Extracellular serotonin and 5-hydroxyindoleacetic acid in hypothalamus of the unanesthetized rat measured by in vivo dialysis coupled to high-performance liquid chromatography with electrochemical detection: dialysate serotonin reflects neuronal release

Auerbach, Sidney B.; Minzenberg, Michael; Wilkinson, Lynn O.

doi:10.1016/0006-8993(89)90776-2

Cited by 185 publications

(91 citation statements)

References 19 publications

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“…Increased firing seems reasonable as high cortical dialysate 5-HT and low 5-HIAA values also occur on both handling (Kalen et al, 1989) and stimulation with K+ ( Figure 2). The latter finding agrees with previous dialysis studies (Kalen et al, 1988;Auerbach et al, 1989;Carboni & DiChiara, 1989). It is relevant that transport of 5-HIAA from neurones has been suggested to be impaired during the depolarized state which occurs when 5-HT is actively released (Miyamoto et al, 1990).…”

Section: Discussionsupporting

confidence: 92%

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Effect of p‐chlorophenylalanine on release of 5‐hydroxytryptamine from the rat frontal cortex in vivo

O’Connell

Portas

Sarna

et al. 1991

British J Pharmacology

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1 Rats were given p-chlorophenylalanine (PCPA, 150mgkg-1, i.p.) to inhibit partially 5-hydroxytryptamine (5-HT) synthesis so that its concentration in the frontal cortex fell by about half. The effects of this treatment on frontal cortex dialysate 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were determined before and after stimulation by increasing K+ concentration in the perfusion fluid by 100 mm for 20 min. Rates of 5-HT synthesis as indicated by the effects of 3-hydroxybenzylhydrazine (NSD 1015, 150mg kg-, i.p.) on frontal cortex tissue and dialysate 5-hydroxytryptophan (5-HTP) and dialysate 5-HIAA were also measured in rats that had not been stimulated with K+. 2 Dialysate 5-HT and 5-HIAA concentrations of both vehicle-and PCPA-treated rats fell into major (group 1) and minor (group 2) populations statistically distinguishable from each other by the high 5-HT and low 5-HIAA values of the latter group. 3 In group 1 animals, PCPA decreased both the dialysate 5-HT concentration and its rise following stimulation by K+ in proportion with the decrease of 5-HT in frontal cortex tissue. 5-HIAA fell more markedly than 5-HT and in similar proportion in both tissue and dialysate. The fall of dialysate 5-HIAA on stimulation by K+ was also attenuated to the same degree. The elevated 5-HT/5-HIAA ratios after PCPA treatment imply increased conservation of the depleted 5-HT stores. 4 PCPA decreased the above 5-HIAA values and the effects of NSD 1015 on tissue 5-HTP or dialysate 5-HIAA concentrations in similar proportion. However, PCPA had little effect on corresponding dialysate 5-HTP values. 5 The results are discussed with respect to relationships between synthesis, storage and release of 5-HT. They indicate that (under the conditions of the present study) the availability of 5-HT to receptors is directly proportional to total vesicular stores under both basal conditions and during neuronal firing.

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Section: Discussionsupporting

confidence: 92%

“…Recent investigations on 5-hydroxytryptamine (5-HT) by Auerbach et al (1989), Kalen et al (1988) and Carboni & DiChiara (1989) show that various drug treatments influence dialysate 5-HT levels in the expected direction. Other studies reveal that levels rise during motor activity or handling (Kalen et al, 1989).…”

Section: Introduction Methodsmentioning

confidence: 99%

Effect of p‐chlorophenylalanine on release of 5‐hydroxytryptamine from the rat frontal cortex in vivo

O’Connell

Portas

Sarna

et al. 1991

British J Pharmacology

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“…One of our initial predictions was that fenfluramine would deplete serotonin stores during continual application, because fenfluramine causes a peak and subsequent decline in serotonin levels over the course of tens of minutes to several hours when administered systemically (Auerbach et al 1989;Carboni and Di Chiara 1989;LaFerrere and Wurtman 1989;Rothman et al 1999;Tao et al 2002;Rothman et al 2003), and more rapidly when administered locally (Schwartz et al 1989). Refuting this prediction, the effects of fenfluramine did not decay appreciably over the course of several minutes.…”

Section: Fenfluramine and Serotonin Effects Are Similarmentioning

confidence: 92%

The serotonin releaser fenfluramine alters the auditory responses of inferior colliculus neurons

Hall

Hurley

2007

Hearing Research

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Local direct application of the neuromodulator serotonin strongly influences auditory response properties of neurons in the inferior colliculus (IC), but endogenous stores of serotonin may be released in a distinct spatial or temporal pattern. To explore this issue, the serotonin releaser fenfluramine was iontophoretically applied to extracellularly recorded neurons in the IC of the Mexican free-tailed bat (Tadarida brasiliensis). Fenfluramine mimicked the effects of serotonin on spike count and first spike latency in most neurons, and its effects could be blocked by co-application of serotonin receptor antagonists, consistent with fenfluramine-evoked serotonin release. Responses to fenfluramine did not vary during single applications or across multiple applications, suggesting that fenfluramine did not deplete serotonin stores. A predicted gradient in the effects of fenfluramine with serotonin fiber density was not observed, but neurons with fenfluramine-evoked increases in latency occurred at relatively greater recording depths compared to other neurons with similar characteristic frequencies. These findings support the conclusion that there may be spatial differences in the effects of exogenous and endogenous sources of serotonin, but that other factors such as the identities and locations of serotonin receptors are also likely to play a role in determining the dynamics of serotonergic effects.

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“…To test this possibility further, extracellular hippocampal levels of 5-HT were reduced by peripheral injection of the 5-HTlA receptor agonist, 8-OH-DPAT. This compound stimulates the somatodendritic 5-HT autoreceptor in the raphe nuclei to reduce terminal release of 5-HT in the forebrain (Maidment et al, 1986;Auerbach et al, 1989;Hutson et al, 1989;Sharp et al, 1989). The ability of renzapride still to enhance extracellular hippocampal 5-HT levels, which had been reduced beforehand with 8-OH-DPAT, suggests that the prevention of the renzapride-induced response by GRI 13808 was due to pharmacological antagonism of the 5-HT4 receptor.…”

Section: Gr125487dmentioning

confidence: 99%

5‐HT₄ receptor‐mediated modulation of 5‐HT release in the rat hippocampus in vivo

Jin

Barnes

1996

British J Pharmacology

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1 In the present study, the ability of the 5-hydroxytryptamine4 receptor (5-HT4 receptor) to modulate the release of 5-HT in the hippocampus of freely-moving rats was investigated by the in vivo microdialysis technique. 2 The 5-HT4 receptor agonist, renzapride (1.0-100 gIM, administered via the microdialysis probe) increased extracellular hippocampal levels of 5-HT in a concentration-dependent manner (approximately 200% maximal increase). The ability of renzapride (100 Mm, administered via the microdialysis probe) to elevate extracellular levels of 5-HT remained in the presence of the selective 5-HT reuptake blocker, paroxetine (1.0 gM, administered via the microdialysis probe). Furthermore, another 5-HT4 receptor agonist 5-methoxytryptamine (5-MeOT; 10 gM, administered via the microdialysis probe, in the presence of the non-5-HT4 5-HT receptor antagonists pindolol (10 gM) and methysergide (10 gM)) maximally elevated extracellular levels of 5-HT by approximately 450% in the rat hippocampus. The elevation of extracellular 5-HT levels induced by either renzapride (100 gM) or 5-MeOT (10 gM) was completely prevented by combined administration of the selective 5-HT4 receptor antagonist, GRI13808 (100 nM, administered via the microdialysis probe). GRI13808 (100 nM, administered via the microdialysis probe) administered alone, however, reduced extracellular hippocampal 5-HT levels by some 60%. In conclusion, the present study provides evidence that activation of the 5-HT4 receptor facilitates 5-HT release in the rat hippocampus in vivo.

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Extracellular serotonin and 5-hydroxyindoleacetic acid in hypothalamus of the unanesthetized rat measured by in vivo dialysis coupled to high-performance liquid chromatography with electrochemical detection: dialysate serotonin reflects neuronal release

Cited by 185 publications

References 19 publications

Effect of p‐chlorophenylalanine on release of 5‐hydroxytryptamine from the rat frontal cortex in vivo

Effect of p‐chlorophenylalanine on release of 5‐hydroxytryptamine from the rat frontal cortex in vivo

The serotonin releaser fenfluramine alters the auditory responses of inferior colliculus neurons

5‐HT₄ receptor‐mediated modulation of 5‐HT release in the rat hippocampus in vivo

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Extracellular serotonin and 5-hydroxyindoleacetic acid in hypothalamus of the unanesthetized rat measured by in vivo dialysis coupled to high-performance liquid chromatography with electrochemical detection: dialysate serotonin reflects neuronal release

Cited by 185 publications

References 19 publications

Effect of p‐chlorophenylalanine on release of 5‐hydroxytryptamine from the rat frontal cortex in vivo

Effect of p‐chlorophenylalanine on release of 5‐hydroxytryptamine from the rat frontal cortex in vivo

The serotonin releaser fenfluramine alters the auditory responses of inferior colliculus neurons

5‐HT4 receptor‐mediated modulation of 5‐HT release in the rat hippocampus in vivo

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5‐HT₄ receptor‐mediated modulation of 5‐HT release in the rat hippocampus in vivo