Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

MAOIs Dopamine

Monoamine Oxidase Inhibitors. MAOIs inactivate the enzyme MAO, which is responsible for the oxidative deamination of a variety of endogenous and exogenous substances. Among the endogenous substances are the neurotransmitters, norepinephrine, dopamine, and serotonin. The prototype MAOI is iproniazid [54-92-2] (25), originally tested as an antitubercular dmg and a close chemical relative of the effective antitubercular, isoniazid [54-85-3] (26). Tubercular patients exhibited mood elevation, although no reHef of their tuberculosis, following chronic administration of iproniazid. In... [Pg.465]

The discovery that MAO has two isoenzymes with different distributions, substrate specificity and inhibitor sensitivity has helped to rehabilitate the MAOIs to some extent. These isoenzymes are the products of different genes on the X-chromosome and share about 70% sequence homology. Whereas noradrenaline and 5-HT are metabolised preferentially by MAOa, tyramine and dopamine can be metabolised by either isoenzyme. Selective inhibitors of MAOa (e-g- moclobemide Da Prada et al. 1989) should therefore be safe and effective antidepressants whereas the selective MAOb inhibitor, selegiline, should not have any appreciable antidepressant activity (Table 20.5). [Pg.435]

MAOI, monoamine oxidase inhibitor NaSSA, noradrenergic and specific serotonergic antidepressant NDRI, norepinephrine and dopamine reuptake inhibitor SARI, serotonin antagonist and reuptake inhibitor SNRI, serotonin and norepinephrine reuptake inhibitor SSRI, selective serotonin reuptake inhibitor TCA, tricyclic antidepressant. [Pg.577]

Synergy of unwanted pharmacological effect ginseng and its products will inhibit the central nervous system (CNS) when they are applied with luminal, chloral hydrate, or ephedrine, which can increase the release of dopamine, noradrenaline, and serotonin in the CNS thus inducing a hypertensive crisis if monoamine oxidase inhibitors (MAOIs) are given simultaneously. [Pg.121]

MAOI (Monoamine Oxidase Inhibitors) will intensify and prolong the effects of NN-DMT, however this is never recommended. Foolish combinations of MAOIs and other drugs can lead to serious health problems and even death. The tryptamines are normally metabolized by an MAO in the body. MAO metabolizes serotonin, norepinephrine, and dopamine. By inhibiting this, MAOIs increase levels of those neurotransmitters. Tyramine will not be metabolized and will cause an increase in tyramine levels in blood. [Pg.5]

DA, dopamine 5-HT, serotonin LSD, lysergic acid diethylamide, MAOI, monoamine oxidase inhibitor, NE, norepinephrine PCP,... [Pg.770]

DA, dopamine GABA, y-aminobutyric acid 5-HT, serotonin MAOI, monoamine oxidase inhibitor NE, norepinephrine. [Pg.772]

The 5-HT syndrome can also be produced by a number of treatments whose primary actions are not expressed at serotonergic receptors. For example, in MAOI-pretreated rats, the intraventricular administration of dopamine or systemic treatment with the dopamine precursor /-dihydroxyphenylalanine (/-DOPA) in combination with an MAOI results in the 5-HT syndrome... [Pg.36]

Listing of antidepressants grouped by principal mechanism of action in the synapse. Abbreviations MAOI—irreversible = irreversible monoamine oxidase inhibitor MAOI—reversible = reversible monoamine oxidase inhibitor NDRl = norepinephrine/ dopamine reuptake inhibitor NRI = norepinephrine reuptake inhibitor NSRl = norepinephrine/serotonin reuptake inhibitor NSSA = norepinephrine/specific serotonin agonist SRI = serotonin reuptake inhibitor SRl/serotonin-2 blocker = serotonin reuptake inhibitor and serotonin-2 receptor antagonist. [Pg.48]

The MAO enzymes, which come in two types known as MAO-A and MAO-B, perform a scavenger function by metabolizing and thereby eliminating certain molecules from nerve cells. This prevents the accumulation of toxic levels of these substances. In the brain, the MAO-A enzyme metabolizes a variety of substances including norepinephrine and serotonin, and the MAO-B enzyme metabolizes dopamine and several other substances. The effectiveness of MAOIs primarily comes from their ability to inhibit the MAO-A enzyme and thereby boost the availability of norepinephrine and serotonin. [Pg.50]

Third is the presence of other psychiatric or medical disorders. This can help gnide antidepressant selection in several ways. In some cases, an antidepressant may be preferred becanse it can treat both disorders. For example, the extensive evidence that flnoxetine is an effective treatment for bnlimia nervosa makes it preferable for patients with depression and bnlimia. Similarly, the depressed Parkinson s disease patient whose nenrological illness results from a lack of dopamine in a particular area of the brain may have both her depression and her Parkinson s disease improved by bnpropion, which increases brain dopamine activity. In other cases, an antidepressant shonld be avoided if it worsens the other illness or interacts adversely with a medication needed to treat the other illness. For example, TCAs and MAOIs can complicate glncose control in diabetics and shonld not rontinely be used by depressed diabetics. (See Table 3.11.)... [Pg.63]

Yet another MAOI is selegiline (Eldepryl). Unlike the other MAOls, selegiline is seldom used to treat depression. At low doses, selegiline only inhibits the M AO-B enzyme. Therefore, it increases dopamine activity but does not have any pronounced effect on norepinephrine or serotonin. For this reason, it has been less useful as an antidepressant however, its primary use has been to treat Parkinson s disease. Of course, this selectivity for dopamine suggests that it may be helpful for ADHD as well. [Pg.245]

Monoamine Oxidase Inhibitors (MAOIs). The MAOls work in a unique fashion by blocking the activity of an enzyme that degrades each of three key brain transmitters norepinephrine, dopamine, and serotonin. These widespread effects on several brain transmitter systems make the MAOls a potentially very effective class of medications for a variety of disorders. A few small studies have evaluated the usefulness of the MAOls in the treatment of BPD and found them moderately helpful for the impulsivity associated with this illness. Unfortunately, the requirements for strict dietary restrictions due to a risk of hypertensive crisis severely limit the usefulness of MAOls in the treatment of BPD. These restrictions are a particular concern when treating patients who have problems with impulsivity and are therefore likely to have difficulty maintaining the dietary regimen. For this reason, although they may theoretically be helpful, MAOls should only be used to treat BPD after other more easily tolerated medications have been tried and have failed. In the near future, so-called reversible MAOls that appear to avoid the need for diet restrictions may become available. If so, this will allow us to reconsider their use in the treatment of BPD. For more information regarding the use of MAOls, please refer to Chapter 3. [Pg.326]

A third way of promoting norepinephrine activity is to interfere with the enzyme that inactivates norepinephrine, monoamine oxidase (MAO). The monoamine oxidase inhibitors (MAOIs) work in this way. Incidentally, inhibiting monoamine oxidase also increases serotonin and dopamine activity. [Pg.361]

Iproniazid, an MAOI no longer available because of its hepatotoxicity, was the first effective antidepressant to be discovered it was introduced shortly before the discovery of imipramine. All MAOIs are presumed to have a similar mode of action, namely to inhibit the intra- and interneuronal metabolism of the biogenic amine neurotransmitters (noradrenaline, dopamine and serotonin). These amines are primarily metabolized by MAO-A (noradrenaline and serotonin) or MAO-B (dopamine). The irreversible MAOIs are inhibitors of MAO-A while selegiline (deprenyl), used as an adjunctive treatment for Parkinson s disease, is a selective, irreversible inhibitor of MAO-B. [Pg.170]

The side effects of the MAOIs include, somewhat surprisingly, orthostatic h)rpotension. This is thought to be due to the accumulation of dopamine in the sympathetic cervical ganglia where it acts as an inhibitory transmitter. [Pg.170]

Dopamine (Intropin) [Vasopressor/Adrenergic] Uses Short-tOTn use in cardiac decompensation secondary to X contractility when no hypovolemia is present T organ p fusion (at low dose) Action Renal dose 2-5 mcg/kg/min Inotropic dose 5-10 mcg/kg/min Pressor dose >10 mcg/kg/min Dose Adults Feds. 5-20 mcg/kg/min by cont inf, start at 5 and t by 5 mcg/kg/min to 20 mcg/kg/min max to effect (mix 400 mg in 250 mL DjW to make 1600 mcg/mL) (see Table 1-3) Caution [C, ] Contra Pheochromocytoma (adrenal gland tumor), VF, sulfite sensitivity Disp Inj 40, 80, 160 mg/mL, premixed 0.8, 1.6, 3.2 mg/mL SE Tach, vasoconstriction, 4- BP, HA, N/V, dyspnea Notes >10 mcg/kg/min X renal p fiision Interactions t Effects W/ a-blockers, diuretics, ergot alkaloids, MAOIs, BBs, anesthetics, phenytoin X effects W/ guanethidine EMS Correct hypovolemia before use use microdrip set or inf pump check soln- discolored... [Pg.15]

Uses Obesity Action Blocks uptake of norepinephrine, serotonin, dopamine Dose 10 mg/d PO, may to 5 mg after 4 wk Caution [C, -] w/ SSRIs, Li, dextromethorphan, opioids Contra MAOI w/in 14 d, uncontrolled HTN, arrhythmias Disp Caps SE HA, insomnia, xerostomia, constipation, rhinitis, tach, HTN Interactions T Risk of serotonin synd W/ dextromethorphan, ergots, fentanyl, Li, meperidine, MAOIs, naratriptan, pentazocine, rizatriptan, sumatriptan, SSRIs, tryptophan, zolmitriptan, St. John s wort effects W/ cimetidine, erythromycin, ketoconazole T CNS depression W/ EtOH EMS Use fentanyl w/ caution, may T risk of serotonin synd concurrent EtOH use can T CNS depression OD May cause tach, HTN, diaphoresis, HA, fever, agitation, muscle tremors, and Szs symptomatic and supportive... [Pg.282]

Mechanism of Action An MAOI that inhibits the activity of the enzyme monoamine oxidase at CNS storage sites, leading to increased levels of the neurotransmitters epinephrine, norepinephrine, serotonin, and dopamine at neuronal receptor sites. Therapeutic Effect Relieves depression. [Pg.970]

Monoamine oxidase inhibitors. The monoamine oxidase inhibitors (MAOIs) inhibit the intracellular catabolic enzyme monoamine oxidase. There are two types of monoamine oxidase MAO-A and MAO-B, both of which metabolize tyramine and dopamine. In addition, MAO-A preferentially metabolizes norepinephrine, epinephrine, and serotonin, and MAO-B preferentially metabolizes phenylethylamine (an endogenous amphetamine-like substance) and N-methylhistamine (Ernst, 1996). Some MAOIs are selective for A or B and some are nonselective (mixed). In addition, irreversible MAOIs (e.g., phenelzine, tranylcypromine) are more susceptible to the cheese effect than are the reversible agents (e.g., moclobemide). [Pg.454]

Two types of the MAO enzymes have been found. They are called MAO-A and MAO-B. MAO-A is found in norepinephrine and serotonin synapses, while MAO-B is found in dopamine synapses. Scientists believe that the therapeutic effects of MAOIs are a result of inhibiting MAO-A, while most of the side effects result from actions at MAO-B. The traditional, older MAOIs cannot select which MAO type they affect, so current studies are investigating drugs that might be more selective. [Pg.82]

DA=dopamine XR=extended-release 5-HT2=serotonin type 2 receptor MAOIs=monoamine oxidase inhibitors MAO=... [Pg.20]

Monoamine oxidase A (MAO A) acts selectively on the substrates norepinephrine and serotonin, whereas monoamine oxidase B (MAO B) preferentially affects phenylethylamine. Both MAO A and MAO B oxidize dopamine and tyramine. MAO A inhibition appears to be most relevant to the antidepressant effects of these drugs. Drugs that inhibit both MAO A and MAO B are called non-selective. The MAOI antidepressants currently available in the United States are nonselective inhibitors. Because tyramine can be metabolized by either MAO A or MAO B, drugs that selectively inhibit one of these enzymes but not the other do not require dietary... [Pg.46]

The enzyme MAO metabolizes some of the neurotransmitters affected by some drugs of abuse, namely epinephrine, norepinephrine, dopamine, and serotonin. Dangerously high levels can result if an inhibitor of this enzyme, or monoamine oxidase inhibitor (MAOI), is used along with the drug of abuse. [Pg.29]

The effect of dopamine is prolonged and intensified by monoamine oxidase inhibitors (MAOIs). If dopamine must be administered to a patient on these drugs, the dose should be reduced to one-tenth or less of that normally used. Concomitant medication with tricyclic... [Pg.153]

The enzyme, monoamine oxidase, exists in two forms MAO-A (intestinal mucosa and intraneuronally in the brain) and MAO-B (platelets and mainly extraneuronally in the brain). Serotonin is preferentially metabolised by MAO-A and noradrenaline (NA norepinephrine), and dopamine and lyramine by both forms. The first generation MAOI antidepressants (phenelzine, tranylcypromine, and isocarboxazid) inhibit both MAO-A and MAO-B and are thought to work by increasing the availability of 5-HT and NA in the synapse—with longer-term adaptive effects occurring as for the TCAs. These MAOls are irreversible, i.e. they permanently inactivate MAO. Thus, recovery of activity occurs slowly, over days, as new MAO molecules are synthesised. [Pg.177]


See other pages where MAOIs Dopamine is mentioned: [Pg.30]    [Pg.158]    [Pg.238]    [Pg.36]    [Pg.334]    [Pg.364]    [Pg.95]    [Pg.99]    [Pg.147]    [Pg.207]    [Pg.221]    [Pg.265]    [Pg.277]    [Pg.287]    [Pg.317]    [Pg.691]    [Pg.692]    [Pg.485]    [Pg.149]    [Pg.42]    [Pg.84]    [Pg.53]    [Pg.289]    [Pg.29]   
See also in sourсe #XX -- [ Pg.893 ]




SEARCH



MAOI

© 2024 chempedia.info