By Neuroscience Education Institute
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Additional resources for Diagnosis and Treatment of Sleep Wake Disorders
Like methylphenidate, amphetamines are Schedule II drugs. There is a subtly greater dopamine release by amphetamines than methylphenidate in the prefrontal cortex, which is thought to account for the subtle differences in effects of these drugs on behavioral tolerance. 6 The precise mechanism of action of modaﬁnil (Provigil) is yet to be fully elucidated. It binds to the DAT and requires its presence as well as that of alpha adrenergic receptors, especially alpha 1. In contrast, modaﬁnil does not appear to require the norepinephrine transporter or postsynaptic dopamine receptors.
It is intimately involved in feelings of tiredness and initiation of sleep. Its synthesis is predominantly controlled by the retinohypothalamic tract (RHT), via the suprachiasmatic nucleus (SCN). From here, the pineal gland can be stimulated either via the paraventricular nucleus (PVN) of the hypothalamus, or via norepinephrine release from the superior cervical ganglion (SCG) in the brainstem/spinal cord, initiated when the SCN is inhibited. The receptors MT1 and MT2 control the relevant actions of melatonin, suppressing neuronal ﬁring and inducing phase shifts respectively.
Immediate release formulations are recommended for excessive sleepiness, dosed 2–3 times per day for a total daily dose of 20–60 mg (racemic) or 5–20 mg (d-enantiomer). Notable side effects include insomnia, headache, nervousness, irritability, overstimulation, tremor, and dizziness. Methylphenidate has high abuse potential and is Schedule II, with greater risk for immediate release formulations, although methylphenidate may be less reinforcing than amphetamines. 5 Amphetamine, like methylphenidate, binds to the DAT and prevents it from taking up dopamine.
Diagnosis and Treatment of Sleep Wake Disorders by Neuroscience Education Institute