Localization and Dynamic Regulation of Biogenic Amine Transporters in the Mammalian Central Nervous System

Hoffman, Beth J.; Hansson, Stefan R.; Mezey, Éva; Palkovits, Miklós

doi:10.1006/frne.1998.0168

Cited by 217 publications

(147 citation statements)

References 177 publications

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“…These studies proved RBL-2H3 cells as an ideal model for studying the SERT. In addition, SERT is also widely expressed in the front cortexes of the brain and the hippocampus which are closely associated with the pathogenesis of depression (23,25), so we verified the effects of LPS in isolated E18 primary rat cortical neurons and gained the same observation.…”

Section: Discussionsupporting

confidence: 57%

Lipopolysaccharide-induced serotonin transporter up-regulation involves PKG-I and p38MAPK activation partially through A3 adenosine receptor

Zhao

Wang

Huang

et al. 2015

BST

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Section: Discussionsupporting

confidence: 57%

Lipopolysaccharide-induced serotonin transporter up-regulation involves PKG-I and p38MAPK activation partially through A3 adenosine receptor

Zhao

Wang

Huang

et al. 2015

BST

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“…Relatively high drug concentrations are commonly used in experiments with C. elegans because drugs are supplied in growth media and only small amounts of a drug enter animals (Lewis et al 1980). It has been reported that in the CNS of rodents and humans SERT is expressed in many neurons that do not express the enzymes essential for 5-HT biosynthesis (D'Amato et al 1987;Hoffman et al 1998;Lebrand et al 1998;Verney et al 2002). Thus, in mammals as well as in C. elegans there are two distinctive populations of serotonergic neurons: neurons synthesizing 5-HT and neurons absorbing 5-HT from extracellular space.…”

Section: Resultsmentioning

confidence: 99%

A Genetic Survey of Fluoxetine Action on Synaptic Transmission in Caenorhabditis elegans

et al. 2010

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Fluoxetine is one of the most commonly prescribed medications for many behavioral and neurological disorders. Fluoxetine acts primarily as an inhibitor of the serotonin reuptake transporter (SERT) to block the removal of serotonin from the synaptic cleft, thereby enhancing serotonin signals. While the effects of fluoxetine on behavior are firmly established, debate is ongoing whether inhibition of serotonin reuptake is a sufficient explanation for its therapeutic action. Here, we provide evidence of two additional aspects of fluoxetine action through genetic analyses in Caenorhabditis elegans. We show that fluoxetine treatment and null mutation in the sole SERT gene mod-5 eliminate serotonin in specific neurons. These neurons do not synthesize serotonin but import extracellular serotonin via MOD-5/SERT. Furthermore, we show that fluoxetine acts independently of MOD-5/SERT to regulate discrete properties of acetylcholine (Ach), gamma-aminobutyric acid (GABA), and glutamate neurotransmission in the locomotory circuit. We identified that two G-protein-coupled 5-HT receptors, SER-7 and SER-5, antagonistically regulate the effects of fluoxetine and that fluoxetine binds to SER-7. Epistatic analyses suggest that SER-7 and SER-5 act upstream of AMPA receptor GLR-1 signaling. Our work provides genetic evidence that fluoxetine may influence neuronal functions and behavior by directly targeting serotonin receptors.

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“…The vesicular monoamine transporter type 2 (VMAT2) has an important role in this process (Hoffman et al, 1998). An early indication that VMAT2 might contribute to stress-related pathology stemmed from the serendipitous discovery that pharmacological inhibition of VMAT by reserpine treatment produced striking depressive-like symptoms in humans (Freis, 1954).…”

Section: Serotonin Vesicular Packagingmentioning

confidence: 99%

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

Holmes

2008

Neuroscience & Biobehavioral Reviews

239

166

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The serotonin system is strongly implicated in the pathophysiology and therapeutic alleviation of stress-related disorders such as anxiety and depression. Serotonergic modulation of the acute response to stress and the adaptation to chronic stress is mediated by a myriad of molecules controlling serotonin neuron development (Pet-1), synthesis (tryptophan hydroxylase 1 and 2 isozymes), packaging (vesicular monoamine transporter 2), actions at presynaptic and postsynaptic receptors (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3A, 5-HT4, 5-HT5A, 5-HT6, 5-HT7), reuptake (serotonin transporter), and degradation (monoamine oxidase A). A growing body of evidence from preclinical rodents models, and especially genetically modified mice and inbred mouse strains, has provided significant insight into how genetic variation in these molecules can affect the development and function of a key neural circuit between the dorsal raphe nucleus, medial prefrontal cortex and amygdala. By extension, such variation is hypothesized to have a major influence on individual differences in the stress response and risk for stress-related disease in humans. The current article provides an update on this rapidly evolving field of research.

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Localization and Dynamic Regulation of Biogenic Amine Transporters in the Mammalian Central Nervous System

Cited by 217 publications

References 177 publications

Lipopolysaccharide-induced serotonin transporter up-regulation involves PKG-I and p38MAPK activation partially through A3 adenosine receptor

Lipopolysaccharide-induced serotonin transporter up-regulation involves PKG-I and p38MAPK activation partially through A3 adenosine receptor

A Genetic Survey of Fluoxetine Action on Synaptic Transmission in Caenorhabditis elegans

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

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