Effect of fluoxetine on the spontaneous electrical activity of fronto-cortical neurons

Ceci, Angelo; Baschirotto, A.; Borsini, Franco

doi:10.1016/0014-2999(93)90034-f

Cited by 13 publications

(6 citation statements)

References 12 publications

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“…Therefore, the observation of l of NMDA and WAY 100135. The observa- Ceci et al (1993) that peripherally administered fluoxetine intrflow of the two amino acids was sensitive to creased overall cortical activity in the rat was unexpected. s that the phenomenon observed is due to re-However, the authors explain this by citing a microdialysis inals of pyramidal neurones by exocytosis ra-study where fluoxetine preferentially increased 5-HT con-:oplasmic release or decreased reuptake.…”

Section: Discussionmentioning

confidence: 99%

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT_1A antagonist

Dijk¹,

Francis²,

Stratmann³

et al. 1995

British J Pharmacology

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1 We have investigated an aspect of the regulation of cortical pyramidal neurone activity. Microdialysis was used to assess whether topical application of drugs (in 10 M1) to fill a burr hole over the frontal cortex, where part of the corticostriatal pathway originates, would change concentrations of the excitatory amino acids glutamate and aspartate in the striatum of the anaesthetized rat. 2 Topical application of N-methyl-D-aspartate (NMDA, 2 and 20 mM) dose-dependently increased glutamate and aspartate concentrations in the striatum. Coapplication of tetrodotoxin (10 ,uM) blocked the NMDA-evoked rise in these amino acids. A calcium-free medium, perfused through the probe also blocked the rise, indicating that it was due to an exocytotic mechanism in the striatum. 3 It was hypothesized that the rise observed was due to an increase in the activity of the corticostriatal pathway. As 5-hydroxytryptaminelA (5-HTIA) receptors are enriched on cell bodies of corticostriatal neurones, a selective 5-HTIA-antagonist (WAY 100135)

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Section: Discussionmentioning

confidence: 99%

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT_1A antagonist

Dijk¹,

Francis²,

Stratmann³

et al. 1995

British J Pharmacology

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“…In fact, it should be pointed out that 8-OH-DPAT and buspirone do not behave as agonists in the frontal cortex (Borsini et al 1995b). Single doses of 8-OH-DPAT and buspirone (Borsini et al 1995a), imipramine (Ceci et al 1992) or fluoxetine (Ceci et al 1993) increase the firing rate of frontocortical neurons, whereas BIMT 17 decreases the firing rate by activating 5-HT 1A receptors (Borsini et al 1995a). In addition, BIMT 17 has a direct action on postsynaptic 5-HT receptors (Borsini et al 1995a;Cesana et al 1995), whereas all the other compounds referred to seem to activate presynaptic 5-HT mechanisms.…”

Section: Drl 72-smentioning

confidence: 94%

BIMT 17: a putative antidepressant with a fast onset of action?

et al. 1997

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BIMT 17, the only compound reported to be a full 5-HT1A agonist and a 5-HT2A antagonist at the frontal cortex, was assessed in three animal paradigms sensitive to antidepressants in rats: olfactory bulbectomy (OB), differential-reinforcement-of-low rate 72-s (DRL 72-s) and learned helplessness (LH). In the OB rats, BIMT 17, given once daily for 14 consecutive days at an i.p. dose of 10 mg/kg, but not of 20 mg/kg, reduced the increase in ambulation of OB rats, 24 h after the last administration. In the DRL 72-s test, BIMT 17 had a different profile than imipramine. A single i.p. injection of 5, 10, 15 or 20 mg/kg BIMT 17, in contrast to the same doses of imipramine, did not affect response and reinforcement rate in DRL 72-s 1 h after the administration. On the other hand, BIMT 17 slightly shifted the peak of the interresponse time (IRT) distribution towards shorter IRT duration, while imipramine shifted the peak of the IRT distribution towards longer IRT duration. In the LH test, acute oral doses (36, 48 or 60 mg/kg) of BIMT 17, given 30 min before testing, reduced the number of escape failures in LH without altering the intertrial crossings. This effect was also induced by a repeated, but not single, administration with 8 or 16 mg/kg imipramine. The plasma levels following i.p. 10 or oral 48 mg/kg BIMT 17 were in the same range. These results indicate that BIMT 17 does not behave like imipramine in all the tests, and suggest that BIMT 17 acts through different mechanisms of action than imipramine. Only clinical trials will tell whether these mechanisms will be relevant, but if so, BIMT 17 might induce a faster onset of therapeutic activity.

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“…For instance, depletion of forebrain serotonin by approximately 92 %, via 5,7-DHT injections into the medial forebrain bundle, prevented the reduction in amphetamine-self administration induced by ßuoxetine pretreatment (Leccese and Lyness 1984). Similarly, 5-HT depletion has been shown to abolish the reduction in VTA-DAergic activity induced by ßuoxetine (Prisco and Esposito 1995), to antagonize ßuoxetine-induced increases in basal Þring rate of cortical neurons (Ceci et al 1993), and to prevent the ßuoxetine-induced decrease in K + -evoked norepinephrine release in the hippocampus (Matsumoto et al 1995).…”

Section: Discussionmentioning

confidence: 93%

The potentiating effect of sertraline and fluoxetine on amphetamine-induced locomotor activity is not mediated by serotonin

et al. 1999

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Sertraline dose-dependently increased the locomotor stimulating effect of amphetamine. At the highest dose, 20 mg/kg sertraline had a biphasic effect on amphetamine-induced hyperactivity, producing an initial reduction in amphetamine-induced hyperactivity that was later followed by an augmentation of amphetamine-induced hyperactivity in the last hour of the 3-h test. Sertraline, at doses of 5 and 10 mg/kg, produced an augmentation of amphetamine-induced hyperactivity over the last 2 h of the 3-h test session. Further, there was an increase in the concentration of amphetamine in the brain in rats pretreated with 5 mg/kg sertraline. Both sertraline (5 mg/kg) and fluoxetine (5 mg/kg) produced an augmentation of amphetamine-induced hyperactivity that was unaltered by a serotonergic lesion of the median and dorsal raphe nuclei that resulted in a greater than 90% depletion of serotonin in hippocampus, striatum, and nucleus accumbens. Further, both sertraline and fluoxetine inhibited spontaneous locomotor activity and this effect was also unaltered by the depletion of serotonin. Thus, serotonergic neurotransmission is not essential for the effects of sertraline and fluoxetine on spontaneous and amphetamine-induced locomotion. It is probable that sertraline and fluoxetine augment the locomotor stimulatory effect of amphetamine by decreasing the metabolism of amphetamine, perhaps via actions on cytochrome P450 isozymes.

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Effect of fluoxetine on the spontaneous electrical activity of fronto-cortical neurons

Cited by 13 publications

References 12 publications

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT_1A antagonist

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT_1A antagonist

BIMT 17: a putative antidepressant with a fast onset of action?

The potentiating effect of sertraline and fluoxetine on amphetamine-induced locomotor activity is not mediated by serotonin

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Effect of fluoxetine on the spontaneous electrical activity of fronto-cortical neurons

Cited by 13 publications

References 12 publications

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT1A antagonist

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT1A antagonist

BIMT 17: a putative antidepressant with a fast onset of action?

The potentiating effect of sertraline and fluoxetine on amphetamine-induced locomotor activity is not mediated by serotonin

Contact Info

Product

Resources

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NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT_1A antagonist

NMDA‐induced glutamate and aspartate release from rat cortical pyramidal neurones: evidence for modulation by a 5‐HT_1A antagonist