O-methyltransferases involved in the biosynthesis of volatile phenolic derivatives in rose petals.
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Rose (Rosa hybrida) flowers produce and emit a diverse array of volatiles, characteristic to their unique scent. One of the most prominent compounds in the floral volatiles of many rose varieties is the methoxylated phenolic derivative 3,5-dimethoxytoluene (orcinol dimethyl ether). Cell-free extracts derived from developing rose petals displayed O-methyltransferase (OMT) activities toward several phenolic substrates, including 3,5-dihydroxytoluene (orcinol), 3-methoxy,5-hydroxytoluene (orcinol monomethyl ether), 1-methoxy, 2-hydroxy benezene (guaiacol), and eugenol. The activity was most prominent in rose cv Golden Gate, a variety that produces relatively high levels of orcinol dimethyl ether, as compared with rose cv Fragrant Cloud, an otherwise scented variety but which emits almost no orcinol dimethyl ether. Using a functional genomics approach, we have identified and characterized two closely related cDNAs from a rose petal library that each encode a protein capable of methylating the penultimate and immediate precursors (orcinol and orcinol monomethyl ether, respectively) to give the final orcinol dimethyl ether product. The enzymes, designated orcinol OMTs (OOMT1 and OOMT2), are closely related to other plant methyltransferases whose substrates range from isoflavones to phenylpropenes. The peak in the levels of OOMT1 and OOMT2 transcripts in the flowers coincides with peak OMT activity and with the emission of orcinol dimethyl ether. (+info)
Mechanism of regulation of casein kinase I activity by group I metabotropic glutamate receptors.
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Previously, we reported that (S)-3,5-dihydroxypenylglycine (DHPG), an agonist for group I metabotropic glutamate receptors (mGluRs), stimulates CK1 and Cdk5 kinase activities in neostriatal neurons, leading to enhanced phosphorylation, respectively, of Ser-137 and Thr-75 of DARPP-32 (dopamine and cAMP-regulated phosphoprotein, 32 kDa). We have now investigated the signaling pathway that leads from mGluRs to casein kinase 1 (CK1) activation. In mouse neostriatal slices, the effect of DHPG on phosphorylation of Ser-137 or Thr-75 of DARPP-32 was blocked by the phospholipase Cbeta inhibitor, the Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA/AM), and the calcineurin inhibitor cyclosporin A. In neuroblastoma N2a cells, the effect of DHPG on the activity of transfected HA-tagged CK1(epsilon) was blocked by BAPTA/AM and cyclosporin A. In neostriatal slices, the effect of DHPG on Cdk5 activity was also abolished by BAPTA/AM and cyclosporin A, presumably through blocking activation of CK1. Metabolic labeling studies and phosphopeptide mapping revealed that a set of C-terminal sites in HA-CK1epsilon were transiently dephosphorylated in N2a cells upon treatment with DHPG, and this was blocked by cyclosporin A. A mutant CK1epsilon with a nonphosphorylatable C-terminal domain was not activated by DHPG. Together, these studies suggest that DHPG activates CK1(epsilon) via Ca(2+)-dependent stimulation of calcineurin and subsequent dephosphorylation of inhibitory C-terminal autophosphorylation sites. (+info)
Different metabotropic glutamate receptors play opposite roles in synaptic plasticity of the rat medial vestibular nuclei.
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In the medial vestibular nuclei (MVN) of rat brainstem slices, the role of group II and III metabotropic glutamate receptors (mGluRs) and of the subtypes of group I mGluRs: mGluR1, mGluR5, was investigated in basal synaptic transmission and in the induction and maintenance of long-term potentiation (LTP). We used selective antagonists and agonists for mGluRs and we analysed the field potentials evoked by vestibular afferent stimulation before and after high-frequency stimulation (HFS) to induce LTP. The group II and III mGluR antagonist, (R,S)-alpha-2-methyl-4sulphonophenylglycine (MSPG), induced LTP per se and caused a reduction of the paired-pulse facilitation (PPF) ratio indicating an enhancement of glutamate release. This suggests that group II and III mGluRs are activated under basal conditions to limit glutamate release. Both the group II and III mGluR selective antagonists, 2S-2-amino-2-(1S,2S-2-carboxycycloprop-1-yl)-3-(xanth-9-yl)propanoate (LY341495) and (R,S)-alpha-methylserine-O-phosphate (MSOP), induced LTP, and the selective agonists, (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC) and L(+)-2-amino-4-phosphonobutyric acid (L-AP4) depressed the field potentials and prevented HFS-LTP, with a prevailing contribution of group II mGluRs over that of group III mGluRs. The mGluR1 antagonist, 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester (CPCCOEt) prevented the full development and maintenance of HFS-LTP. By contrast, the mGluR5 antagonist, 2-methyl-6-phenylethynylpyridine (MPEP) induced LTP per se, which was impeded by CPCCOEt, and it had no effect on LTP once induced by HFS. The PPF analysis showed an enhancement of glutamate release during MPEP potentiation. The group I mGluR agonist, (R,S)-3,5-dihydroxyphenylglycine (DHPG) induced LTP per se, which was blocked by CPCCOEt. By contrast the mGluR5 agonist, (R,S)-2-chloro-5-hydroxypheylglycine (CHPG) prevented LTP elicited by HFS and DHPG as well. In conclusion vestibular LTP is inhibited by group II and III mGluRs during the early induction phase while it is facilitated by mGluR1 for achieving its full expression and consolidation. An additional inhibitory control is exerted by mGluR5 at the level of this facilitatory phase. (+info)
The group I metabotropic glutamate receptor agonist (S)-3,5-dihydroxyphenylglycine induces a novel form of depotentiation in the CA1 region of the hippocampus.
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The ability of activation of group I metabotropic glutamate receptor (mGluR) to induce depotentiation was investigated at Schaffer collateral-CA1 synapses of rat hippocampal slices. Brief bath application (5 min) of group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG) (10 microm) induced a long-term depression of synaptic transmission or depotentiation (DEP) of previously established long-term potentiation (LTP), which was independent of NMDA or A(1) adenosine receptor activation. This DHPG-DEP was observed when DHPG was delivered 3 min after LTP induction. However, when DHPG was applied at 10 or 30 min after LTP induction, significantly less depotentiation was found. DHPG-DEP (1) is reversible and has the ability to unsaturate LTP, (2) is synapse specific, (3) does not require concurrent synaptic stimulation, (4) is mechanistically distinct from NMDA receptor-dependent depotentiation, (5) requires mGluR5 activation, (6) requires rapamycin-sensitive mRNA translation signaling, (7) does not require phospholipase C or protein phosphatase activation, and (8) is not associated with a change in paired-pulse (PP) facilitation. In addition, the ability of DHPG to reverse LTP was mimicked by a long train of low-frequency (1 Hz/15 min) PP stimulation. Moreover, the expression of DHPG-DEP is associated with a reduction in the increase of the surface expression of AMPA receptors seen with LTP. These results suggest that the activation of mGluR5 and in turn the triggering of a protein synthesis-dependent internalization of synaptic AMPA receptors may contribute to the DHPG-DEP in the CA1 region of the hippocampus. (+info)
Ardisiphenols and other antioxidant principles from the fruits of Ardisia colorata.
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Novel alkylphenols, ardisiphenols A-C (1-3) and a novel bergenin derivative, demethoxybergenin (10) were isolated from the fruits of Ardisia colorata (Myrsinaceae), together with known alkylresorcinols (4-6), embelin (7), myricetin (8), quercetin (9), bergenin (11), norbergenin (12), kaempferol (13), quercetin-3-O-beta-D-glucopyranoside (14) and gallic acid (15). Their structures were determined by NMR, MS(/MS) analyses and other spectroscopic methods. Ardisiphenols showed moderate scavenging activities toward 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals and showed cytotoxicity against the murine breast cancer cell line, FM3A. (+info)
Biosynthesis of bisorbicillinoid in Trichoderma sp. USF-2690; evidence for the biosynthetic pathway, via sorbicillinol, of sorbicillin, bisorbicillinol, bisorbibutenolide, and bisorbicillinolide.
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An incorporation study of [1-(13)C] and [1,2-(13)C2] labeled sodium acetates into sorbicillinol 1 established a ring closure system between C-1 and C-6 and the positions that were oxidized and/or methylated on a hexaketide chain. Subsequent investigations, using 13C-labeled 1 prepared from [1-(13)C] labeled sodium acetate, clearly demonstrated that both bisorbicillinol 2 and sorbicillin 6 incorporated 13C-labeled 1 into their carbon skeletons. 13C-labeled bisorbicillinols 2 derived from [1-(13)C]- and [2-(13)C]-labeled sodium acetates clearly indicate that these were on the biosynthetic route from 1 to bisorbibutenolide (bislongiquinolide) 3 and bisorbicillinolide 4 via 2 as a branching point in the fungus. (+info)
Distinct functional roles of the metabotropic glutamate receptors 1 and 5 in the rat globus pallidus.
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Group I metabotropic glutamate receptors (mGluRs) 1 and 5 frequently colocalize in the same neurons throughout the CNS. Because both receptors can couple to the same effector systems, the purpose of their cellular coexpression remains unclear. Here, we report that group I mGluR1 and mGluR5 have distinct functional roles in type II neurons of the rat globus pallidus (GP). Type II GP neurons form a large population of GABAergic projection neurons that are characterized by the presence of inwardly rectifying current I(h), low-threshold voltage-activated calcium current I(t), and activity at rest. Although immunocytochemical analysis reveals a high degree of neuronal colocalization of the two group I mGluRs in the GP, activation of mGluR1 only directly depolarizes type II GP neurons. Interestingly, blockade of mGluR5 by a highly selective antagonist, methylphenylethynylpyridine, leads to the potentiation of the mGluR1-mediated depolarization in this neuronal subpopulation. Metabotropic GluR1 desensitizes during repeated activation with the agonist in type II GP neurons, and blocking mGluR5 prevents the desensitization of the mGluR1-mediated depolarization. Elimination of the activity of protein kinase C (PKC) by an application of 1 microm bisendolylmaleimide or 1 microm chelerythrine, both protein kinase C inhibitors, potentiates the mGluR1-mediated response and prevents the desensitization of mGluR1 in type II GP neurons, suggesting that the effect of mGluR5 on mGluR1 signaling may involve PKC. Together, these data illustrate a novel mechanism by which mGluR1 and mGluR5, members of the same family of G-protein-coupled receptors, can interact to modulate neuronal activity in the rat GP. (+info)
New surgical technique of left ventricular free wall rupture: double patch sealing method.
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We experienced two cases of left ventricular free wall rupture (LVFWR) following acute myocardial infarction (AMI). Case 1, with the blowout type of LVFWR was initially closed by direct suture, followed by hemostasis using a double patch sealing method (DPS) by which the tear was doubly sealed with large and small bovine pericardium patches to which GRF glue was applied. Case 2 with the oozing type of LVFWR was treated only using DPS. Complete hemostasis was achieved in both cases, and aneurysmal dilatation or constrictive heart failure were not detected by postoperative left ventriculography. Therefore, DPS may be useful for treating LVFWR following AMI. (+info)