Carbamazepine increases extracellular serotonin concentration: lack of antagonism by tetrodotoxin or zero Ca2+

Dailey, John W.; Reith, Maarten E. A.; Yan, Qing‐Shan; Li, Ming-Ya; Jobe, Phillip C.

doi:10.1016/s0014-2999(97)83041-5

Cited by 76 publications

(25 citation statements)

References 26 publications

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“…If fluoxetine increases serotonin activity in D. magna (Campos et al, 2012a), then it is likely that by doing so also alters its response to light stimulus. The main target of carbamazepine in humans is blocking voltage dependant sodium channels (Ambrósio et al, 2002), but there is reported information indicating that carbamazepine also causes increases in extracellular serotonin levels (Dailey et al, 1997). There is also evidences that in mammals carbamazepine activates dopamine receptors (Montezinho et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Low environmental levels of neuro-active pharmaceuticals alter phototactic behaviour and reproduction in Daphnia magna

2016

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Section: Discussionmentioning

confidence: 99%

Low environmental levels of neuro-active pharmaceuticals alter phototactic behaviour and reproduction in Daphnia magna

2016

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“…Furthermore, using para-chlorophenylalanine to deplete brain 5-HT, it has been found that the fluoxetine + 5-HT receptor blocker combination lost most of its anticonvulsant activity [120]. In other studies, it has been shown that carbamazepine in GEPRs has antiepileptic effects as reflected by increasing 5-HT in the cerebral extracellular fluid [133,134]. Increments of 5-HT concentrations are linked to carbamazepine's anticonvulsant effects.…”

Section: Ars Scorementioning

confidence: 99%

Genetically epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic reflex epilepsy for the evaluation of new generation AEDs

Sarro¹,

Russo²,

Citraro³

et al. 2017

Epilepsy & Behavior

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“…Moreover, in rats receiving four times the ED dose of carba-50 mazepine against maximal electroshock seizure, the peak brain extracellular fluid concentration is approximately 11 Ž . mM Dailey et al, 1997 . However, the concentrations used in the present work were not different from the Ž concentrations reported previously Stefani et al, 1995;Dailey et al, 1997;Nonaka et al, 1998;Benes et al, .…”

Section: Neurotoxic Effect Caused By Antiepileptic Drugs In Cultured mentioning

confidence: 99%

“…mM Dailey et al, 1997 . However, the concentrations used in the present work were not different from the Ž concentrations reported previously Stefani et al, 1995;Dailey et al, 1997;Nonaka et al, 1998;Benes et al, . 1999a;Lingamaneni and Hemmings, 1999 .…”

Section: Neurotoxic Effect Caused By Antiepileptic Drugs In Cultured mentioning

confidence: 99%

Neurotoxic/neuroprotective profile of carbamazepine, oxcarbazepine and two new putative antiepileptic drugs, BIA 2-093 and BIA 2-024

Ambrósio

Silva

Araújo

et al. 2000

European Journal of Pharmacology

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We investigated and compared the toxicity profile, as well as possible neuroprotective effects, of some antiepileptic drugs in cultured Ž . Ž . w x rat hippocampal neurons. We used two novel carbamazepine derivatives, S -y -10-acetoxy-10,11-dihydro-5H-dibenz b,f azepine-5-Ž . w x Ž . carboxamide BIA 2-093 and 10,11-dihydro-10-hydroxyimino-5H-dibenz b,f azepine-5-carboxamide BIA 2-024 , and compared their effects with the established compounds carbamazepine and oxcarbazepine. The assessment of neuronal injury was made by using the Ž . Ž . 3-4,5-dimethylthiazol-2-yl -2,5-diphenyl MTT assay, as well as by analysing morphology and nuclear chromatin condensation Ž . propidium iodide staining , after hippocampal neurons were exposed to the drugs for 24 h. The putative antiepileptic drugs, BIA 2-093 or Ž . BIA 2-024 at 300 mM , only slightly decreased MTT reduction, whereas carbamazepine or oxcarbazepine were much more toxic at lower concentrations. Treatment with the antiepileptic drugs caused nuclear chromatin condensation in some neurons, which is characteristic of apoptosis, and increased the activity of caspase-3-like enzymes, mainly in neurons treated with carbamazepine and Ž . oxcarbazepine. The toxic effect caused by carbamazepine was not mediated by N-methyl-D-aspartate NMDA or by a-amino-3-hydroxy-Ž . 5-methyl-isoxazole-4-propionate AMPA receptors. Moreover, the antiepileptic drugs failed to protect hippocampal neurons from the toxicity caused by kainate, veratridine, or ischaemia-like conditions. q

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Carbamazepine increases extracellular serotonin concentration: lack of antagonism by tetrodotoxin or zero Ca2+

Cited by 76 publications

References 26 publications

Low environmental levels of neuro-active pharmaceuticals alter phototactic behaviour and reproduction in Daphnia magna

Low environmental levels of neuro-active pharmaceuticals alter phototactic behaviour and reproduction in Daphnia magna

Genetically epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic reflex epilepsy for the evaluation of new generation AEDs

Neurotoxic/neuroprotective profile of carbamazepine, oxcarbazepine and two new putative antiepileptic drugs, BIA 2-093 and BIA 2-024

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