Fluoxetine attenuates the dl-fenfluramine-induced increase in extracellular serotonin as measured by in vivo dialysis

Sabol, Karen E.; Richards, Jerry B.; Seiden, Lewis S.

doi:10.1016/0006-8993(92)91249-e

Cited by 60 publications

(41 citation statements)

References 23 publications

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“…As expected (Sabol et al 1992b;Rutter and Auerbach, 1993), a high dose of the serotonin reuptake inhibitor (SRI) citalopram also caused increased extracellular concentrations of serotonin in the hippocampus; however, this effect was less pronounced than that of mCPP.…”

Section: Discussionsupporting

confidence: 54%

Effects of mCPP on the Extracellular Concentrations of Serotonin and Dopamine in Rat Brain

Eriksson

Engberg²,

Bing³

et al. 1999

Neuropsychopharmacology

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Intravenous administration of m-chloro-phenylpiperazine (mCPP) (0.25 or 2.5 mg/kg) induced a marked and doserelated increase in extracellular concentrations of serotonin in hippocampus (300-1,400% of baseline) as measured using in vivo microdialysis in awake male Wistar rats of the spontaneously hypertensive (SH) strain. Indicating that the effect of mCPP was caused by a reversal of the serotonin transporter, it was antagonized by pretreatment with the serotonin re-uptake inhibitor citalopram (10 mg/kg) but was unaffected by local administration of the sodium channel blocker tetrodotoxin (TTX; 1 m). mCPP was also shown to induce an increase in extracellular concentrations of dopamine in the nucleus accumbens and the striatum of SH rats and in the nucleus accumbens of rats of the Sprague-Dawley (SD) Dopamine, In vivo microdialysis; Hippocampus; Striatum, Nucleus accumbens; Citalopram; Rat m-Chloro-phenylpiperazine (mCPP), the metabolite of the antidepressant drug trazodone, has recently gained marked attention as a putative probe of serotonergic function in clinical psychiatric research. Thus, the prolactin, ACTH, and cortisol responses to mCPP frequently have been used as putative markers of postsynaptic serotonin receptor function in various psychiatric disorders. Moreover, administration of mCPP has been shown to elicit, and/or aggravate, anxiety attacks in patients with panic disorder, obsessions in patients with obsessive compulsive disorder (OCD), elation in alcoholics and cocaine addicts, and positive symptoms in schizophrenic patients (see Murphy et al. 1991;Kahn and Wetzler 1991;Krystal et al. 1993;Buydens-Branchey et al. 1993;Krystal et al. 1994).mCPP displays high affinity to 5-HT2C receptors and moderate, or low, affinity to 5-HT1A, 5-HT1B, 5-HT2A, 5-HT2B, and 5-HT3 receptors; in addition, the compound has some affinity for alpha-2-adrenoceptors. At the 5-HT2C receptor, mCPP seems to act as a partial agonist with relatively high intrinsic efficacy, whereas, at the other serotonin receptors, the intrinsic efficacy of mCPP is moderate or low (see Murphy et al. 1991 NO . 3 and Wetzler 1991). The behavioral and endocrine effects of mCPP observed in clinical studies are generally attributed to the direct effects of mCPP on various subtypes of serotonin receptors; in contrast, little attention has been paid to the report by Baumann et al. (1993) suggesting that mCPP may also stimulate serotonin release by means of an interaction with the serotonin transporter (see also Baumann et al. 1995).To further elucidate the possible influence of mCPP on the release of serotonin, we studied the effects of a high dose of mCPP on extracellular, hippocampal concentrations of serotonin in awake, freely moving rats using in vivo microdialysis.Enhanced dopaminergic neurotransmission has been suggested as a mechanism of importance both for the positive symptoms of schizophrenia and for the euphoria induced by such central stimulants as cocaine. The observations that mCPP may aggravate psychotic symptoms in schizophr...

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Section: Discussionsupporting

confidence: 54%

Effects of mCPP on the Extracellular Concentrations of Serotonin and Dopamine in Rat Brain

Eriksson

Engberg²,

Bing³

et al. 1999

Neuropsychopharmacology

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“…Our results agree with those of others (Wolf and Kuhn 1991) and show the selectivity of dFEN and mCPP for SERT sites relative to DAT sites. Interestingly, mCPP is much more potent than dFEN at inhibiting binding to rat SERTs la- (Fuxe et al 1975;Garattini et al 1975;Berger et al 1992) Yes (Pettibone and Williams 1984;Wolf and Kuhn 1991) Large but transient elevations of extracellular 5-HT in vivo Yes (present study; Schwartz et al 1989;Series et al 1994) Yes (present study; Baumann et al 1993;Eriksson et al 1999) Tetrodotoxin-insensitive elevations of extracellular 5-HT in vivo Yes (Carboni and DiChiara 1989) Yes (Eriksson et al 1999) SSRI-reversible elevations of extracellular 5-HT in vivo Yes (Sabol et al 1992;Gundlah et al 1997) Yes (Baumann et al 1993;Eriksson et al 1999) FEN, dFEN, and mCPP release endogenous 5-HT from neurons by a similar mechanism involving SERTs. FEN and dFEN cause long-term depletion of tissue 5-HT in the brain whereas mCPP does not.…”

Section: Discussionmentioning

confidence: 68%

“…SERTs play a pivotal role in the release process because they serve as 'gateways' for the flow of drug molecules into the cell in exchange for 5-HT molecules that flow out (Levi and Raiteri 1993;Rudnick 1997). Interestingly, 5-HT-selective reuptake inhibitors (SSRIs) such as fluoxetine are known to prevent acute 5-HT release and long-term 5-HT depletion produced by FEN administration (Clineschmidt et al 1978;Steranka and Sanders-Bush 1979;Sabol et al 1992).…”

mentioning

confidence: 99%

“…Based on the information discussed above, investigators have speculated that FEN-induced 5-HT release might somehow be involved in mediating the longterm 5-HT deficits seen after high doses of the drug (Berger et al 1992;Sabol et al 1992). For example, there is evidence that drug-induced release of 5-HT can lead to the formation of reactive 5-HT metabolites, such as 5,6-dihydroxytryptamine (5,6-DHT), that cause cellular damage (Commins et al 1987;Seiden and Sabol 1996).…”

mentioning

confidence: 99%

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1-(m-Chlorophenyl)piperazine (mCPP) Dissociates In Vivo Serotonin Release from Long-Term Serotonin Depletion in Rat Brain

Baumann

Ayestas

Dersch

et al. 2001

Neuropsychopharmacology

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“…The most common pharmacological treatment for depression is selective serotonin reuptake inhibitors (SSRIs), which can acutely increasing synaptic serotonin levels throughout the brain, including within the medial prefrontal cortex (Beyer and Cremers, 2008) and the hippocampus (Sabol et al, 1992). To determine whether serotonin increases influence VH-IL coherence, we recorded from the same rats that had received DBS or sham treatments after they had been injected with the SSRI fluoxetine (n = 15) and, during a separate session, injected with saline (n = 7).…”

Section: Effects Of Fluoxetine On Vh-il Coherencementioning

confidence: 99%

Chronic deep brain stimulation of the rat ventral medial prefrontal cortex disrupts hippocampal–prefrontal coherence

Insel

Pilkiw

Nóbrega

et al. 2015

Experimental Neurology

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Deep brain stimulation (DBS) of the subgenual cingulate gyrus (SCG) has been used to treat patients with treatment-resistant depression. As in humans, DBS applied to the ventromedial prefrontal cortex of rats induces antidepressant-like responses. Physiological interactions between structures that play a role in depression and antidepressant treatment are still unknown. The present study examined the effect of DBS on inter-region communication by measuring the coherence of local field potentials in the rat infralimbic cortex (IL; homologue of the SCG) and one of its major afferents, the ventral hippocampus (VH). Rats received daily IL DBS treatment (100 μA, 90 μs, 130 Hz; 8 h/day). Recordings were conducted in unrestrained, behaving animals on the day before treatment, after 1 and 10 days of treatment, and 10 days stimulation offset. VH-IL coherence in the 2-4 Hz range was reduced in DBS-treated animals compared with shams after 10 days, but not after only 1 day of treatment. No effect of DBS was observed in the 6-10 Hz (theta) range, where coherence was generally high and could be further evoked with a loud auditory stimulus. Finally, coherence was not affected by fluoxetine (10 mg/kg), suggesting that the effects of DBS were not likely mediated by increased serotonin levels. While these data support the hypothesis that DBS disrupts communication between regions important for expectation-based control of emotion, they also suggest that lasting physiological effects require many days of treatment and, furthermore, may be specific to lower-frequency patterns, the nature and scope of which await further investigation.☆ NI, MP and CH designed the experiments; NI and MP performed the experiments; NI analyzed the data; NI, JN, WDH, KT, and CH wrote the paper.

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Fluoxetine attenuates the dl-fenfluramine-induced increase in extracellular serotonin as measured by in vivo dialysis

Cited by 60 publications

References 23 publications

Effects of mCPP on the Extracellular Concentrations of Serotonin and Dopamine in Rat Brain

Effects of mCPP on the Extracellular Concentrations of Serotonin and Dopamine in Rat Brain

1-(m-Chlorophenyl)piperazine (mCPP) Dissociates In Vivo Serotonin Release from Long-Term Serotonin Depletion in Rat Brain

Chronic deep brain stimulation of the rat ventral medial prefrontal cortex disrupts hippocampal–prefrontal coherence

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