Effect of Carbamazepine on the <i>In Vitro</i> Uptake and Release of Norepinephrine in Adrenergic Nerves of Rabbit Aorta and in Whole Brain Synaptosomes

Purdy, Ralph E.; Julien, Robert M.; Fairhurst, Alan S.; Terry, Michelle D.

doi:10.1111/j.1528-1157.1977.tb04474.x

Cited by 63 publications

(15 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Its main effect is related to DA release, since in the same concentration M ) it releases -60% of the accumulated [3H]DA. Modification of reuptake of another catecholamine, norepinephrine (NE), by CBZ has already been described (Purdy et al, 1977). It has been observed that CBZ inhibited more or less 20% of the reuptake of [3H]NE, in brain synaptosomes, at a concentration of M .…”

Section: Discussionmentioning

confidence: 97%

Effect of Carbamazepine on Dopamine Release and Reuptake in Rat Striatal Slices

1986

View full text Add to dashboard Cite

Carbamazepine has been shown to enhance dopaminergic agonist behavioral effects, but not to displace [3H]spiroperidol binding. To verify if carbamazepine acts presynaptically on dopaminergic neurons, reuptake and release of [3H]dopamine were measured in rat striatal slices in vitro. It was observed that carbamazepine blocked 20% of the reuptake of [3H]dopamine, while cocaine blocked 82% of the reuptake, compared with control. Carbamazepine released 62% and tyramine released 92% of the accumulated [3H]dopamine, compared with control. It was concluded that carbamazepine acts presynaptically on striatal neurons, mainly through enhancement of dopamine release. This finding can be related to some behavioral effects described for carbamazepine; however, the importance of its effects in epileptic and manic-depressive patients remains to be clarified.

show abstract

Section: Discussionmentioning

confidence: 97%

Effect of Carbamazepine on Dopamine Release and Reuptake in Rat Striatal Slices

1986

View full text Add to dashboard Cite

show abstract

“…However, unlike imipramine and desipramine, carbamazepine only weakly inhibits neuronal monoamine reuptake (16). In our studies of the reversal modulation of chloroquine resistance in W2 by car- bamazepine, carbamazepine had no intrinsic antimalarial activity at concentrations up to 10 p.g/ml and failed to modulate chloroquine resistance in W2 at concentrations up to 10 ,ug/ml (Table 1).…”

mentioning

confidence: 84%

“…However, unlike imipramine and desipramine, carbamazepine only weakly inhibits neuronal monoamine reuptake (16 …”

mentioning

confidence: 99%

Neuronal monoamine reuptake inhibitors enhance in vitro susceptibility to chloroquine in resistant Plasmodium falciparum

Coutaux¹,

Mooney²,

Wirth³

1994

Antimicrob Agents Chemother

View full text Add to dashboard Cite

Chloroquine resistance in Plasmodiumfalciparum was reversed in vitro by the neuronal monoamine reuptake inhibitors and antidepressants desipramine, sertraline, fluoxetine, and norfluoxetine but not by carbamazepine, an antiseizure and mood-stabilizing tricyclic drug resembling desipramine which only weakly inhibits neuronal monoamine reuptake. These findings have important clinical implications for drug combination therapy.The goal of this work was to investigate the potential use of clinically relevant antidepressants as combination therapy with antimalarial drugs in drug-resistant malarial infections. Previous studies have shown that antidepressants such as desipramine, imipramine, protriptyline, nortriptyline, doxepin, and fluoxetine modify chloroquine resistance in Plasmodium falciparum in vitro (1, 4, 11). These tricyclic antidepressants and fluoxetine block the sodium-dependent neuronal reuptake of either norepinephrine or serotonin, and tricyclic antidepressants such as imipramine also block the H+-ATPase-regulated monoamine uptake by monoamine storage granules (5). More recently, it has been shown that the monoamine transport proteins in the neuronal plasma cell membrane (10, 18) and neuronal monoamine storage vesicles (10) belong to a superfamily of transport proteins with 12 transmembrane domains which also include the malaria parasite protein mdrl (7,19) and the P glycoprotein in tumor cells (9). In this article, we report that the two antidepressants and neuronal monoamine reuptake inhibitors sertraline and norfluoxetine modify antimalarial resistance to chloroquine in vitro; Taken together with previous studies (1, 4, 11), these findings suggest that antidepressants which act as neuronal monoamine reuptake inhibitors may also enhance the antimalarial activity of chloroquine against drug-resistant forms of P. falciparum.The organisms used in these studies were (i) the chloroquine-resistant clone W2 of P. falciparum from Indochina and (ii) the chloroquine-sensitive clone HB3 of P. falciparum from Honduras. We examined the reversal of chloroquine resistance in the W2 clone of P. falciparum by several neuronal monoamine reuptake inhibitors, namely, desipramine, fluoxetine, norfluoxetine, and sertraline. The monoamine reuptake inhibitors had intrinsic antimalarial activities only at very high concentrations. The IC50s obtained for the W2 clone for each drug are as follows: chloroquine, 65 ng/ml; desipramine, 2,770 ng/ml; fluoxetine, 2,455 ng/ml; norfluoxetine, 1,045 ng/ml; and sertraline, 1,458 ng/ml. The drug IC50s determined for the chloroquine-sensitive clone HB3 are as follows: chloroquine, 10 ng/ml;. desipramine, 4,000 ng/ml; and sertraline, 1,590 ng/ml.In Table 1, we present the response modification index (RMI) for each monoamine reuptake inhibitor, which reflects modulation of susceptibility to chloroquine in the presence of one of the monoamine reuptake inhibitors at predetermined concentrations. The RMI for each monoamine reuptake inhibitor decreased as the concentration of psychotropic drug wa...

show abstract

“…The drug is chemically related to antidepressants (McNamara, 2001). In addition, the drug interacts with alpha adrenoceptors (Dilsaver et al, 1993;Mosqueda-Garcia, 1991) and decreases noradrenaline release (Purdy et al, 1977;Yoshimura et al, 1995). Some of the studies have shown that GABAergic systems are involved in the pharmacological property of carbamazepine (Waldmeier et al, 1995;Asahi & Yonehara, 2001).…”

mentioning

confidence: 98%

On the Mechanism of Carbamazepin-Induced Antinociception in the Formalin Test

Sahebgharani

Hossein-Abad

Zarrindast

2006

International Journal of Neuroscience

View full text Add to dashboard Cite

In the present study, the effect of lidocaine (a sodium channel blocker) on carbamazepine-induced antinociception, in formalin test was investigated. Intraperitoneal (i.p.) administration of different doses of carbamazepine (3.5, 7, 15, and 30 mg/kg) induced a dose-dependent antinociception in mice, in the first and second phases of the test. Different doses of lidocaine as a sodium channel blocker (5, 10, and 20 mg/kg, i.p.) also induced antinociception in both phases of the formalin test. It is noted that lidocaine could potentiate the response of carbamazepine in the first, but not in the second, phase of the formalin test. Meanwhile i.p. administration of different doses of Prazosin, alpha1 adrenoceptor antagonist (0.125, 0.25, and 0.5 mg/kg), Yohimbine, alpha2 adrenoceptor antagonist (0.25, 0.5, and 1 mg/kg), Bicuculline, GABAA receptor antagonist (1.5 and 3 mg/kg), and CGP 35348, GABAB receptor antagonist (100 and 200 mg/kg) exert dose-dependent antinociceptive effect in both phases of the formalin test. It should be noted that bicuculline 0.75 mg/kg by itself increased pain score in the second phase of the formalin test, indicating that blockade of GABAA receptor subtype may induce chronic pain. None of the aforementioned drugs could alter the antinociceptive response of carbamazepine in the formalin test. It is concluded that sodium channel mechanisms may be involved partly in the antinociceptive induced by carbamazepine.

show abstract

Effect of Carbamazepine on the In Vitro Uptake and Release of Norepinephrine in Adrenergic Nerves of Rabbit Aorta and in Whole Brain Synaptosomes

Cited by 63 publications

References 19 publications

Effect of Carbamazepine on Dopamine Release and Reuptake in Rat Striatal Slices

Effect of Carbamazepine on Dopamine Release and Reuptake in Rat Striatal Slices

Neuronal monoamine reuptake inhibitors enhance in vitro susceptibility to chloroquine in resistant Plasmodium falciparum

On the Mechanism of Carbamazepin-Induced Antinociception in the Formalin Test

Contact Info

Product

Resources

About