How serotonin receptors regulate morphogenic signalling in neurons

Wirth, Alexander; Holst, Katrin; Ponimaskin, Evgeni

doi:10.1016/j.pneurobio.2016.03.007

Cited by 88 publications

(73 citation statements)

References 359 publications

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“…Behavioral studies show that mid-gestational CPF causes long-term deficits in adult working memory accompanied by decreased susceptibility to the amnestic effect of muscarinic cholinergic blockade indicating a decreased reliance on cholinergic circuits for memory function (Icenogle and others 2004). Both serotonin (5HT) and AChE are expressed prior to synaptogenesis and act as neurotropic factors early during brain development (Abreu-Villaça and others 2011; Nordquist and Oreland 2010; Wirth and others 2016). CPF at doses too low to inhibit AChE nevertheless interferes with its morphogenic activity (Yang and others 2008).…”

Section: Organophosphates (Ops)mentioning

confidence: 99%

“…Nitric oxide synthase expression is transiently decreased in most cortical regions (Naseh and others 2013) whereas there are late-emergent increases in the hypothalamus (Naseh and Vatanparast 2014) and amygdala (Vatanparast and others 2013). Effects on neurotransmitter systems such as the cholinergic, serotonergic and nitrergic likely have pervasive consequences since they have established trophic roles in developmental events including neurogenesis, differentiation and synaptogenesis and also neuroplasticity (Abreu-Villaça and others 2011; Cossenza and others 2014; Okamoto and Lipton 2015; Wirth and others 2016). Most studies focus on effects on neurons, however, protein markers not only for developing axons but also for oligodendrocytes are enhanced shortly after exposure while, during adolescence, there are deficits (Garcia and others 2003), which indicates that glial cells are also impacted by CPF.…”

Section: Organophosphates (Ops)mentioning

confidence: 99%

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Developmental neurotoxicity of succeeding generations of insecticides

Abreu‐Villaça

Levin

2017

Environment International

124

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Insecticides are by design toxic. They must be toxic to effectively kill target species of insects. Unfortunately, they also have off-target toxic effects that can harm other species, including humans. Developmental neurotoxicity is one of the most prominent off-target toxic risks of insecticides. Over the past seven decades several classes of insecticides have been developed, each with their own mechanisms of effect and toxic side effects. This review covers the developmental neurotoxicity of the succeeding generations of insecticides including organochlorines, organophosphates, pyrethroids, carbamates and neonicotinoids. The goal of new insecticide development is to more effectively kill target species with fewer toxic side effects on non-target species. From the experience with the developmental neurotoxicity caused by the generations of insecticides developed in the past advice is offered how to proceed with future insecticide development to decrease neurotoxic risk.

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Section: Organophosphates (Ops)mentioning

confidence: 99%

Section: Organophosphates (Ops)mentioning

confidence: 99%

Developmental neurotoxicity of succeeding generations of insecticides

Abreu‐Villaça

Levin

2017

Environment International

124

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“…It has been described by Dr Barnes as the happy hormone2, involved in natural reward-related physiology and behaviour3, from feeding to sexual activity. Serotonin is biochemically derived from tryptophan and has various functions in different phyla, including both vertebrates and invertebrates, and plays a modulatory role in numerous physiological processes such as feed intake, reproduction, immunity and stress responses456.…”

mentioning

confidence: 99%

Identification and functional characterisation of 5-HT4 receptor in sea cucumber Apostichopus japonicus (Selenka)

Wang

Yang

Zhou

et al. 2017

Sci Rep

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Serotonin (5-HT) is an important neurotransmitter and neuromodulator that controls a variety of sensory and motor functions through 5-HT receptors (5-HTRs). The 5-HT4R subfamily is linked to Gs proteins, which activate adenylyl cyclases (ACs), and is involved in many responses in peripheral organs. In this study, the 5-HT4R from Apostichopus japonicus (Aj5-HT4R) was identified and characterised. The cloned full-length Aj5-HT4R cDNA is 1,544 bp long and contains an open reading frame 1,011 bp in length encoding 336 amino acid proteins. Bioinformatics analysis of the Aj5-HT4R protein indicated this receptor was a member of class A G protein coupled receptor (GPCR) family. Further experiments using Aj5-HT4R-transfected HEK293 cells demonstrated that treatment with 5-HT triggered a significant increase in intracellular cAMP level in a dose-dependent manner and induced a rapid internalisation of Aj5-HT4R fused with enhanced green fluorescent protein (Aj5-HT4R-EGFP) from the cell surface into the cytoplasm. In addition, the transcriptional profiles of Aj5-HT4R in aestivating A. japonicas and phosphofructokinase (AjPFK) in 5-HT administrated A. japonicus have been analysed by real-time PCR assays. Results have led to a basic understanding of Aj5-HT4R in A. japonicus, and provide a foundation for further exploration of the cell signaling and regulatory functions of this receptor.

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“…Remarkably, about 90% of the human body’s total serotonin (and hence TPH biosynthetic systems) are located in the neuroendocrine entero-chromaffin cells in the human gastrointestinal (GI) tract, where it is used to regulate intestinal movements and participate in GI-neural tract signaling; the other 10% is synthesized by serotonergic neurons of the CNS where it functions in the regulation of neurite outgrowth, somatic morphology, growth cone motility, synaptogenesis, and control of dendritic spine shape and density, and behaviorally anger, aggression, mood, body temperature, appetite, sleep, pain and cognition. Serotonin acts via a heterogenic receptor family that includes G protein-coupled receptors and ligand-gated ion channels (New et al, 1998; Craig et al, 2004; Shearer et al, 2016; Wirth et al, 2016). TPH is encoded by two separate enzymes: TPH1 produces serotonin in the pineal gland and entero-chromaffin cells, while TPH2 produces serotonin in the Raphe nuclei of the brain stem and myenteric plexus.…”

Section: Discussionmentioning

confidence: 99%

Genetics of Aggression in Alzheimer’s Disease (AD)

Lukiw

Rogaev

2017

Front. Aging Neurosci.

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Alzheimer’s disease (AD) is a terminal, age-related neurological syndrome exhibiting progressive cognitive and memory decline, however AD patients in addition exhibit ancillary neuropsychiatric symptoms (NPSs) and these include aggression. In this communication we provide recent evidence for the mis-regulation of a small family of genes expressed in the human hippocampus that appear to be significantly involved in expression patterns common to both AD and aggression. DNA array- and mRNA transcriptome-based gene expression analysis and candidate gene association and/or genome-wide association studies (CGAS, GWAS) of aggressive attributes in humans have revealed a surprisingly small subset of six brain genes that are also strongly associated with altered gene expression patterns in AD. These genes encoded on five different chromosomes (chr) include the androgen receptor (AR; chrXq12), brain-derived neurotrophic factor (BDNF; chr11p14.1), catechol-O-methyl transferase (COMT; chr22q11.21), neuronal specific nitric oxide synthase (NOS1; chr12q24.22), dopamine beta-hydroxylase (DBH chr9q34.2) and tryptophan hydroxylase (TPH1, chr11p15.1 and TPH2, chr12q21.1). Interestingly, (i) the expression of three of these six genes (COMT, DBH, NOS1) are highly variable; (ii) three of these six genes (COMT, DBH, TPH1) are involved in DA or serotonin metabolism, biosynthesis and/or neurotransmission; and (iii) five of these six genes (AR, BDNF, COMT, DBH, NOS1) have been implicated in the development, onset and/or propagation of schizophrenia. The magnitude of the expression of genes implicated in aggressive behavior appears to be more pronounced in the later stages of AD when compared to MCI. These recent genetic data further indicate that the extent of cognitive impairment may have some bearing on the degree of aggression which accompanies the AD phenotype.

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How serotonin receptors regulate morphogenic signalling in neurons

Cited by 88 publications

References 359 publications

Developmental neurotoxicity of succeeding generations of insecticides

Developmental neurotoxicity of succeeding generations of insecticides

Identification and functional characterisation of 5-HT4 receptor in sea cucumber Apostichopus japonicus (Selenka)

Genetics of Aggression in Alzheimer’s Disease (AD)

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