Voltammetric measurements of 5-hydroxyindole compounds in the suprachiasmatic nuclei: Circadian fluctuations

Faradji, H.; Cespuglio, Raymond; Jouvet, Michel

doi:10.1016/0006-8993(83)90168-3

Cited by 84 publications

(36 citation statements)

References 30 publications

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“…As shown previously by ourselves (Martin & Marsden, 1986) and other workers (Faradji et al, 1983) an increase in the height of peak 3 occurred as the carbon fibre working electrode was lowered towards the SCN. However, once the electrode entered the nucleus the magnitude of peak 3 decreased (Figure 1).…”

Section: Resultssupporting

confidence: 82%

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Involvement of 5‐HT_1A‐ and α₂‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Marsden

Martin

1986

British J Pharmacology

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1 The 5-hydroxytryptamine1A-receptor agonist 8-hydroxy-2-(n-dipropylamino) tetralin (8-OH-DPAT, 0.1 mg kg-' i.v.) decreased the height of the extracellular 5-hydroxyindoleacetic acid (5-HIAA) oxidation peak recorded in the suprachiasmatic nucleus (SCN) of the anaesthetized rat by use of differential pulse voltammetry. -2 The decrease in extracellular 5-HIAA produced by 8-OH-DPAT could be partially attenuated by prior administration of the non-selective 5-HT receptor antagonist methiothepin (1 mg kg-i.v.). The 5-HT2-receptor antagonist ritanserin (0.2 mg kg-' i.v.) did not appear to block the effects of 8-OH-DPAT.3 The selective ligand for 5-HTIA recognition sites TVX Q 7821 (isapirone, 1 mg kg-' i.v.) decreased the extracellular level of 5-HIAA in the SCN but to a lesser extent than 8-OH-DPAT. The response to 8-OH-DPAT was attenuated by prior administration of TVX Q 7821 to a level suggesting that TVX Q 7821 had blocked the effect of intravenous 8-OH-DPAT. 4 Idazoxan (0.2mg kg-i.v.) an X2-adrenoceptor antagonist, completely blocked the effect of 8-OH-DPAT on the 5-HIAA oxidation peak recorded in the SCN, whilst having no effect on the 5-HIAA oxidation peak when given alone. 5 At a dose of 0.5mg kg-' i.v. idazoxan induced a 120% increase in the height ofthe indole oxidation peak, suggesting that 5-HT release and metabolism in the rat SCN may be influenced by tonic adrenergic inputs. 6 The data in this paper suggest that 5-HTIA-and a2-receptors are involved in the effects of i.v. administered 8-OH-DPAT on 5-HT release and metabolism in the SCN in vivo.

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Section: Resultssupporting

confidence: 82%

“…The working electrodes used in this study were similar to those used in previous studies (Ponchon et al, 1979;Maidment & Marsden, 1985 (Crespi et al, 1983;Faradji et al, 1983;Sharp et al, 1984). In common with other studies using similar carbon fibre electrodes, we have termed this oxidation peak, 'peak 3'.…”

Section: Electrode Preparationmentioning

confidence: 76%

Involvement of 5‐HT_1A‐ and α₂‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Marsden

Martin

1986

British J Pharmacology

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“…These data agree with previous reports (19,22). A specificity for GAERS rats is, however, indicated by the tight opposition existing in the occurrence of PS and SWDs.…”

Section: Discussionsupporting

confidence: 93%

Sleep and Epilepsy: A Key Role for Nitric Oxide?

Faradji¹,

Rousset²,

Debilly³

et al. 2000

Epilepsia

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Summary:Purpose: It has been suggested that nitric oxide (NO) is involved in sleep mechanisms and in the pathophysiology of epilepsy. Data are, however, controversial because it is not clear whether NO facilitates sleep or waking, or whether it exerts pro-or antiepileptic influences.Methods: The question was considered through NO voltammetric measurements and electroencephalographic recordings performed in GAERS rats (Genetic Absence Epilepsy Rat from Strasbourg): an experimental model of "petit-mal" human disease. Regulatory processes of sleep and epilepsy were studied after administration of a NO synthase inhibitor LL-arginine-pnitroanilide (L-ANA) 100 mg/kg i.p.1, a NO donor (SIN-] 100 ng/2 pl i.c.v.), and the antiepileptic drugs used in clinic [valproate (VPA 200 mg/kg i.p.) and ethosuximide (ESM 100 mg/ kg i.p.)I.Results: In GAERS rats, spontaneous circadian organizations of spike-wave discharges and paradoxical sleep (PS) occur in an opposite way; spontaneous NO concentrations are higher during seizures than during wakefulness, slow-wave sleep, and PS, respectively. L-ANA induces a disappearance of NO peak, an epileptic induction, and a loss of PS while SIN-I induces opposite effects. Antiepileptic effects of VPA and ESM are associated with a PS increase and a significant release of NO.Conclusions: These results indicate that NO could be, in GAERS rats, a central piece in the reciprocal inhibitory mechanisms regulating the induction of PS and spike-wave discharges. NO could prevent absence epilepsy and act as an antiepileptic substance in facilitating PS. Antiepileptic efficiency of VPA and ESM may work through their ability to release NO. A track for a new treatment of petit-ma1 disease in children can be envisioned. Key Words: GAERS ratElectroencephalography-Voltammetry-NO sensorAntiepileptic drugs.Nitric oxide (NO) is a gaseous compound produced in brain neuronal elements equimolarly with citrulline and through biochemical processes involving calmodulin/ Ca2+-dependent NO synthase (NOS) (1,2). NO is involved in various physiological and pathological processes, including regulation of the sleep-wake cycle (3-9) and the electroencephalographic manifestation of epilepsy (10-14). Data reported with respect to sleep, wakefulness (W), and epilepsy are controversial because it is not clear whether NO is associated with the maintenance of sleep or wakefulness, whether it acts as a proor an antiepileptic substance (convulsions or absence seizures). Contrasting conclusions relate both to absence seizures (12) and convulsive phenomena elicited either by electrical stimulation (13) For clarification, we used the animal model of GAERS rats (Genetic Absence Epilepsy Rat from Strasbourg) (15), known to exhibit spontaneous seizures characterized by the occurrence of spike-wave discharges (SWDs). These SWDs are phenomena prevalent in cortical and thalamic structures (16) occurring, at least partly, through GABAergic (17) and glutamatergic processes (18). For our purpose, we analyzed in GAERS rats the part played by NO ...

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“…After incubation of SCA taken from males or OVX, the levels of 5-HT and 5-HIAA measured in the corresponding medium increased, reflecting an increase in 5-HT release induced by the stimulation of GABA transmission. Indeed, as we have already discussed (3) and as has been shown by different studies (23)(24)(25), the increase in 5-HIAA in the medium reflected an increase in 5-HT release, rather than the metabolism of an excess of stored 5-HT which was metabolized without being released. In the SCA of males and OVX, the increase in 5-HT release was accompanied by an increase in 5-HT synthesis.…”

Section: Discussionsupporting

confidence: 66%

Analysis of the Inhibitory Effect of Oestradiol on Functional GABA/5‐HT Relationship in the Rat Suprachiasmatic Area

François‐Bellan¹,

Héry²,

Faudon³

et al. 1989

J Neuroendocrinology

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The purpose of this study was to test the capacity of oestradiol to modulate the stimulating effect of a-aminobutyric acid (GABA) on serotonin (5-HT) metabolism, previously described in the suprachiasmatic area of the male rat. After an in vivo stimulation of GABA transmission by systemic administration of a GABA-transaminase inhibitor (amino-oxyacetic acid) or a GABA, agonist (RS-baclofen), the 5-HT metabolism was studied in the suprachiasmatic area of ovariectomized, and ovariectomized oestradiol-treated rats.Amino-oxyacetic acid or RS-baclofen treatment increased the endogenous content of 5-HT in the suprachiasmatic area of males and ovariectomized rats. These two treatments were without effect in ovariectomized oestradiol-treated rats. GABA transmission stimulation induced by amino-oxyacetic acid treatment failed to affect the release and synthesis of 5-HT in ovariectomized oestradiol-treated rats while it increased these two parameters of 5-HT metabolism in the suprachiasmatic area of male and ovariectomized rats. To investigate the main target of oestradiol effect, comparative studies of the serotoninergic and GABAergic metabolism in the suprachiasmatic area were performed in the three experimental groups. Under our experimental conditions the endogenous 5-HT metabolism was similar between ovariectornized and ovariectomized oestradiol-treated rats. Nevertheless, 5-HT metabolism was higher in the two female groups than in the male group. Neither GABA metabolism nor GABAergic response to GABA-related drug treatment differed between ovariectomized, and ovariectomized oestradiol-treated rats. However, the turnover of GABA was higher when compared to the two female groups. It is concluded that the lack of 5-HT responsiveness to GABA transmission stimulation in ovariectomized oestradiol-treated rats was not related to an effect of oestradiol on 5-HT metabolism or to an effect of the steroid on GABA turnover. Furthermore, our results suggest a sex difference in the activity of serotoninergic and GABAergic systems in the suprachiasmatic area.Recently, an anatomical relationship between GABAergic and szrotoninergic terminals in the suprachiasmatic nucleus (SCN) has been reported (1). Parallel to previous reports we have shown the existence of a metabolic interaction between these two neurotransmitters. The stimulation of y-aminobutyric acid (GABA) transmission leads to an increase in serotonin (5-HT) metabolism la GABA, receptor activation in the rat's suprachiasmatic area (SCA) (2, 3). The ability of oestradiol (E,) to influence neurotransmission has long been recognized. There are numerous (4-6) examples of mechanisms by which E, may act on neurotransmitter systems. These include the modulation of neurotransmitter metabolism and effects on neurotransmitter receptor concentrations. Data concerning the effects of the steroid on 5-HT and GABA metabolism in the hypothalamus are conflicting. While some authors report that E, administration to ovariectomized animals (OVX) results in no change in 5-HT content of...

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Voltammetric measurements of 5-hydroxyindole compounds in the suprachiasmatic nuclei: Circadian fluctuations

Cited by 84 publications

References 30 publications

Involvement of 5‐HT_1A‐ and α₂‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Involvement of 5‐HT_1A‐ and α₂‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Sleep and Epilepsy: A Key Role for Nitric Oxide?

Analysis of the Inhibitory Effect of Oestradiol on Functional GABA/5‐HT Relationship in the Rat Suprachiasmatic Area

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Voltammetric measurements of 5-hydroxyindole compounds in the suprachiasmatic nuclei: Circadian fluctuations

Cited by 84 publications

References 30 publications

Involvement of 5‐HT1A‐ and α2‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Involvement of 5‐HT1A‐ and α2‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Sleep and Epilepsy: A Key Role for Nitric Oxide?

Analysis of the Inhibitory Effect of Oestradiol on Functional GABA/5‐HT Relationship in the Rat Suprachiasmatic Area

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Involvement of 5‐HT_1A‐ and α₂‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin

Involvement of 5‐HT_1A‐ and α₂‐receptors in the decreased 5‐hydroxytryptamine release and metabolism in rat suprachiasmatic nucleus after intravenous 8‐hydroxy‐2‐ (n‐dipropylamino) tetralin