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Norepinephrine-dopamine reuptake

Monoamine oxidase inhibition Serotonin reuptake inhibition Norepinephrine reuptake inhibition Dopamine reuptake inhibition a2-Adrenergic receptor blockade Serotonin-2A receptor blockade Serotonin-2C receptor blockade Serotonin-3 receptor blockade op-Adrenergic receptor blockade Histamine-1 receptor blockade Muscarinic cholinergic receptor blockade... [Pg.573]

Bupropion is a monocyclic antidepressant that inhibits the reuptake of norepinephrine and dopamine. Bupropion is effective for relieving symptoms of ADHD in children but is... [Pg.638]

Carboni E Silvagni A. (2004). Dopamine reuptake by norepinephrine neurons exception or rule Crit. Rev. Neurobiol. 16, 121-8. [Pg.208]

Bupropion is another alternative pharmacological approach to tobacco abstinence. It is an antidepressant drug that blocks reuptake of norepinephrine and dopamine, and also blocks nicotinic receptors in the low to intermediate micromolar range (Fryer and Lukas 1999). Thus, the effects of bupropion on nicotine addiction may be through dual effects on dopaminergic and nicotinic systems. Further, it has been an effective treatment in controlled studies, both alone and in combination with the nicotine patch. Bupropion alone or in combination with a nicotine patch was more effective than placebo or the nicotine patch alone. [Pg.117]

Monoamine The primary psychoactive mechanism of cocaine is blocking reuptake of the monoamine neurotransmitters dopamine, norepinephrine, and serotonin, leading to increased available synaptic transmitters (O Brien 1996). Chronic use is associated with changes in... [Pg.134]

Tricyclic drugs have, as the name implies, a three-ring structure, and interfere with reuptake of norepinephrine and/or serotonin into axon terminals. Tricyclic drugs include imipramine (Tofranil), amitriptyline (Elavil), clomipramine (Anafranil), and nortriptyline (Pamelor, Aventil). Tricyclics have the occasional but unfortunate cardiovascular side effects of arrhythmia and postural hypotension. Newer, nontricyclic antidepressants have been developed that are collectively referred to as SSRIs. These have a potent and selective action on serotonin, and lack the cardiovascular side effects of the tricyclics. These include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), and fluvoxamine (Luvox). A fifth SSRI, citalopram (Celexa) has been used in Europe and has recently been approved in the United States. Venlafaxine (Effexor) blocks reuptake of norepinephrine and serotonin, while bupropion (Wellbutrin) acts on both dopamine and norepinephrine. [Pg.251]

Bupropion (Wellbutrin). Bupropion is the only antidepressant that works by blocking the reuptake of norepinephrine and dopamine. It is used to treat depression and... [Pg.56]

The TCAs have affinity for both receptors and transporters of monoamine transmitters and behave as antagonists in both respects. Thus, the neuronal reuptake of norepinephrine (p. 82) and serotonin (p. 116) is inhibited, with a resultant increase in activity. Muscarinic acetylcholine receptors, a-adrenocep-tors, and certain 5-HT and hista-mine(Hi) receptors are blocked. Interference with the dopamine system is relatively minor. [Pg.230]

It is believed that trazodone, in therapeutic doses, inhibits the neuronal reuptake of serotonin. It is not a MAO inhibitor or a CNS stimulator. It has a minor influence on the reuptake of norepinephrine and dopamine. In addition, it does not bind with cholinergic or a-adrenergic receptors. Synonyms of this drag are thrombran, pragmarel, desyrel, and others. [Pg.114]

Pharmacology Dexmethylphenidate hydrochloride is a CNS stimulant. It is the more pharmacologically active enantiomer of the d- and /-enantiomers and is thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. Pharmacokinetics ... [Pg.1147]

Mechanism of Action A CNS stimulant that blocks the reuptake of norepinephrine and dopamine into presynaptic neurons, increasing the release of these neurotransmitters into the synaptic cleft. Therapeutic Effect Decreases motor restlessness and fatigue increases motor activity, mental alertness, and attention span elevates mood. [Pg.348]

PCP and ketamine bind to the NMDA receptor and block the neurotransmitter glutamate. PCP also blocks reuptake of dopamine, norepinephrine, and serotonin. Because so many neurotransmitters are affected, the signs and symptoms of PCP intoxication are numerous and varied. [Pg.107]

Of the clinically tested new antipsychotics, ziprasidone has the highest 5-HT2A/D2 receptor-affinity ratio. Ziprasidone is an antagonist at the a -adrenoreceptor, but its affinity is half that of its D 2 affinity. In addition, compared with its affinity for D 2 and 5-HT2A receptors, ziprasidone has a relatively low affinity for histamine receptors (pKJ = 7.33). In vitro, ziprasidone is a moderately potent inhibitor of neuronal reuptake of norepinephrine, serotonin, and, to a lesser extent, dopamine. This property is shared with some antidepressants, and contrasts with risperidone, which is inactive at all three monoamine uptake sites. [Pg.62]

Pharmacologic targeting of monoamine transporters. Commonly used drugs such as antidepressants, amphetamines, and cocaine target monoamine (norepinephrine, dopamine and serotonin) transporters with different potencies. A shows the mechanism of reuptake of norepinephrine (NE) back into the noradrenergic neuron via the norepinephrine transporter (NET), where a proportion is sequestered in presynaptic vesicles through the vesicular monoamine transporter (VMAT). and C show the effects of amphetamine and cocaine on these pathways. See text for details. [Pg.178]

How precisely does cocaine achieve these effects in the brain As described in Chapter i, once a neurotransmitter is released from its neuronal terminal, its actions within the synapse are ended principally by reuptake into the presynaptic terminal. Cocaine primarily blocks the reuptake of dopamine but also acts similarly on norepinephrine and serotonin reuptake. If your neuronal terminals can be seen as acting like little vacuum cleaners, then cocaine essentially clogs the vacuum nozzle. As a consequence of this blockade, the concentrations of dopamine, norepinephrine, and serotonin within the synaptic cleft between two neurons increases dramatically. Withinmillions of synapses in the brain, these neurotransmitters are now free to continue to stimulate their receptors over and over, again and again. There are neuronal terminals for dopamine, norepinephrine, and serotonin scattered throughout the entire brain, and thus the consequences of cocaine on brain function are also widespread. [Pg.71]

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. [Pg.412]

Dopamine-norepinephrine reuptake inhibitors Bupropion (Wellbutrin)... [Pg.43]

This drug is a central nervous system stimulant that is considered to prevent the reuptake of norepinephrine and dopamine into the presynaptic neurones and increase the release of these neurotransmitters to the extraneuronal space. A high-fat meal increases its absorption. Methylphenidate in animal experiments was found to inhibit CYP1A and CYP2E1 by 50%. It is metabolized by de-esterification to inactive metabolites. [Pg.153]

Figure 10.11. Presynaptic reuptake of norepinephrine and dopamine by sodium and chloride cotransport (a), and functional consequences of inhibition of reuptake (b). Figure 10.11. Presynaptic reuptake of norepinephrine and dopamine by sodium and chloride cotransport (a), and functional consequences of inhibition of reuptake (b).
Again, there are various dmgs with different ranges and specificities. Cocaine has a particularly broad spectrum, affecting the reuptake of norepinephrine, dopamine, and serotonin alike. The effect of cocaine can be quantitatively studied in mice by observing their excitement in response to being placed into a new environment, which is measured simply as the distance travelled within their new home over time. In experiments with transgenic mice, the reuptake transporters for both dopamine and serotonin had to be deleted in order to abolish the increase in excitement induced by cocaine. [Pg.96]

As noted in Chapter 3, stimulant drugs such as cocaine and the amphetamines are thought to affect the brain primarily through complex actions on monoamine neurotransmitters dopamine, norepinephrine, and serotonin. For example, both cocaine and the amphetamines block rcuptake of norepinephrine, serotonin, and particularly dopamine (Meyer 8c Quenzer, 2005). In addition, the amphetamines and methylphenidatc also increase the release of dopamine (Sulzer, Sonders, Poulsen, 8c Galli, 2005). Thus, the initial effect of stimulants is to produce a storm of activity in neural pathways that are sensitive to the monoamine transmitters. Because of this increased activity, however, and particularly because reuptake is blocked so that enzymes break down the neurotransmitters, the long-term effects of stimulant use involve depletion of monoamines. If you remember that low levels of monoamines are linked to clinical depression (see Chapter 3), tlien you have the basis for one theory of why the aftereffects of heavy cocaine use involve depression (Dackis 8c Gold, 1985). To explain this hypothesis, we must turn briefly to data from the animal laboratory. [Pg.144]

Chlorpromazine also inhibits the reuptake of norepinephrine and 5-hydroxy-tryptamine in rat cerebral cortex but does not affect reuptake of gamma-aminobutyric acid. It is also a potent competitive inhibitor of the stimulatory effects of dopamine on adenylate cyclase. [Pg.580]

Neurons in the central nervous system communicate by chemical transmission. Of relevance to the present discussion are monoamine neurons that release dopamine, norepinephrine, or serotonin as one of their transmitters in response to an action potential. Reuptake transporter proteins embedded in the neuronal plasma membrane then clear the synapse of monoamines, typically taking up 70-80%) of the released transmitter. This reuptake is thought to be the major termination mechanism for the monoamine chemical signaling process. [Pg.179]

Cocaine is a potent CNS stimulant that elicits a state of increased alertness and euphoria with its actions similar to those of amphetamine but of shorter duration. These CNS effects are thought to be largely associated with the ability of cocaine to block dopamine reuptake at nerve synapses and thereby prolong the action of dopamine in the CNS. It is this response that leads to recreational abuse of cocaine. Cocaine also blocks the reuptake of norepinephrine at presynaptic nerve terminals this produces a sympathomimetic response (including an increase in blood pressure, heart rate, and body temperature). Cocaine is effective as a local anesthetic and vasoconstrictor of mucous membranes and is therefore used clinically for nasal surgery, rhinoplasty, and emergency nasotracheal intubation. [Pg.1335]

Dexmethylphenidate is a CNS stimulant that blocks the reuptake of norepinephrine and dopamine into presynaptic... [Pg.194]

Sibutramine hydrochloride is an anorexiant that inhibits reuptake of norepinephrine, serotonin and dopamine. It may stimulate the satiety center in brain, causing appetite suppression. It is indicated as an adjunct to a reduced calorie diet for the management of obesity, including weight loss and maintenance of weight loss. Recommended for patients with an initial body mass index greater than 30 kg/m2 or greater than 27 kg/m in the presence of other risk factors (e.g., hypertension, diabetes, dyslipidemia). [Pg.643]


See other pages where Norepinephrine-dopamine reuptake is mentioned: [Pg.322]    [Pg.61]    [Pg.168]    [Pg.51]    [Pg.114]    [Pg.1038]    [Pg.243]    [Pg.105]    [Pg.59]    [Pg.76]    [Pg.82]    [Pg.82]    [Pg.27]    [Pg.92]    [Pg.76]    [Pg.30]    [Pg.455]    [Pg.693]    [Pg.113]   


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