共查询到20条相似文献,搜索用时 31 毫秒
1.
Erin R. Slaten Melissa C. Hernandez Ricardo Albay III Rachel Lavian Skirmantas Janušonis 《Developmental neurobiology》2010,70(3):165-181
The serotonin 5‐HT4 receptor (5‐HT4‐R) is an unusually complex G‐protein coupled receptor that is likely to play important roles in brain development and that may underlie the comorbidity of central and peripheral abnormalities in some developmental disorders. We studied the expression of 5‐HT4‐Rs in the developing mouse forebrain at embryonic days 13, 15, 17, and at postnatal days 3 and 14 by using immunohistochemistry, tract tracing, and quantitative RT‐PCR. The developing thalamocortical projections transiently expressed 5‐HT4‐Rs in the embryonic brain and the 5‐HT4‐R expression in the forebrain changed from axonal to somatic around birth. From embryonic days 13–17, the forebrain mRNA levels of the 5‐HT4(a)‐R and 5‐HT4(b)‐R splice variants increased nine‐ and fivefold, respectively, whereas the levels of the 5‐HT4(e)‐R and 5‐HT4(f)‐R variants remained relatively low throughout the studied period of embryonic development. These results suggest that during development 5‐HT4‐R expression undergoes a dynamic regulation and that this regulation may be important for the normal development of sensory and limbic processing. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2010. 相似文献
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The role of 5‐hydroxytryptamine (5‐HT, serotonin) in the control of leech behavior is well established and has been analyzed extensively on the cellular level; however, hitherto little is known about the effect of 5‐HT on the cytosolic free calcium concentration ([Ca2+]i) in leech neurons. As [Ca2+]i plays a pivotal role in numerous cellular processes, we investigated the effect of 5‐HT on [Ca2+]i (measured by Fura‐2) in identified leech neurons under different experimental conditions, such as changed extracellular ion composition and blockade of excitatory synaptic transmission. In pressure (P), lateral nociceptive (N1), and Leydig neurons, 5‐HT induced a [Ca2+]i increase which was predominantly due to Ca2+ influx since it was abolished in Ca2+‐free solution. The 5‐HT‐induced Ca2+ influx occurred only if the cells depolarized sufficiently, indicating that it was mediated by voltage‐dependent Ca2+ channels. In P and N1 neurons, the membrane depolarization was due to Na+ influx through cation channels coupled to 5‐HT receptors, whereby the dose‐dependency suggests an involvement in excitatory synaptic transmission. In Leydig neurons, 5‐HT receptor‐coupled cation channels seem to be absent. In these cells, the membrane depolarization activating the voltage‐dependent Ca2+ channels was evoked by 5‐HT‐triggered excitatory glutamatergic input. In Retzius, anterior pagoda (AP), annulus erector (AE), and median nociceptive (N2) neurons, 5‐HT had no effect on [Ca2+]i. © 2004 Wiley Periodicals, Inc. J Neurobiol, 2005 相似文献
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V. S. Naumenko D. V. Bazovkina E. M. Kondaurova E. A. Zubkov A. V. Kulikov 《Genes, Brain & Behavior》2010,9(5):519-524
In the present study, the 5‐HT2A and 5‐HT1A receptors functional activity and 5‐HT2A receptor gene expression were examined in the brain of ASC/Icg and congenic AKR.CBAD13Mit76C mouse strains (genetically predisposed to catalepsy) in comparison with the parental catalepsy‐resistant AKR/J and catalepsy‐prone CBA/Lac mouse strains. The significantly reduced 5‐HT2A receptor functional activity along with decreased 5‐HT2A receptor gene expression in the frontal cortex was found in all mice predisposed to catalepsy compared with catalepsy‐resistant AKR/J. 5‐HT2A agonist DOI (0.5 and 1 mg/kg, i.p.) significantly reduced catalepsy in ASC/Icg and CBA/Lac, but not in AKR.CBAD13Mit76C mice. Essential increase in 5‐HT1A receptor functional activity was shown in catalepsy‐prone mouse strains in comparison with catalepsy‐resistant AKR/J mice. However, in AKR.CBAD13Mit76C mice it was lower than in ASC/Icg and CBA/Lac mice. The inter‐relation between 5‐HT2A and 5‐HT1A receptors in the regulation of catalepsy was suggested. This suggestion was confirmed by prevention of DOI anticataleptic effect in ASC/Icg and CBA/Lac mice by pretreatment with 5‐HT1A receptor antagonist p‐MPPI (3 mg/kg, i.p.). At the same time, the activation of 5‐HT2A receptor led to the essential suppression of 5‐HT1A receptor functional activity, indicating the opposite effect of 5‐HT2A receptor on pre‐ and postsynaptic 5‐HT1A receptors. Thus, 5‐HT2A/5‐HT1A receptor interaction in the mechanism of catalepsy suppression in mice was shown. 相似文献
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Yukiko Nakamura Yusuke Ishida Takahiro Yamada Makoto Kondo Shoichi Shimada 《Journal of neurochemistry》2013,125(1):7-15
The 5‐hydroxytryptamine (serotonin, 5‐HT) type 3 (5‐HT3) receptor belongs to the superfamily of Cys‐loop ligand‐gated ion channels, and can be either homopentameric (5‐HT3A) or heteropentameric (5‐HT3AB) receptor. Several modulators are known, which either inhibit or potentiate this channel, but few have any appreciable selectivity between the two subtypes or can modulate one receptor differently to the other. In this study, we show that the anticancer drug, topotecan, bidirectionally modulates the 5‐HT3 receptor using a two‐electrode voltage clamp technique. Topotecan inhibited 5‐HT‐gated current through homomeric 5‐HT3A receptors. Interestingly, however, additional expression of the 5‐HT3B subunit changed the response to topotecan dramatically from an inhibitory to a potentiatory one. This effect was dependent on the level of 5‐HT3B subunit expression. Moreover, the effect was reduced in the receptors containing the 5‐HT3B(Y129S) polymorphic variant. These finding could explain individual differences in the sensitivity to topotecan‐induced nausea and vomiting. 相似文献
6.
Chiung‐Chun Huang Che‐Ming Yeh Mei‐Ying Wu Kuei‐Sen Hsu 《Journal of neurochemistry》2013,125(6):809-821
The nucleus accumbens (NAc) is a crucial forebrain nucleus implicated in reward‐based decision‐making. While NAc neurons are richly innervated by serotonergic fibers, information on the functional role of serotonin 5‐hydroxytryptamine (5‐HT) in the NAc is still sparse. Here, we demonstrate that brief application of 5‐HT or 5‐HT1B receptor agonist CP 93129 induced a long‐term depression (LTD) of glutamatergic transmission in NAc neurons. This LTD was presynaptically mediated and inducible by endogenous 5‐HT. Remarkably, a single cocaine exposure impaired the induction of LTD by 5‐HT or CP 93129. The inhibition was blocked when a selective dopamine D1 receptor antagonist SCH23390 was coadministered with cocaine. Cocaine treatment resulted in increased phosphorylation of presynaptic proteins, rabphilin 3A and synapsin 1, and significantly attenuated CP 93129‐induced decrease in rabphilin 3A and synapsin 1 phosphorylation. Application of cAMP‐dependent protein kinase inhibitor KT5720 caused a prominent synaptic depression in NAc neurons of mice with a history of cocaine exposure. Our results reveal a novel 5‐HT1B receptor‐mediated LTD in the NAc and suggest that cocaine exposure may result in elevated phosphorylation of presynaptic proteins involved in regulating glutamate release, which counteracts the presynaptic depressant effects of 5‐HT1B receptors and thereby impairs the induction of LTD by 5‐HT. 相似文献
7.
Discovering the mechanisms underlying serotonin (5‐HT)2A and 5‐HT2C receptor regulation following nicotine withdrawal in rats
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Magdalena Zaniewska Natalia Alenina Karolina Wydra Sebastian Fröhler Maciej Kuśmider Andrew C. McCreary Wei Chen Michael Bader Małgorzata Filip 《Journal of neurochemistry》2015,134(4):704-716
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β‐arrestin1 phosphorylation by GRK5 regulates G protein‐independent 5‐HT4 receptor signalling
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Elizabeth Cassier Breann Barker Florence Gaven Marion Pillot Bérénice Framery Lucie P Pellissier Julie Augier Dong Soo Kang Sylvie Claeysen Eric Reiter Jean‐Louis Banères Jeffrey L Benovic Philippe Marin Joël Bockaert Aline Dumuis 《The EMBO journal》2009,28(18):2706-2718
G protein‐coupled receptors (GPCRs) have been found to trigger G protein‐independent signalling. However, the regulation of G protein‐independent pathways, especially their desensitization, is poorly characterized. Here, we show that the G protein‐independent 5‐HT4 receptor (5‐HT4R)‐operated Src/ERK (extracellular signal‐regulated kinase) pathway, but not the Gs pathway, is inhibited by GPCR kinase 5 (GRK5), physically associated with the proximal region of receptor’ C‐terminus in both human embryonic kidney (HEK)‐293 cells and colliculi neurons. This inhibition required two sequences of events: the association of β–arrestin1 to a phosphorylated serine/threonine cluster located within the receptor C‐t domain and the phosphorylation, by GRK5, of β–arrestin1 (at Ser412) bound to the receptor. Phosphorylated β‐arrestin1 in turn prevented activation of Src constitutively bound to 5‐HT4Rs, a necessary step in receptor‐stimulated ERK signalling. This is the first demonstration that β‐arrestin1 phosphorylation by GRK5 regulates G protein‐independent signalling. 相似文献
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The interactions of cobalt(II)–4‐[(5‐chloro‐2‐pyridyl)azo]‐1,3‐diaminobenzene (5‐Cl‐PADAB) complex with different kinds of homopolymer oligonucleotides in basic medium were investigated based on the measurements of resonance light scattering, UV–vis, circular dichroism spectra and dark field light‐scattering imaging. Experiments showed that only thymidine homopolymer (poly T) oligonucleotides with the length in the range of poly T6 to poly T18 could interact with the Co(II)–5‐Cl‐PADAB complex in alkaline conditions and cause evident color and spectral change. Thus, the binary complex of Co(II)–5‐Cl‐PADAB could be employed as a visual probe for selectively recognizing the poly T oligonucleotides. Copyright © 2009 John Wiley & Sons, Ltd. 相似文献
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Alexandre Julien Chu Loucif Patricia Bonnavion Batrice Macri Jean‐Louis Golmard Claudette Boni Maxette Melfort Grgoire Leonard Klaus‐Peter Lesch Joëlle Adrien Thierry Didier Jacquin 《Developmental neurobiology》2006,66(13):1475-1488
Agonists at G‐protein‐coupled receptors in neurons of the dorsal raphe nucleus (DRN) of knock‐out mice devoid of the serotonin transporter (5‐HTT?/?) exhibit lower efficacy to inhibit cellular discharge than in wild‐type counterparts. Using patch‐clamp whole‐cell recordings, we found that a G‐protein‐gated inwardly rectifying potassium (GIRK) current is involved in the inhibition of spike discharge induced by 5‐HT1A agonists (5‐carboxamidotryptamine (5‐CT) and (±)‐2‐dipropylamino‐8‐hydroxy‐1,2,3,4‐tetrahydronaphthalene hydrobromide (8‐OH‐DPAT); 50 nM–30 μM) in both wild‐type and 5‐HTT?/? female and male mice. These effects were mimicked by 5′‐guanylyl‐imido‐diphosphate (Gpp(NH)p; 400 μM) dialysis into cells with differences between genders. The 5‐HTT?/? knock‐out mutation reduced the current density induced by Gpp(NH)p in females but not in males. These data suggest that the decreased response of 5‐HT1A receptors to agonists in 5‐HTT?/? mutants reflects notably alteration in the coupling between G‐proteins and GIRK channels in females but not in males. Accordingly, gender differences in central 5‐HT neurotransmission appear to depend—at least in part—on sex‐related variations in corresponding receptor‐G protein signaling mechanisms. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 相似文献
13.
Tongtong Ge Zhuo Zhang Jiayin Lv Yunong Song Jie Fan Wei Liu Xuefeng Wang F. Scott Hall Bingjin Li Ranji Cui 《Journal of biochemical and molecular toxicology》2017,31(6)
Corticosterone plays an important role in feeding behavior. However, its mechanism remains unclear. Therefore, the present study aimed to investigate the effect of corticosterone on feeding behavior. In this study, cumulative food intake was increased by acute corticosterone administration in a dose‐dependent manner. Administration of the 5‐HT2c receptor agonist m‐chlorophenylpiperazin (mCPP) reversed the effect of corticosterone on food intake. The anorectic effects of mCPP were also blocked by the 5‐HT2c receptor antagonist RS102221 in corticosterone‐treated mice. Both corticosterone and mCPP increased c‐Fos expression in hypothalamic nuclei, but not the nucleus of the solitary tract. RS102221 inhibited c‐Fos expression induced by mCPP, but not corticosterone. In addition, mCPP had little effect on TH and POMC levels in the hypothalamus. Furthermore, mCPP antagonized decreasing effect of the leptin produced by corticosterone. Taken together, our findings suggest that 5‐HT2c receptors and leptin may be involved in the effects of corticosterone‐induced hyperphagia. 相似文献
14.
5—羟色胺抑制谷氨酸对海马神经元的毒性作用 总被引:5,自引:1,他引:5
为探讨5-羟色胺(5-HT)对过量谷氨酸(glutamate,Glu)神经毒性的影响。观察了5-HT存在时,过量Glu对海马细胞存活率、海马脑片CA1区群锋电位(population spike,PS)及神经细胞膜Ga^2 电流的影响。结果发现:5-HT可明显提高过量Glu作用下海马神经细胞的存活率,减缓Glu对海马脑片CA1区PS的降低作用;在细胞膜上,5-HT可明显减弱Glu诱导的Ca^2 内向电流,推测,一定浓度的5-HT具有抑制过量Glu神经毒性的作用。在细胞膜上5-HT可明显减弱Glu诱导的Ca^2 内向电流,推测,一定浓度的5-HT具有抑制过量Glu神经毒性的作用,其机制可能在于5-HT与细胞膜上特定的受体结合,抑制了Glu诱导的Ca^2 内流。 相似文献
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H. Gu C. Liu C. Liu M. Chen Q. Zhang J. Zhai K. Wang F. Ji Z. Xu Q. Shen X. Bao X. Chen J. Li Q. Dong C. Chen 《Genes, Brain & Behavior》2013,12(1):133-139
Decision making ability has been reported to be impaired in schizophrenia patients, but no research has examined the genetic bases of this impairment. This study investigated how decision making was affected by the genetic variants in the serotonin transporter gene (triallelic 5‐ HTTLPR) and serotonin receptor 1A gene (rs6295) and their interaction in 465 schizophrenia patients and 448 healthy controls. The Iowa Gambling Task (IGT) was used to evaluate decision making under ambiguity (the first 40 trials) and decision making under risk (the last 60 trials). Results showed that, among the patients, the main effects of 5‐ HTTLPR (F2,16 = 6.54, P = 0.002) and HTR1A rs6295 (F2,16 = 3.87, P = 0.021) polymorphisms and their interaction effect (F4,16 = 3.32, P = 0.005) were significant for the first 40 trials, with the GG genotype of HTR1A rs6295, the L′L′ genotype of 5‐ HTTLPR and the GG‐L′L′ combination showing poorer IGT performance than their counterparts. Results for the healthy controls showed a similar pattern but did not reach statistical significance. No significant effects were found for the last 60 trials. These results are discussed in terms of their implications for our understanding of the genetic mechanisms of decision making in schizophrenia patients as well as healthy adults. 相似文献
17.
Sabah Kelaï Thibault Renoir Laurent Chouchana Françoise Saurini Naïma Hanoun Michel Hamon Laurence Lanfumey 《Journal of neurochemistry》2008,107(6):1660-1670
Alcoholism is a complex disorder involving, among others, the serotoninergic (5‐HT) system, mainly regulated by 5‐HT1A autoreceptors in the dorsal raphe nucleus. 5‐HT1A autoreceptor desensitization induced by chronic 5‐HT reuptake inactivation has been associated with a decrease in ethanol intake in mice. We investigated here whether, conversely, chronic ethanol intake could induce 5‐HT1A autoreceptor supersensitivity, thereby contributing to the maintenance of high ethanol consumption. C57BL/6J mice were subjected to a progressive ethanol intake procedure in a free‐choice paradigm (3–10% ethanol versus tap water; 21 days) and 5‐HT1A autoreceptor functional state was assessed using different approaches. Acute administration of the 5‐HT1A receptor agonist ipsapirone decreased the rate of tryptophan hydroxylation in striatum, and this effect was significantly larger (+75%) in mice that drank ethanol than in those drinking water. Furthermore, ethanol intake produced both an increased potency (+45%) of ipsapirone to inhibit the firing of 5‐HT neurons, and a raise (+35%) in 5‐HT1A autoreceptor‐mediated stimulation of [35S]GTP‐γ‐S binding in the dorsal raphe nucleus. These data showed that chronic voluntary ethanol intake in C57BL/6J mice induced 5‐HT1A autoreceptor supersensitivity, at the origin of a 5‐HT neurotransmission deficit, which might be causally related to the addictive effects of ethanol intake. 相似文献
18.
The advanced glycation end product Nϵ‐carboxymethyllysine and its precursor glyoxal increase serotonin release from Caco‐2 cells
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Ann‐Katrin Holik Barbara Lieder Nicole Kretschy Mark M. Somoza Jakob P. Ley Joachim Hans Veronika Somoza 《Journal of cellular biochemistry》2018,119(3):2731-2741
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This paper presents novel evidence to address mechanisms by which trematode parasites effect behavioural changes in naturally infected fish hosts. California killifish Fundulus parvipinnis infected with the brain‐encysting trematode Euhaplorchis californiensis display conspicuous swimming behaviours that render them 30 times more likely to be eaten by birds, the parasite's final host. Prevalence of E. californiensis reaches nearly 100% in most F. parvipinnis populations, with parasite biomass constituting almost 2% of F. parvipinnis biomass in some locations. Despite having thousands of cysts on their brains, infected fish grow and mature at rates comparable to those of uninfected populations. The lack of general pathology combined with the specificity of the altered behaviours suggests that the behavioural changes are due to parasite manipulation. The monoamine neurotransmitters serotonin and dopamine, which control locomotion and social behaviour in fishes and other vertebrates, were examined to explore the underlying mechanisms of this behaviour modification. Whereas previous studies were similarly conducted with experimentally infected fish, in this study, brain dopaminergic and serotonergic activity were analysed in naturally infected fish to assess how E. californiensis may alter F. parvipinnis monoamines in a naturally occurring system. A parasite density‐associated decrease in serotonergic activity occurred in the hippocampus of naturally infected fish, as well as a decrease in dopaminergic activity in the raphe nuclei, suggesting that E. californiensis inhibits serotonin and dopamine signaling in naturally infected F. parvipinnis. The neurochemical profile of infected fish is consistent with the hypothesis that E. californiensis affects brain monoaminergic systems in order to induce impulse‐driven, active, and aggressive behaviour in its hosts. 相似文献
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Ui Joung Youn Jun‐Ho Lee Yoo Jin Lee Joo Won Nam Hyunsu Bae Eun‐Kyoung Seo 《化学与生物多样性》2010,7(9):2296-2302
Four known alkyl 4‐hydroxybenzoates, i.e., methyl 4‐hydroxybenzoate ( 1 ), ethyl 4‐hydroxybenzoate ( 2 ), propyl 4‐hydroxybenzoate ( 3 ), and butyl 4‐hydroxybenzoate ( 4 ), were isolated from the seeds of Nelumbo nucifera Gaertner (Nymphaeaceae) for the first time. The structures of the isolates were identified by 1D‐ and 2D‐NMR spectroscopy and comparison with published values. The compounds were evaluated for their effects on the 5‐HT‐stimulated inward current (I5‐HT) mediated by the human 5‐HT3A receptors expressed in Xenopus oocytes. Compounds 1 and 2 enhanced the I5‐HT, but 4 reduced it. These results indicate that 4 is an inhibitor of the 5‐HT3A receptors expressed in Xenopus oocytes. 相似文献