Non-cholinergic functions of acetylcholinesterase

Appleyard, Margaret E.

doi:10.1042/bst0220749

Cited by 48 publications

(12 citation statements)

References 9 publications

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“…The structure, location and function of acetylcholinesterase will be briefly summarized (for reviews, see [10,11]). The first convincing evidence for chemical neurotransmission was obtained by Loewi in 1921, with the demonstration that electrical stimulation of the vagal nerve inhibited contraction of the heart by release of an inhibitory substance, which was subsequently identified as acetylcholine [12].…”

Section: Degradation Of Acetylcholinementioning

confidence: 99%

Regulatory mechanisms that modulate signalling by G-protein-coupled receptors

Böhm

Grady

Bunnett

1997

Biochemical Journal

476

322

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The large and functionally diverse group of G-protein-coupled receptors includes receptors for many different signalling molecules, including peptide and non-peptide hormones and neurotransmitters, chemokines, prostanoids and proteinases. Their principal function is to transmit information about the extracellular environment to the interior of the cell by interacting with the heterotrimeric G-proteins, and they thereby participate in many aspects of regulation. Cellular responses to agonists of these receptors are usually rapidly attenuated. Mechanisms of signal attenuation include removal of agonists from the extracellular fluid, receptor desensitization, endocytosis and downregulation. Agonists are removed by dilution, uptake by transporters and enzymic degradation. Receptor desensitization is mediated by receptor phosphorylation by G-protein receptor kinases and second-messenger kinases, interaction of phosphorylated receptors with arrestins and receptor uncoupling from

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Section: Degradation Of Acetylcholinementioning

confidence: 99%

Regulatory mechanisms that modulate signalling by G-protein-coupled receptors

Böhm

Grady

Bunnett

1997

Biochemical Journal

476

322

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Section: Introductionmentioning

confidence: 99%

“…AChE has been implicated in several non-cholinergic actions including cell proliferation, neurite outgrowth and other responses to various insults including stress and amyloid formation. [19][20][21] Although, the neurotoxic effect of (PhTe) 2 has been reported, the interaction of this organotellurium compound with cholinergic system has not been documented.Based on these considerations, the purpose of the present study was to investigate if acute exposure to (PhTe) 2 causes impairment of developmental behavioral performance in rat pups. To better understand the effect of (PhTe) 2 in the developmental period of life (14 to 21 days), parameters of neurotoxicity, such as histology, myelin content and activity of AChE, were studied in brain of rat pups.…”

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confidence: 99%

Diphenyl ditelluride induces neurotoxicity and impairment of developmental behavioral in rat pups

Pinton¹,

Luchese²,

Stangherlin³

et al. 2010

J. Braz. Chem. Soc.

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O objetivo deste estudo foi investigar se a exposição aguda ao ditelureto de difenila [(PhTe) 2 ] causaria prejuízo no desenvolvimento comportamental de filhotes de ratos. Os filhotes receberam uma injeção subcutânea de (PhTe) 2 (0,1 mg kg -1 , 3 mL kg -1 ) ou veículo (3 mL kg -1 ) no 14º dia após o nascimento (DPN). Do 15º ao 21º DPN, foram realizados testes comportamentais nos filhotes e, imediatamente após estes testes, os filhotes foram submetidos à eutanásia. As análises histológicas, a determinação do conteúdo de mielina e a atividade da acetilcolinesterase (AChE) foram realizadas. O período crítico de intoxicação ocorreu no 4º e 5º dias após a injeção de (PhTe) 2 , quando os sinais de toxicidade foram mais evidentes, caracterizados pelo aparecimento de sinais sistêmicos de toxicidade, disfunções comportamentais, neurotoxicidade e uma alteração no sistema colinérgico. Desta forma, conclui-se que o (PhTe) 2 induziu neurotoxicidade e prejuízos no desenvolvimento comportamental de filhotes de ratos.The purpose of the present study was to investigate if acute exposure to diphenyl ditelluride (PhTe) 2 causes impairment of developmental behavioral performance in rat pups. Rat pups received a single subcutaneous injection of (PhTe) 2 (0.1 mg kg -1 , 3 mL kg -1 ) or vehicle (3 mL kg -1 ) at 14 th postnatal day. After exposure to (PhTe) 2 , the general parameters of neurotoxicity, behavioral tasks, cerebral myelin content, histological analysis and acetilcholinesterase (AChE) activity were performed during seven days. The appearance of classic signs of toxicity, behavioral alterations and the reduction in myelin content were dependent on the time after (PhTe) 2 exposure to pups. Neuronal damage, reduction of myelin content, and the increase in AChE activity occurred mainly at 4 th and 5 th day after (PhTe) 2 exposure, indicating that the critical period of neurotoxicity is coincident with the major behavioral alterations. In conclusion, exposure to (PhTe) 2 induced neurotoxicity and impairment of developmental behavioral in rat pups.Keywords: tellurium, neurotoxicity, developmental behavioral, myelin, acetylcholinesterase IntroductionTellurium (Te) is a metalloid with increasing utilization in rubber, metallurgic and electronics industry because of its unique chemical and physical properties. Similarly, the use of organic Te compounds will increase due to its importance in organic synthesis.1,2 Thus, the incidence of occupational exposure to Te either in elemental, organic or inorganic form has growing rapidly, but the biochemistry and clinical significance of such exposure are poorly understood.Diphenyl ditelluride (PhTe) 2 is an organotellurium compound widely used as intermediate in organic synthesis.2 Besides its use as an organic reactant, (PhTe) 2 has been reported as a neurotoxic compound in adult rodents.3-5 (PhTe) 2 , administered to dams, is teratogenic to rat fetuses, changes behavioral parameters related to neural function and causes oxidative stress in cerebral areas in young rats. [6][7][8] Moretto an...

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“…In recent years, AChE has been associated with non-cholinergic functions within the central nervous system, e.g., degradation of amides (Checler et al 1994), neuronal differentiation and development (Coleman and Taylor 1996;Jones et al 1995;Willbold, 1994,1995), and interactions with excitatory amino acid (Appleyard 1994) and monoaminergic (Abo et al 1992;Ennis and Shipley 1992) neurotransmitters. The relationship of non-cholinergic AChE to monoamines has been best studied in the dopaminergic neurons of the substantia nigra (Greenfield 1991(Greenfield ,1995, and the method described here may prove particularly helpful in examining such functions in noradrenergic and serotonergic nuclei.…”

Section: Discussionmentioning

confidence: 99%

A Simple Enzyme Histochemical Method for the Simultaneous Demonstration of Acetylcholinesterase and Monoamine Oxidase in Fixed-Frozen Sections

Dunning

McHaffie

Stein

1997

J Histochem Cytochem.

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SUMMARYWe describe an enzyme histochemical technique for the simultaneous demonstration of acetylcholinesterase (AChE) and monoamine oxidase (MAO) (Types A, B, or A ϩB) in fixed-frozen sections. Several regions in the mesencephalon and brainstem were examined for both somatic and neuropil labeling. The results obtained are equivalent or superior to those obtained using previous methods for the individual localization of these enzymes. The simultaneous visualization of AChE and MAO in the same section allows the relationship of the two enzymes to be easily assessed with brightfield microscopy.

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Non-cholinergic functions of acetylcholinesterase

Cited by 48 publications

References 9 publications

Regulatory mechanisms that modulate signalling by G-protein-coupled receptors

Regulatory mechanisms that modulate signalling by G-protein-coupled receptors

Diphenyl ditelluride induces neurotoxicity and impairment of developmental behavioral in rat pups

A Simple Enzyme Histochemical Method for the Simultaneous Demonstration of Acetylcholinesterase and Monoamine Oxidase in Fixed-Frozen Sections

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