Neuronal 5-HT metabotropic receptors: fine-tuning of their structure, signaling, and roles in synaptic modulation

Bockaert, Joël; Claeysen, Sylvie; Bécamel, Carine; Dumuis, Aline; Marin, Philippe

doi:10.1007/s00441-006-0286-1

Cited by 231 publications

(192 citation statements)

References 147 publications

(212 reference statements)

Supporting

Mentioning

188

Contrasting

Unclassified

Order By: Relevance

Section: Bdnfmentioning

confidence: 99%

“…Fifteen genes encoding 5-HT receptors have been identified in the mammalian brain (Bockaert et al, 2006). All of the 5-HT receptors are G-protein-coupled receptors except for the 5-HT 3 receptor, which uses an ionotropic mechanism (Bockaert et al, 2006). The 5-HT 1 receptors (5-HT 1A , 5-HT 1B , 5-HT 1D , 5-HT 1E , 5-HT 1F ) are coupled to Ga i /Ga o signaling proteins; the 5-HT 2 receptors (5-HT 2A , 5-HT 2B, 5-HT 2C ) are coupled to Ga q signaling proteins; the 5-HT 4 , 5-HT 6 , and 5-HT 7 receptors are coupled to Gs proteins.…”

Section: Bdnfmentioning

confidence: 99%

See 1 more Smart Citation

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

686

458

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are two seemingly distinct signaling systems that play regulatory roles in many neuronal functions including survival, neurogenesis, and synaptic plasticity. A common feature of the two systems is their ability to regulate the development and plasticity of neural circuits involved in mood disorders such as depression and anxiety. BDNF promotes the survival and differentiation of 5-HT neurons. Conversely, administration of antidepressant selective serotonin reuptake inhibitors (SSRIs) enhances BDNF gene expression. There is also evidence for synergism between the two systems in affective behaviors and genetic epitasis between BDNF and the serotonin transporter genes.

show abstract

Section: Bdnfmentioning

confidence: 99%

Section: Bdnfmentioning

confidence: 99%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

686

458

View full text Add to dashboard Cite

show abstract

“…The interaction could occur proximally or distally to glutamate receptor activation. For example, glutamate-induced changes in intracellular Ca 2+ can suppress serotonin receptor responsiveness (Bockaert et al, 2006). Conversely, the interaction could occur further downstream from glutamate receptor activation.…”

Section: Glutamate Inhibition Of Serotonergic Phase Shifts May Occur mentioning

confidence: 99%

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

2008

View full text Add to dashboard Cite

Alcohol abuse is associated with sleep problems, which are often linked to circadian rhythm disturbances. However, there is no information on the direct effects of ethanol on the mammalian circadian clock. Acute ethanol inhibits glutamate signaling, which is the primary mechanism through which light resets the mammalian clock in the suprachiasmatic nucleus (SCN). Glutamate and light also inhibit circadian clock resetting induced by non-photic signals, including serotonin. Thus, we investigated the effects of acute ethanol on both glutamatergic and serotoninergic resetting of the SCN clock in vitro. We show that ethanol dose-dependently inhibits glutamate-induced phase shifts and enhances serotonergic phase shifts. The inhibition of glutamate-induced phase shifts is not affected by excess glutamate, glycine or D-serine, but is prevented by excess brain-derived neurotrophic factor (BDNF). BDNF is known to augment glutamate signaling in the SCN and to be necessary for glutamate/light-induced phase shifts. Thus, ethanol may inhibit glutamate-induced clock resetting at least in part by blocking BDNF enhancement of glutamate signaling. Ethanol enhancement of serotonergic phase shifts is mimicked by treatments that suppress glutamate signaling in the SCN, including antagonists of glutamate receptors, BDNF signaling and nitric oxide synthase. The combined effect of ethanol with these treatments is not additive, suggesting they act through a common pathway. Our data indicate further that the interaction between serotonin and glutamate in the SCN may occur downstream from nitric oxide synthase activation. Thus, acute ethanol disrupts normal circadian clock phase regulation, which could contribute to the physiological and psychological problems associated with alcohol abuse. Keywords suprachiasmatic nucleus; circadian rhythms; ethanol; glutamate; serotonin; brain-derived neurotrophic factorThe development of alcoholism and the likelihood of relapse drinking are associated with poor sleep quality and the deleterious effects of ethanol on sleep (Landolt and Gillin, 2001;Brower et al., 2001). Alcohol consumption reduces sleep quality (Kubota et al., 2002;Ehler and Slawecki, 2000;Landolt et al., 1996), which is closely linked to the circadian system. For example, the inability to fall asleep at the desired time can result from improper synchronization *Corresponding author: Dept. Biochemistry and Cellular and Molecular Biology, University of Tennessee, Knoxville, TN 37996, phone: (865) 974-2722, FAX: (865)-974-6306, rprosser@utk.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal per...

show abstract

“…Conditional expression of 5-HT 1A in hippocampal and cortical regions is sufficient to normalize anxietylike behavior in mutant mice. 178 Interestingly, the conditional loss of forebrain 5-HT 1A function does not induce the anxiety-like phenotype when the deletion 174,175 Receptor tyrosine kinase signaling, typified by BDNF (brain-derived neurotrophic factor), is shown in yellow. BDNF or other ligand binds a homo-or heterodimer of the receptor (for example, TrkB) that, in turn, phosphorylates proteins downstream, such as GRB2 (growth factor receptor-bound protein).…”

Section: Autism Candidate Genes and Synaptic Functionmentioning

confidence: 99%

Advances in behavioral genetics: mouse models of autism

2007

View full text Add to dashboard Cite

Autism is a neurodevelopmental syndrome with markedly high heritability. The diagnostic indicators of autism are core behavioral symptoms, rather than definitive neuropathological markers. Etiology is thought to involve complex, multigenic interactions and possible environmental contributions. In this review, we focus on genetic pathways with multiple members represented in autism candidate gene lists. Many of these pathways can also be impinged upon by environmental risk factors associated with the disorder. The mouse model system provides a method to experimentally manipulate candidate genes for autism susceptibility, and to use environmental challenges to drive aberrant gene expression and cell pathology early in development. Mouse models for fragile X syndrome, Rett syndrome and other disorders associated with autistic-like behavior have elucidated neuropathology that might underlie the autism phenotype, including abnormalities in synaptic plasticity. Mouse models have also been used to investigate the effects of alterations in signaling pathways on neuronal migration, neurotransmission and brain anatomy, relevant to findings in autistic populations. Advances have included the evaluation of mouse models with behavioral assays designed to reflect disease symptoms, including impaired social interaction, communication deficits and repetitive behaviors, and the symptom onset during the neonatal period. Research focusing on the effect of gene-by-gene interactions or genetic susceptibility to detrimental environmental challenges may further understanding of the complex etiology for autism.

show abstract

Neuronal 5-HT metabotropic receptors: fine-tuning of their structure, signaling, and roles in synaptic modulation

Cited by 231 publications

References 147 publications

Interaction between BDNF and Serotonin: Role in Mood Disorders

Interaction between BDNF and Serotonin: Role in Mood Disorders

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

Advances in behavioral genetics: mouse models of autism

Contact Info

Product

Resources

About