Database : MEDLINE
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PMID:28951257
Author:Meyer M; Garay LI; Kruse MS; Lara A; Gargiulo-Monachelli G; Schumacher M; Guennoun R; Coirini H; De Nicola AF; Gonzalez Deniselle MC
Address:Laboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Obligado 2490, 1428, Buenos Aires, Argentina.
Title:Protective effects of the neurosteroid allopregnanolone in a mouse model of spontaneous motoneuron degeneration.
Source:J Steroid Biochem Mol Biol; 174:201-216, 2017 Nov.
ISSN:1879-1220
Country of publication:England
Language:eng
Abstract:Amyotrophic lateral sclerosis (ALS) is a devastating disorder characterized by progressive death of motoneurons. The Wobbler (WR) mouse is a preclinical model sharing neuropathological similarities with human ALS. We have shown that progesterone (PROG) prevents the progression of motoneuron degeneration. We now studied if allopregnanolone (ALLO), a reduced metabolite of PROG endowed with gabaergic activity, also prevents WR neuropathology. Sixty-day old WRs remained untreated or received two steroid treatment regimens in order to evaluate the response of several parameters during early or prolonged steroid administration. ALLO was administered s.c. daily for 5days (4mg/kg) or every other day for 32days (3, 3mg/kg), while another group of WRs received a 20mg PROG pellet s.c. for 18 or 60days. ALLO administration to WRs increased ALLO serum levels without changing PROG and 5 alpha dihydroprogesterone (5α-DHP), whereas PROG treatment increased PROG, 5α-DHP and ALLO. Untreated WRs showed higher basal levels of serum 5α-DHP than controls. In the cervical spinal cord we studied markers of oxidative stress or associated to trophic responses. These included nitric oxide synthase (NOS) activity, motoneuron vacuolation, MnSOD immunoreactivity (IR), brain derived neurotrophic factor (BDNF) and TrkB mRNAs, p75 neurotrophin receptor (p75NTR) and, cell survival or death signals such as pAKT and the stress activated kinase JNK. Untreated WRs showed a reduction of MnSOD-IR and BDNF/TrkB mRNAs, associated to high p75NTR in motoneurons, neuronal and glial NOS hyperactivity and neuronal vacuolation. Also, low pAKT, mainly in young WRs, and a high pJNK in the old stage characterized WRs spinal cord. Except for MnSOD and BDNF, these alterations were prevented by an acute ALLO treatment, while short-term PROG elevated MnSOD. Moreover, after chronic administration both steroids enhanced MnSOD-IR and BDNF mRNA, while attenuated pJNK and NOS in glial cells. Long-term PROG also increased pAKT and reduced neuronal NOS, parameters not modulated by chronic ALLO. Clinically, both steroids improved muscle performance. Thus, ALLO was able to reduce neuropathology in this model. Since high oxidative stress activates p75NTR and pJNK in neurodegeneration, steroid reduction of these molecules may provide adequate neuroprotection. These data yield the first evidence that ALLO, a gabaergic neuroactive steroid, brings neuroprotection in a model of motoneuron degeneration.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Brain-Derived Neurotrophic Factor); 0 (Neuroprotective Agents); 0 (Receptors, Nerve Growth Factor); 0 (TNFRSF16 protein, mouse); 4G7DS2Q64Y (Progesterone); BXO86P3XXW (Pregnanolone); EC 1.14.13.39 (Nitric Oxide Synthase); EC 1.15.1.1 (Superoxide Dismutase); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 2.7.10.1 (Receptor, trkB)


  2 / 7684 MEDLINE  
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PMID:28916328
Author:Del Pino J; Moyano P; Díaz GG; Anadon MJ; Diaz MJ; García JM; Lobo M; Pelayo A; Sola E; Frejo MT
Address:Department of Toxicology and Pharmacology, Veterinary School, Complutense University of Madrid, 28040 Madrid, Spain. Electronic address: jdelpino@pdi.ucm.es.
Title:Primary hippocampal neuronal cell death induction after acute and repeated paraquat exposures mediated by AChE variants alteration and cholinergic and glutamatergic transmission disruption.
Source:Toxicology; 390:88-99, 2017 Sep 01.
ISSN:1879-3185
Country of publication:Ireland
Language:eng
Abstract:Paraquat (PQ) is a widely used non-selective contact herbicide shown to produce memory and learning deficits after acute and repeated exposure similar to those induced in Alzheimer's disease (AD). However, the complete mechanisms through which it induces these effects are unknown. On the other hand, cholinergic and glutamatergic systems, mainly in the hippocampus, are involved on learning, memory and cell viability regulation. An alteration of hippocampal cholinergic or glutamatergic transmissions or neuronal cell loss may induce these effects. In this regard, it has been suggested that PQ may induce cell death and affect cholinergic and glutamatergic transmission, which alteration could produce neuronal loss. According to these data, we hypothesized that PQ could induce hippocampal neuronal loss through cholinergic and glutamatergic transmissions alteration. To prove this hypothesis, we evaluated in hippocampal primary cell culture, the PQ toxic effects after 24h and 14 consecutive days exposure on neuronal viability and the cholinergic and glutamatergic mechanisms related to it. This study shows that PQ impaired acetylcholine levels and induced AChE inhibition and increased CHT expression only after 14days exposure, which suggests that acetylcholine levels alteration could be mediated by these actions. PQ also disrupted glutamate levels through induction of glutaminase activity. In addition, PQ induced, after 24h and 14days exposure, cell death on hippocampal neurons that was partially mediated by AChE variants alteration and cholinergic and gultamatergic transmissions disruption. Our present results provide new view of the mechanisms contributing to PQ neurotoxicity and may explain cognitive dysfunctions observed after PQ exposure.
Publication type:JOURNAL ARTICLE
Name of substance:0 (GPI-Linked Proteins); 0 (Herbicides); 0 (Membrane Transport Proteins); 0 (choline transporter); 3KX376GY7L (Glutamic Acid); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.7 (Ache protein, rat); EC 3.5.1.2 (Glutaminase); N9YNS0M02X (Acetylcholine); PLG39H7695 (Paraquat)


  3 / 7684 MEDLINE  
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PMID:28910446
Author:Takahama S; Adetunji MO; Zhao T; Chen S; Li W; Tomarev SI
Address:Section on Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Institutes of Health, Bethesda, Maryland, United States.
Title:Retinal Astrocytes and GABAergic Wide-Field Amacrine Cells Express PDGFRα: Connection to Retinal Ganglion Cell Neuroprotection by PDGF-AA.
Source:Invest Ophthalmol Vis Sci; 58(11):4703-4711, 2017 Sep 01.
ISSN:1552-5783
Country of publication:United States
Language:eng
Abstract:Purpose: Our previous experiments demonstrated that intravitreal injection of platelet-derived growth factor-AA (PDGF-AA) provides retinal ganglion cell (RGC) neuroprotection in a rodent model of glaucoma. Here we used PDGFRα-enhanced green fluorescent protein (EGFP) mice to identify retinal cells that may be essential for RGC protection by PDGF-AA. Methods: PDGFRα-EGFP mice expressing nuclear-targeted EGFP under the control of the PDGFRα promoter were used. Localization of PDGFRα in the neural retina was investigated by confocal imaging of EGFP fluorescence and immunofluorescent labeling with a panel of antibodies recognizing different retinal cell types. Primary cultures of mouse RGCs were produced by immunopanning. Neurobiotin injection of amacrine cells in a flat-mounted retina was used for the identification of EGFP-positive amacrine cells in the inner nuclear layer. Results: In the mouse neural retina, PDGFRα was preferentially localized in the ganglion cell and inner nuclear layers. Immunostaining of the retina demonstrated that astrocytes in the ganglion cell layer and a subpopulation of amacrine cells in the inner nuclear layer express PDGFRα, whereas RGCs (in vivo or in vitro) did not. PDGFRα-positive amacrine cells are likely to be Type 45 gamma-aminobutyric acidergic (GABAergic) wide-field amacrine cells. Conclusions: These data indicate that the neuroprotective effect of PDGF-AA in a rodent model of glaucoma could be mediated by astrocytes and/or a subpopulation of amacrine cells. We suggest that after intravitreal injection of PDGF-AA, these cells secrete factors protecting RGCs.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Neuroprotective Agents); 0 (Platelet-Derived Growth Factor); 0 (enhanced green fluorescent protein); 0 (neurobiotin); 0 (platelet-derived growth factor A); 147336-22-9 (Green Fluorescent Proteins); 56-12-2 (gamma-Aminobutyric Acid); 6SO6U10H04 (Biotin); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)


  4 / 7684 MEDLINE  
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PMID:28874448
Author:Bardóczi Z; Pál B; Koszeghy Á; Wilheim T; Watanabe M; Záborszky L; Liposits Z; Kalló I
Address:Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, HAS, 1083, Budapest, Hungary.
Title:Glycinergic Input to the Mouse Basal Forebrain Cholinergic Neurons.
Source:J Neurosci; 37(39):9534-9549, 2017 Sep 27.
ISSN:1529-2401
Country of publication:United States
Language:eng
Abstract:The basal forebrain (BF) receives afferents from brainstem ascending pathways, which has been implicated first by Moruzzi and Magoun (1949) to induce forebrain activation and cortical arousal/waking behavior; however, it is very little known about how brainstem inhibitory inputs affect cholinergic functions. In the current study, glycine, a major inhibitory neurotransmitter of brainstem neurons, and gliotransmitter of local glial cells, was tested for potential interaction with BF cholinergic (BFC) neurons in male mice. In the BF, glycine receptor α subunit-immunoreactive (IR) sites were localized in choline acetyltransferase (ChAT)-IR neurons. The effect of glycine on BFC neurons was demonstrated by bicuculline-resistant, strychnine-sensitive spontaneous IPSCs (sIPSCs; 0.81 ± 0.25 × 10 Hz) recorded in whole-cell conditions. Potential neuronal as well as glial sources of glycine were indicated in the extracellular space of cholinergic neurons by glycine transporter type 1 (GLYT1)- and GLYT2-IR processes found in apposition to ChAT-IR cells. Ultrastructural analyses identified synapses of GLYT2-positive axon terminals on ChAT-IR neurons, as well as GLYT1-positive astroglial processes, which were localized in the vicinity of synapses of ChAT-IR neurons. The brainstem raphe magnus was determined to be a major source of glycinergic axons traced retrogradely from the BF. Our results indicate a direct effect of glycine on BFC neurons. Furthermore, the presence of high levels of plasma membrane glycine transporters in the vicinity of cholinergic neurons suggests a tight control of extracellular glycine in the BF. Basal forebrain cholinergic (BFC) neurons receive various activating inputs from specific brainstem areas and channel this information to the cortex via multiple projections. So far, very little is known about inhibitory brainstem afferents to the BF. The current study established glycine as a major regulator of BFC neurons by (1) identifying glycinergic neurons in the brainstem projecting to the BF, (2) showing glycine receptor α subunit-immunoreactive (IR) sites in choline acetyltransferase (ChAT)-IR neurons, (3) demonstrating glycine transporter type 2 (GLYT2)-positive axon terminals synapsing on ChAT-IR neurons, and (4) localizing GLYT1-positive astroglial processes in the vicinity of synapses of ChAT-IR neurons. The effect of glycine on BFC neurons was demonstrated by bicuculline-resistant, strychnine-sensitive spontaneous IPSCs recorded in whole-cell conditions.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Glycine Agents); 0 (Glycine Plasma Membrane Transport Proteins); EC 2.3.1.6 (Choline O-Acetyltransferase); H9Y79VD43J (Strychnine); TE7660XO1C (Glycine); Y37615DVKC (Bicuculline)


  5 / 7684 MEDLINE  
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PMID:28867578
Author:Rostami F; Javan M; Moghimi A; Haddad-Mashadrizeh A; Fereidoni M
Address:Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran.
Title:Streptozotocin-induced hippocampal astrogliosis and insulin signaling malfunction as experimental scales for subclinical sporadic Alzheimer model.
Source:Life Sci; 188:172-185, 2017 Nov 01.
ISSN:1879-0631
Country of publication:Netherlands
Language:eng
Abstract:AIMS: Insulin signaling malfunction has recently been suggested as a preliminary event involved in the etiology of Sporadic Alzheimer's disease (SAD). In order to develop insulin resistance-related SAD model, rats were treated with streptozotocin, intracerebroventricularly (icv-STZ). Nevertheless, given the lack of knowledge regarding sub-clinical stages of SAD, the current challenging issue is establishing a practical pre-clinical SAD model. Despite some proposed mechanisms, such as insulin malfunction, neuroinflammation, and gliosis, icv-STZ mechanism of action is not fully understood yet and Streptozotocin-induced rat model of Alzheimer has still major shortcomings. MAIN METHODS: Using three STZ doses (0.5, 1, and 3mg/kg) and three testing time (short-term, medium-term and long-term), we sought the best dose of STZ in order to mimic the characteristic feature of sAD in rats. So, we conducted a series of fifteen-week follow-up cognitive and non-cognitive studies. Besides, IR, tau and ChAT mRNA levels were measured, along with histological analysis of astrocyte, dark neuron numbers, and pyramidal layer thickness, in order to compare the effects of different doses of icv-STZ. KEY FINDINGS: STZ 3mg/kg caused cognitive and insulin signaling disturbance from the very first testing-time. STZ1-injected animals, however, showed an augmented hippocampal astrocyte numbers in a short time; they, also, were diagnosed with disturbed insulin signaling in medium-term post icv-STZ-injection. Moreover, behavioral, molecular and histological impairments induced by 0.5mg/kg icv-STZ were slowly progressing in comparison to high doses of STZ. SIGNIFICANCE: STZ1 and 0.5mg/kg-treated animals are, respectively, suggested as a suitable experimental model of MCI, and sub-clinical stage.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Insulin); 0 (tau Proteins); 5W494URQ81 (Streptozocin); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 2.7.10.1 (Receptor, Insulin)


  6 / 7684 MEDLINE  
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PMID:28833372
Author:Gesslbauer B; Hruby LA; Roche AD; Farina D; Blumer R; Aszmann OC
Address:Christian Doppler Laboratory for Restoration of Extremity Function, Medical University of Vienna, Vienna, Austria.
Title:Axonal components of nerves innervating the human arm.
Source:Ann Neurol; 82(3):396-408, 2017 Sep.
ISSN:1531-8249
Country of publication:United States
Language:eng
Abstract:OBJECTIVE: Axons traveling within the brachial plexus are responsible for the dexterous control of human arm and hand movements. Despite comprehensive knowledge on the topographical anatomy of nerves innervating the human upper limbs, the definite quantity of sensory and motor axons within this neural network remains elusive. Our aim was to perform a quantitative analysis of the axonal components of human upper limb nerves based on highly specific molecular features from spinal cord level to the terminal nerves at wrist level. METHODS: Nerve specimen harvest at predefined harvesting sites (plexus roots and cords as well as major nerves originating from the brachial plexus innervating the arm and hand) was performed in 9 human heart-beating organ donors. Double immunofluorescence staining using antibodies against choline-acetyltransferase and neurofilament was performed to differentiate motor and sensory axons on nerve cross sections. RESULTS: Three hundred fifty thousand axons emerge from the spinal cord to innervate the human upper limb, of which 10% are motor neurons. In all nerves studied, sensory axons outnumber motor axons by a ratio of at least 9:1. The sensory axon contribution increases when moving distally, whereas only 1,700 motor axons reach the hand to innervate the intrinsic musculature. INTERPRETATION: Our results suggest that upper limb motor execution, and particularly dexterous coordination of hand movement, require an unexpectedly low number of motor neurons, with a large convergence of afferent input for feedback control. Ann Neurol 2017;82:396-408.
Publication type:JOURNAL ARTICLE
Name of substance:EC 2.3.1.6 (Choline O-Acetyltransferase)


  7 / 7684 MEDLINE  
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PMID:28791701
Author:López-Hernández GY; Ananth M; Jiang L; Ballinger EC; Talmage DA; Role LW
Address:Department of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Title:Electrophysiological properties of basal forebrain cholinergic neurons identified by genetic and optogenetic tagging.
Source:J Neurochem; 142 Suppl 2:103-110, 2017 Aug.
ISSN:1471-4159
Country of publication:England
Language:eng
Abstract:Recent developments in the generation of neuronal population-specific, genetically modified mouse lines have allowed precise identification and selective stimulation of cholinergic neurons in vivo. Although considerably less laborious than studies conducted with post hoc identification of cholinergic neurons by immunostaining, it is not known whether the genetically based labeling procedures that permit in vivo identification are electrophysiologically benign. In this study, we use mice carrying a bacterial artificial chromosome transgene that drives expression of a tau-green fluorescent fusion protein specifically in cholinergic neurons. This allowed us to visualize basal forebrain cholinergic neurons in acute slice preparations. Using whole cell, patch clamp electrophysiological recording in acute brain slices, here we present original data about the basic electrical properties of these genetically tagged cholinergic neurons including firing rate, resting membrane potential, rheobase, and various characteristics of their action potentials and after-hyperpolarization potentials. The basic electrical properties are compared (i) with non-cholinergic neurons in the same brain regions; (ii) in cholinergic neurons between immature animals and young adults; and (iii) with cholinergic neurons that are expressing light-sensitive channels. Our conclusions based on these data are (i) cholinergic neurons are less excitable then their non-cholinergic neighbors, (ii) the basic properties of cholinergic neurons do not significantly change between adolescence and young adulthood and (iii) these properties are not significantly affected by chronic expression of the excitatory opsin, oChIEF. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
Publication type:JOURNAL ARTICLE
Name of substance:EC 2.3.1.6 (Choline O-Acetyltransferase)


  8 / 7684 MEDLINE  
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PMID:28570646
Author:McGregor R; Shan L; Wu MF; Siegel JM
Address:Department of Psychiatry and Biobehavioral Sciences, University of California at Los Angeles, Los Angeles, California, United States of America.
Title:Diurnal fluctuation in the number of hypocretin/orexin and histamine producing: Implication for understanding and treating neuronal loss.
Source:PLoS One; 12(6):e0178573, 2017.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:The loss of specific neuronal phenotypes, as determined by immunohistochemistry, has become a powerful tool for identifying the nature and cause of neurological diseases. Here we show that the number of neurons identified and quantified using this method misses a substantial percentage of extant neurons in a phenotype specific manner. In mice, 24% more hypocretin/orexin (Hcrt) neurons are seen in the night compared to the day, and an additional 17% are seen after inhibiting microtubule polymerization with colchicine. We see no such difference between the number of MCH (melanin concentrating hormone) neurons in dark, light or colchicine conditions, despite MCH and Hcrt both being hypothalamic peptide transmitters. Although the size of Hcrt neurons did not differ between light and dark, the size of MCH neurons was increased by 15% in the light phase. The number of neurons containing histidine decarboxylase (HDC), the histamine synthesizing enzyme, was 34% greater in the dark than in the light, but, like Hcrt, cell size did not differ. We did not find a significant difference in the number or the size of neurons expressing choline acetyltransferase (ChAT), the acetylcholine synthesizing enzyme, in the horizontal diagonal band (HBD) during the dark and light conditions. As expected, colchicine treatment did not increase the number of these neurons. Understanding the function and dynamics of transmitter production within "non-visible" phenotypically defined cells has fundamental implications for our understanding of brain plasticity.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Hypothalamic Hormones); 0 (Melanins); 0 (Orexins); 0 (Pituitary Hormones); 67382-96-1 (melanin-concentrating hormone); 820484N8I3 (Histamine); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 4.1.1.22 (Histidine Decarboxylase); SML2Y3J35T (Colchicine)


  9 / 7684 MEDLINE  
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PMID:28552584
Author:Fujii T; Mashimo M; Moriwaki Y; Misawa H; Ono S; Horiguchi K; Kawashima K
Address:Department of Pharmacology, Faculty of Pharmaceutical Sciences, Doshisha Women's College of Liberal Arts, Kyotanabe, Kyoto 610-0395, Japan.
Title:Physiological functions of the cholinergic system in immune cells.
Source:J Pharmacol Sci; 134(1):1-21, 2017 May.
ISSN:1347-8648
Country of publication:Japan
Language:eng
Abstract:T and B cells, macrophages and dendritic cells (DCs) all express most of the components necessary for a functional cholinergic system. This includes choline acetyltransferase (ChAT), muscarinic and nicotinic acetylcholine (ACh) receptors (mAChRs and nAChRs, respectively) and acetylcholinesterase (AChE). Immunological activation of T cells up-regulates cholinergic activity, including ChAT and AChE expression. Moreover, toll-like receptor agonists induce ChAT expression in DCs and macrophages, suggesting cholinergic involvement in the regulation of immune function. Immune cells express all five M -M mAChR subtypes and several nAChR subtypes, including α7. Modulation of antigen-specific antibody and pro-inflammatory cytokine production in M /M mAChR gene-knockout (KO) and α7 nAChR-KO mice further support the idea of a non-neuronal cholinergic system contributing to the regulation of immune function. Evidence also suggests that α7 nAChRs are involved in suppressing DC and macrophage activity, leading to suppression of T cell differentiation into effector T cells. These findings suggest the possibility that immune function could be modulated by manipulating immune cell cholinergic activity using specific agonists and antagonists. Therefore, a fuller understanding of the immune cell cholinergic system should be useful for the development of drugs and therapeutic strategies for the treatment of inflammation-related diseases and cancers.
Publication type:JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antibodies); 0 (Antigens); 0 (Cytokines); 0 (Receptors, Cholinergic); 0 (Receptors, Nicotinic); EC 2.3.1.6 (Choline O-Acetyltransferase); N9YNS0M02X (Acetylcholine)


  10 / 7684 MEDLINE  
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PMID:28479505
Author:Zhang X; Li S; Wang C; Tian H; Wang W; Ru S
Address:College of Marine Life Sciences, Ocean University of China, Qingdao 266003, China.
Title:Effects of monocrotophos pesticide on cholinergic and dopaminergic neurotransmitter systems during early development in the sea urchin Hemicentrotus pulcherrimus.
Source:Toxicol Appl Pharmacol; 328:46-53, 2017 Aug 01.
ISSN:1096-0333
Country of publication:United States
Language:eng
Abstract:During early development in sea urchins, classical neurotransmitters, including acetylcholine (ACh), dopamine (DA), and serotonin (5-HT), play important roles in the regulation of morphogenesis and swimming behavior. However, the underlying mechanisms of how organophosphate pesticides cause developmental neurotoxicity by interfering with different neurotransmitter systems are unclear. In this study, we investigated the effects of 0.01, 0.10, and 1.00mg/L monocrotophos (MCP) pesticide on the activity of acetyltransferase (ChAT), acetylcholinesterase (AChE), monoamine oxidase, the concentration of DA, dopamine transporter, and the transcription activity of DA receptor D and tyrosine hydroxylase, during critical periods in cholinergic and dopaminergic nervous system development in sea urchin (Hemicentrotus pulcherrimus) embryos and larvae. At the blastula stages, MCP disrupted DA metabolism but not 5-HT metabolism, resulting in abnormal development. High ChAT and AChE activity were observed at the gastrulation-completed stage and the two-armed pluteus stage, respectively, MCP inhibited ChAT activity and AChE activity/distribution and resulted in developmental defects of the plutei. From the gastrula stage to the two-armed pluteus stage, we found ubiquitous disrupting effects of MCP on ACh, DA, and 5-HT metabolism, particularly at critical periods during the development of these neurotransmitter systems. Therefore, we propose that this disruption is one of the main mechanisms of MCP-related developmental neurotoxicity, which would contribute better understanding insight into the mechanism of MCP pesticide's toxic effects.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Dopamine Plasma Membrane Transport Proteins); 0 (Insecticides); 0 (Neurotransmitter Agents); 0 (Receptors, Dopamine D1); 333DO1RDJY (Serotonin); 6923-22-4 (Monocrotophos); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.4.3.4 (Monoamine Oxidase); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 3.1.1.7 (Acetylcholinesterase); VTD58H1Z2X (Dopamine)



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