantly act only on the dopamine transporter (DAT), inhibiting the reuptake of dopamine with an IC50 value of 4 μM.[26] Accordingly, it produces locomotor activity and extracellular dopamine concentrations in a manner similar to the selective dopamine reuptake inhibitor (DRI) vanoxerine, and blocks methamphetamine-induced dopamine release.[26] As a result, it seems that modafinil exerts its effects by acting as a weak DRI, though it cannot be ruled out that other mechanisms may also be at play.[26] On account of its action as a DRI and lack of abuse potential, modafinil was suggested as a treatment for methamphetamine addiction by the authors of the study.[26] Modafinil - Wikipedia, the free encyclopedia. Fundamental differences in modafinil vs. amphetamine http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum http://www.sciencedirect.com/science...6452298000153t

Amphetamines increase the release of monoamines throughout the brain. Provigil both increases the release of monoamines and histamine levels more specifically in the hypothalamus.
The specific monoamines increased by Provigil are dopamine in the striatum and nucleus accumbens, noradrenaline in the hypothalamus and ventrolateral preoptic nucleus, and serotonin in the amygdala and frontal cortex. Amphetamines increase the levels of norepinephrine, serotonin, and dopamine (in the nigrostriatal region- is a neural pathway that connects the substantia nigra with the striatum. It is one of the four major dopamine pathways in the brain region of the brain)inducing euphoria and with a strongly addictive potential:


Potential Adverse Effects of Amphetamine Treatment on Brain and Behavior: A Review
Amphetamines are a competitive inhibitor of DA. Attaching directly to DA substrate binding sites on DAT. It creates a twofold action
1)- Blocking the reuptake of DA into the neuron.
2)- And at an even more profound level, actually entering the neuron itself. Thus separating the amphetamines m.o. a much more robust class from the allosteric reuptake inhibitors. Once inside the actual cell amphetamine then competitively inhibits DA at the VMAT. Now the function of storing DA into the synaptic vesicles is reversed causing displacement of DA . Building in the front neuronal vesicles until the cell is forced to release the DA back into the synapse by opening a new ion channel. At the same time the DAT cycle is now reversed and instead of releasing the DA into the neuron. It is now pumping it back into the synaptic cleft. Dexamphetamine has a higher proclivity for DAT. While adderall is more inclined to bind to NET. Both affect the two monoamines and release large active amounts of DA and NE into the synapse for use. And draining the cells of the normal levels of both to a high degree. Note, the spanules or xr release of these amps. do not have the same commando type of actions. Even though the pharmacological function is similar. The drugs aggressive actions are slowed significantly and lower the addiction potential, neurotoxicity, and systematic overload in the brain.

Modafinil and its big brother, armodafinil also bind to DAT. Modafinil's lower affinity for binding to DAT, is made up for by its naturally high plasma levels. It's effect on the increase of synaptic DA leads to a tonic firing and a downstream effects on the neurotransmitters histamine and
orexin/hypocretin. The pharmacokinetics suggest the success of its stimulating qualities are also due in part to its slow rise in plasma. The sustained plasma levels of 6-8 hrs reinforcing the tonic DA activity to promote wakefulness. Instead of a phasic DA activity that promotes reinforcement and abuse.. Armodafinil is the active R enantiomer minus the S. Armodafinil has even later times for peak levels, a longer half-life, and higher plasma levels, 6-14 hrs.
Potential Adverse Effects of Amphetamine Treatment on Brain and Behavior: A Review
Armodafinil versus Modafinil in Patients of Excessive Sleepiness Associated with Shift Work Sleep Disorder: A Randomized Double Blind Multicentric Clinical Trial
Practical Use and Risk of Modafinil, a Novel Waking Drug

The future of stimulants and cognitive enhancers

THE AVAILABILITY AND PORTRAYAL OF STIMULANTS OVER THE INTERNET
Ty S. Schepis, Ph.D.,1 Douglas B. Marlowe, J.D., Ph.D.,2,3 and Robert F. Forman, Ph.D.2,3,4 THE AVAILABILITY AND PORTRAYAL OF STIMULANTS OVER THE INTERNET

The Future of Psychopharmacological Enhancements:
Expectations and Policies
Abstract-
The Future of Psychopharmacological Enhancements: Expectations and Policies - Springer
Text-
Home - Springer

[Altered Moment]

I was addicted to meth for five years along time ago. It is a very powerful drug. Large doses over a period of time can have major deliterious effects.

I am not sure how Prozac would effect adderal since it only acts on serotonin. Who knows though the chemistry is so complicated.

I often wish they would give me amphetamine for depression. I think it is rare for a pdoc to do it. With my history probably not a good idea. I know it would work though at proper dosage and extended realease. I will read all the above links when I have some time.

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