China
Africa
Explore chapters and articles related to this topic
Neurotransmitters and pharmacology
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Ronald A. Browning, Richard W. Clough
The use of DA antagonists can be advantageous in controlling the symptoms of psychosis but could impair motivation and cognition. The role of dopamine neurons in motivation and reward as well as in addiction is well established.17 Thus, blocking DA receptors could reduce motivation. Perhaps it would be possible to enhance motivation with a dopamine reuptake inhibitor such as bupropion (Wellbutrin®, Zyban®) or methylphenidate (Ritalin®). There are reports showing that bupropion improves restlessness and methylphenidate improves cognitive function in TBI patients.84,101 Moreover, as expected, there is experimental evidence that DA receptor antagonists (e.g., antipsychotic drugs) can impair recovery of cognitive function after TBI.102 Thus, having knowledge of DA neurotransmission, including receptor populations and the diverse functional circuitry through which DA acts, will promote a better understanding and rationale for DA pharmacotherapy in TBI.
Panic Disorder
Published in Stephen M. Stahl, Bret A. Moore, Anxiety Disorders: A Guide for Integrating Psychopharmacology and Psychotherapy, 2013
Meredith E. Charney, M. Alexandra Kredlow, Eric Bui, Naomi M. Simon
Studies investigating the potential efficacy of bupropion, a norepinephrine, serotonin, and dopamine reuptake inhibitor, have yielded conflicting results, with both negative (Sheehan, Davidson, Manschreck, & Wyck Fleet, 1983) and positive (Simon et al., 2003) open-label trials, with the latter suggesting that lower dosing may be better tolerated.
Stimulants
Published in Clete A. Kushida, Sleep Deprivation, 2004
John A. Caldwell, J. Lynn Caldwell
Amphetamine’s primary effects (increased wakefulness, appetite suppression, and increased locomotor activity) are thought to be mediated by the release of norepinephrine from noradrenergic neurons in the CNS (36). However, research points to the role of plasma transport inhibition of dopamine, norepinephrine, and serotonin as well as inhibition of the vesicular monoamine transporter (138). Wisor et al. (139) summarize evidence that dopamine reuptake inhibition produces a greater alerting effect than norepinephrine transport blockade.
Rethinking the medication management of major depression
Published in Expert Review of Neurotherapeutics, 2023
Our proposed approach needs testing, but is readily usable by psychiatrists. Further studies are needed to guide use of antidepressant blood levels for most newer antidepressants. Ongoing evaluation of pharmacogenetic tests in guiding medication choices for MDD is also needed. The use of generic drugs has steadily increased in the US over the past two decades. Formularies that encourage selection of cheaper medications through copayment or coinsurance tiers have been a principal driver of generic drug use [193]. Despite anecdotal reports that some generics have less bioavailability compared with brand-name drugs, a study using two U.S. large commercial insurance databases reported comparable clinical outcomes with use of generic drugs compared with brand-name products [194]. Research on treatment of depression has appropriately focused over the past two decades on searching for drugs with new mechanism of action and targets, which is crucial but, there have been too few studies on how to better utilize currently available medications. A recent successful example in this regard is the dextromethorphan-bupropion combination, which has just been approved by FDA for MDD treatment [195]. Dextromethorphan has anti-NMDA receptor antagonist and SNRI properties. When combined with the norepinephrine-dopamine reuptake inhibitor bupropion, improvement of depressive symptoms is observed in as short as one week.
Practice patterns of bupropion co-prescription with antipsychotic medications
Published in Journal of Addictive Diseases, 2022
Mohan Gautam, Shivali Patel, Paul Zarkowski
Meyer and colleagues investigated the degree to which bupropion and hydroxybupropion occupy dopamine transporters in human subjects after oral administration of bupropion using positron emission tomography. Eight healthy subjects received no bupropion whereas eight subjects who met DSM-IV criteria for MDD received bupropion sustained release at 100 mg/day for week one, 200 mg/day for week two, and 300 mg/day for week three. The mean change in striatal dopamine transporter binding potential was 7+/-12% for healthy subjects and 14+/-12% for subjects with MDD. Other medications which utilize dopamine reuptake inhibition to exert therapeutic effect, such as methylphenidate, demonstrate at least 50–75% dopamine receptor transporter occupancy even in the lower range of clinically relevant dosages such as 10–20 mg.24 This suggests that bupropion demonstrates minimal to minor dopaminergic activity.
A Single Low-Dose of Methylphenidate Improves Abnormal Visual Field Testing
Published in Current Eye Research, 2021
Amir Sternfeld, Omer Y. Bialer, Dotan Keidar, Elinor Megiddo, Ivan Budnik, Hadas Stiebel-Kalish, Tami Livnat
Methylphenidate (trade name Ritalin™, Novartis Pharmaceuticals Corporation) is a central nervous system stimulant registered and widely used for the treatment of attention-deficit hyperactivity disorder (ADHD) and narcolepsy.17,18 The postulated mechanism of action is as a neuronal norepinephrine–dopamine reuptake inhibitor, thus increasing their bioavailability. It has an approximate duration of action of 2–4 hours for the immediate release drug.19 Common adverse effects include insomnia, anxiety, nervousness, and weight loss. More serious adverse effects include psychosis, tachycardia and hypertension.17,18 Methylphenidate (MPH) is recently gaining popularity as a cognitive enhancer for non-ADHD individuals.20,21 Numerous studies reported improvement in working memory, speed of processing, attention, vigilance, anxiety and motivation following a single-dose MPH.21–23 These properties can be harnessed to improve VF testing performance without inducing a change in the functional architecture of the visual system.11,12