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.