Neutral endopeptidase-24.11, μ and δ opioid receptors after selective brain lesions: an autoradiographic study

Waksman, Gilles; Hamel, Édith; Delay‐Goyet, Philippe; Roques, Bernárd P.

doi:10.1016/0006-8993(87)91663-5

Cited by 57 publications

(31 citation statements)

References 53 publications

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“…Peroxidase immunocytochemistry confirmed the presence of enkephalinase immunostaining along the plasma membrane of both dendritic shafts and dendritic spines. This finding is consistent with the marked decrease in enzymatic activity (Malfroy et al, 1979), enkephalinase immunoreactivity (Pollard et al, 1987b), and binding of tritiated enkephalinase inhibitors (Waksman et al, 1987) reported in the rat neostriatum following local injection of kainic acid. It also conforms to the presence of a large number of neostriatal perikarya reactive for enkephalinase in material processed by histochemistry (Back and Gorenstein, 1989) or found to express enkephalinase mRNA by in situ hybridization (Pollard et al, 1989b;Wilcox et al, 1989).…”

Section: Discussion Topographic Distribution Of Enkephalinase Immunorsupporting

confidence: 78%

“…Consistent with this interpretation are the reports of intense labeling of striatofugal pathways in sections of pig (Barnes et al, 1988a) and rat (Pollard et al, 1987b(Pollard et al, , 1989a brain immunoreacted for enkephalinase, as well as the frequency with which interfaces between myelinated axons and their myelin sheaths were found to be labeled in our immunoradioautographic material. Also consistent with this view is the substantial drop in enkephalinase activity and binding of radiolabeled inhibitors recorded in the globus pallidus and substantia nigra following injection of kainic acid (Waksman et al, 1986b;Pollard et al, 1987b) or colchicine (Waksman et al, 1987) into the caudate putamen.…”

Section: Discussion Topographic Distribution Of Enkephalinase Immunorsupporting

confidence: 60%

“…Others could theoretically correspond to projections from the cerebral cortex, because the latter has been shown to contain both perikarya histochemically reactive for enkephalinase (Back and Gorenstein, 1989) and neurons hybridizing enkephalinase mRNA (Wilcox et al, 1989). A cortical origin appears unlikely, however, given that cortical ablation was found to not modify the binding of the enkephalinase inhibitor 3H-HACBO-gly in the rat neostriatum (Waksman et al, 1987). In contrast, lesions of the dopaminergic neostriatal pathway were found to induce a small but significant decrease of enkephalinase activity in rat striatal membranes, suggesting that a proportion of the enkephalinase-immunoreactive axons might be originating from the substantia nigra (Malfroy et al, 1979).…”

Section: Discussion Topographic Distribution Of Enkephalinase Immunormentioning

confidence: 99%

“…Also, intense enkephalinase activity was observed over fiber bundles linking the neostriatum to the globus pallidus, the entopeduncular nucleus, and the substantia nigra (Waksman et al, 1986b(Waksman et al, , 1987Pollard et al, 1987b;Barnes et al, 1988a). Additional lines of evidence supporting the concept of a neuronal localization of enkephalinase include the presence of intense peptidase activity within synaptosomal membrane fractions (Alstein and Vogel, 1980;De la Baume et al, 198 1) and the decrease of enkephalinase activity (Malfroy et al, 1979) enkephalinase immunoreactivity (Pollard et al, 1987b), and binding of enkephalinase inhibitors (Waksman, 1986b(Waksman, , 1987 observed after intracerebral injections of neurotoxins. Whether enkephalinase is also associated with glial components in the CNS remains a matter of controversy.…”

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Electron microscopic localization of immunoreactive enkephalinase (EC 3.4.24.11) in the neostriatum of the rat

et al. 1990

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The fine structural distribution of the enzyme-neutral endopeptidase EC 3.4.24.11 (enkephalinase) was examined by immunoradioautography (using an iodinated monoclonal antibody) and peroxidase immunocytochemistry (using the same probe in nonradioactive form) in the neostriatum of the rat. At the light microscopic level, both techniques revealed a heterogeneous distribution of immunoreactive enkephalinase in the caudoputamen, characterized by the presence of patches of intense immunolabeling prominent against a relatively strong immunoreactive matrix, a pattern reminiscent of mu opioid receptors radioautographically labeled in the same region. Pilot experiments indicated that fixation of the brain with a mixture of 4% paraformaldehyde, 0.05% glutaraldehyde, and 0.2% picric acid did not modify the distribution and only slightly reduced the intensity of striatal enkephalinase antigenicity, provided that the post-fixation period did not exceed 1 hr. In the neostriatum of animals fixed according to this protocol, enkephalinase immunoreactivity was found by electron microscopic immunoradioautography to be exclusively confined to neuronal and glial membrane interfaces. Immunoperoxidase cytochemistry confirmed the association of immunoreactive enkephalinase with the plasma membrane of neurons and, to a lesser extent, of astrocytes and oligodendrocytes. Both immunoradioautographic and immunoperoxidase techniques revealed a predominant association of the enzyme with neuronal perikarya and dendrites. The morphological features of the labeled perikarya, together with the presence of immunoreactive dendritic spines, suggested that some of these neurons corresponded to striatofugal medium spiny neurons. Immunoreactive enkephalinase was also detected at the level of myelinated and unmyelinated axons and axon terminals. These axons could potentially have originated from intrinsic striatal neurons or from the substantia nigra. Statistical analysis of silver grain distribution in electron microscopic immunoradioautographs indicated that immunoreactive enkephalinase was not preferentially concentrated at the level of specific membrane interfaces, but rather, was more or less uniformly distributed on the surface of neurons and/or glial cells. A similarly diffuse localization of the enzyme was apparent in peroxidase-reacted material, though the latter technique also revealed a microheterogeneity in the deposition of the reaction product along the labeled membranes. Finally, quantitative analysis of immunoradioautographs clearly indicated an absence of enkephalinase enrichment at the level of synaptic junctions. The similarity between the light and electron microscopic distribution of enkephalinase observed in the present study, and that previously reported for mu opioid receptors, lends support to the concept that this ectoenzyme may be involved in the inactivation of endogenous opioids in the mammalian neostriatum.

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Section: Discussion Topographic Distribution Of Enkephalinase Immunorsupporting

confidence: 78%

Section: Discussion Topographic Distribution Of Enkephalinase Immunorsupporting

confidence: 60%

Section: Discussion Topographic Distribution Of Enkephalinase Immunormentioning

confidence: 99%

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Electron microscopic localization of immunoreactive enkephalinase (EC 3.4.24.11) in the neostriatum of the rat

et al. 1990

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“…However, the inhibitory e ect of m-opioids on nigrostriatal DA release seems to be indirect involving other neurotransmitters locally in the striatum. Thus, recent studies have indicated that m-opioid receptors are not located in the terminals of nigrostriatal dopaminergic neurones (Smith et al, 1993;Trovero et al, 1990;Waksman et al, 1987), although selective lesions of nigrostriatal dopaminergic neurones induce considerable loss (about 30%) of m-opioid binding sites in the striatum (Bodnar et al, 1988;Eghbali et al, 1987;Smith et al, 1993). Striatal dopamine release is under the regulatory control of multiple excitatory and inhibitory neurotransmitters including glutamate, acetylcholine, dynorphins, and GABA (Cheramy et al, 1990;Ronken et al, 1993), and morphine might either activate the inhibitory mechanisms or inhibit excitatory mechanisms controlling DA release within the striatum.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Piepponen

Mikkola

Ruotsalainen

et al. 1999

British J Pharmacology

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1 The e ect of intrastriatally-administered morphine on striatal dopamine (DA) release was studied in freely moving rats. Morphine (1, 10 or 100 mM) was given into the striatum by reversed microdialysis, and concentrations of DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were simultaneously measured from the striatal dialysates. 2 Intrastriatally-administered morphine signi®cantly and dose-dependently decreased the extracellular concentration of DA, the concentrations of the acidic DA metabolites were only slightly decreased. The e ect of morphine was antagonized by naltrexone (2.25 mg kg 71 , s.c.). Pretreatment with a preferential k-opioid receptor antagonist, MR2266 [(7)-5,9 alpha-diethyl-2-(3-furylmethyl)-2'-hydroxy-6,7-benzomorphane; 1 mg kg 71 , s.c.], had no e ect on the decrease of extracellular DA evoked by intrastriatal morphine (100 mM). 3 Intrastriatal administration of the selective m-opioid receptor agonist [D-Ala 2 ,MePhe 4 ,Gly-ol 5 ] enkephalin (DAMGO; 1 mM), signi®cantly decreased the extracellular concentration of DA in the striatum. 4 When the rats were given morphine repeatedly in increasing doses (10 ± 25 mg kg 71 , s.c.) twice daily for 7 days and withdrawn for 48 h, the decrease of extracellular DA induced by morphine (100 mM) was signi®cantly less than that seen in saline-treated controls. 5 Our results show that besides the well-known stimulatory e ect there is a local inhibitory component in the action of morphine on striatal DA release in the terminal regions of nigrostriatal DA neurones. Tolerance develops to this inhibitory e ect during repeated morphine treatment. Furthermore, our results suggest that the e ect of intrastriatally-administered morphine is mediated by the m-opioid receptors.

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Effect of cocaine and morphine on neutral endopeptidase activity of human peripheral blood mononuclear cells cultured with lectins

Leoni

Losa

1993

Cell Biochemistry & Function

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We have tested the effect of alkaloids (cocaine, morphine) and enkephalins on neutral endopeptidase of peripheral blood mononuclear cells activated by lectins. When treated with concanavalin A and cocaine, peripheral blood mononuclear cells showed an enhanced activity (+110 per cent) of the membrane neutral endopeptidase, which was not related to the expression of the common acute lymphoblastic leukemia antigen at the cell surface, although both molecules have the identical amino acid sequence. Phytohemagglutinin-P, morphine and synthetic enkephalins did not induce the activity of neutral endopeptidase nor the expression of common acute lymphoblastic leukemia antigen. Our findings suggested that the drugs of abuse, cocaine and morphine, affected specific membrane constituents without altering proliferation, subcellular localization of membrane enzymes or the surface immune phenotype of peripheral blood mononuclear cells.

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Neutral endopeptidase-24.11, μ and δ opioid receptors after selective brain lesions: an autoradiographic study

Cited by 57 publications

References 53 publications

Electron microscopic localization of immunoreactive enkephalinase (EC 3.4.24.11) in the neostriatum of the rat

Electron microscopic localization of immunoreactive enkephalinase (EC 3.4.24.11) in the neostriatum of the rat

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Effect of cocaine and morphine on neutral endopeptidase activity of human peripheral blood mononuclear cells cultured with lectins

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