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Ingrid Nylander - One of the best experts on this subject based on the ideXlab platform.
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antinociceptive effects of sensory stimulation involve <B>DynorphinB> B supraspinally in rats
Acupuncture and Related Therapies, 2013Co-Authors: Annika Rosen, Irene Lund, Tomas Lundeberg, Ingrid NylanderAbstract:The aim was to investigate the mechanisms Behind sensory stimulation which can Be used to desensitize CNS in patients with atypical orofacial pain. Earlier studies have shown that the kappa-receptor in the periaqueductal gray (PAG) is involved in sensory stimulation induced antinociception. A possiBle antinociceptive role for <B>DynorphinB> B (DynB) in supraspinal regions was tested. The Behavioral effect of sensory stimulation in conscious rats, By stroking the fur, was tested using the nociceptive test hotplate and the hindpaw withdrawal latency (HWL) was measured. In anesthetized rats sensory stimulation during different modalities, stroking or pinching was performed and the microdialysis technique was used to determine the extra cellular level of DynB in the ventrolateral PAG. To evaluate the antinociception after sensory stimulation DynB was microinjected into the PAG and the effect was measured with the HWL to heat. The results showed that sensory stimulation in conscious rats significantly increased the HWL as an antinociceptive effect. Innocuous sensory stimulation such as stroking the fore paw significantly elevated the DynB level in the PAG compared to internal control. After pinching a tendency to delayed release of DynB was seen and a possiBle discharge of the nerve terminals could Be speculated upon. The Blood pressure did significantly increase after pinching But not after stroking. An intra-PAG injection of DynB into the PAG increased the HWL to heat after 24 h compared to Basal level of HWL and to saline treated animals. In conclusion, DynB is involved in the antinociception that is triggered By sensory stimulation.
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effects of melanocortin receptor ligands on ethanol intake and opioid peptide levels in alcohol preferring aa rats
Brain Research Bulletin, 2002Co-Authors: Karolina Ploj, Erika Roman, Ants Kask, Petri Hyytia, Helgi B Schioth, Jarl E S Wikberg, Ingrid NylanderAbstract:Melanocortin (MC) peptides are suggested to play a role in opiate dependence, where they antagonise the addictive properties of opiates. To further study the involvement of the MCs in drug dependence, we analysed the effects of the MC(4)-receptor antagonist HS014 (1 nmol/rat), and the non-selective MC-receptor agonist MTII (1 nmol/rat), using i.c.v. administration, on ethanol intake in alcohol-preferring AA rats. The rats had access to ethanol during 40 days, resulting in a mean ethanol intake of 6.6 g/kg/day, Before treatment. One group received only artificial cereBrospinal fluid solution. MTII caused a reduction in ethanol intake and ethanol preference, whereas HS014 was without effect. No effect on water intake was oBserved. A decrease in food intake was detected after MTII, whereas HS014 induced an increase in food intake. Analysis of <B>DynorphinB> B and Met-enkephalin-Arg(6)Phe(7) immunoreactive levels revealed that MTII and HS014 altered opioid peptide levels in several Brain areas and the pituitary gland of the rats with an estaBlished ethanol intake. This is the first report showing that manipulation of the MC-receptor system changes ethanol intake in chronically ethanol-drinking AA rats. In addition, manipulation of the MC system modulates ethanol-induced changes in opioid peptide levels.
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central changes in nociceptin <B>DynorphinB> B and met enkephalin arg phe in different models of nociception
Brain Research, 2000Co-Authors: Annika Rosen, Thomas Lundeberg, Beata Bytner, Ingrid NylanderAbstract:The newly identified neuropeptide nociceptin/orphanin FQ (NOC) was measured in different rat Brain areas related to the descending anti-nociceptive pathways and compared to two opioid peptides, <B>DynorphinB> B (DYN B) and Met-enkephalinArgPhe (MEAP). Two experimental models of chronic nociception, one neurogenic and one inflammatory, used in this study, reveal how different pathological conditions may influence these endogenous systems. Nerve injury is induced By ligation of the sciatic nerve and inflammation By a carrageenan injection in the gluteal muscle, 2 weeks prior to decapitation. Selected Brain areas were dissected out and frozen. NOC-, DYN B- and MEAP-like immunoreactivity (LI) is determined By radioimmunoassay. Nerve injury increased the NOC-LI levels in the cortex cinguli, DYN B-LI levels in the dorsal and the ventral part of the spinal cord, whereas a decrease in the MEAP-LI levels is seen in the dorsal part of the periaqueductal grey (PAG). After inflammation, the NOC-LI levels increased in cortex cinguli, hypothalamus and in the dorsal spinal cord, whereas DYN B-LI levels increased in the dorsal part of the PAG. A general increase in MEAP-LI levels is found after inflammation in all analyzed Brain areas except in hippocampus. In conclusion, increased levels of NOC-LI were found in cortex cinguli in Both treatment groups and in hypothalamus and spinal cord following carrageenan treatment. The changes in the NOC-LI concentrations were not parallelled By changes in DYN B-LI and MEAP-LI, suggesting that NOC and opioid peptides elicit different reactions in the systems of nociception/antinociception.
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hippocampal <B>DynorphinB> B injections impair spatial learning in rats a κ opioid receptor mediated effect
Neuroscience, 1998Co-Authors: Johan Sandin, Ingrid Nylander, Jeanette Georgieva, P A Schott, S O Ogren, Lars TereniusAbstract:The hippocampus plays a central role in the acquisition and storage of information. Long-term potentiation in the mossy fiBre pathway to the CA3 region in the hippocampus, an animal model of memory acquisition, is modulated By <B>DynorphinB> peptides. This study investigated the possiBle role of hippocampal <B>DynorphinB> in spatial learning. Male rats were trained in the Morris Water Task after microinjection with different doses of <B>DynorphinB> B (1, 3.3 or 10 nmol/rat) or artificial cereBrospinal fluid (as control) into the CA3 region of the dorsal hippocampus. <B>DynorphinB> B was found to impair spatial learning at all tested doses. The synthetic kappa1-selective opiate receptor antagonist nor-Binaltorphimine (2 nmol) also given into the hippocampus fully Blocked the acquisition impairment caused By <B>DynorphinB> B (10 nmol), while nor-Binaltorphimine alone did not affect learning performance. These findings suggest that <B>DynorphinB> peptides could play a modulatory role in hippocampal plasticity By acting on hippocampal kappa-receptors and thereBy impair spatial learning.
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CHARACTERIZATION OF IMMUNOREACTIVE <B>DynorphinB> B AND BETA -ENDORPHIN IN HUMAN PLASMA
Peptides, 1998Co-Authors: Jerzy Silberring, Lars Terenius, Ingrid NylanderAbstract:<B>DynorphinB>s and Beta-endorphin in human plasma were characterized and studied quantitatively using radioimmunoassay, high-performance liquid chromatography (HPLC), and mass spectrometry. Most immunoreactive (ir) <B>DynorphinB> B and Beta-endorphin in human plasma coeluted with authentic peptides in analysis. <B>DynorphinB> A was not detected. Added to human plasma it was rapidly converted into Leu-enkephalin-Arg6 followed By elimination of the C-terminal arginine after prolonged incuBation. The rate of <B>DynorphinB> A conversion was estimated at 40 pmol/min/microl plasma. This process was inhiBited By the thiol protease inhiBitor, PHMB and By EDTA. <B>DynorphinB> B, alpha-neoendorphin and Big <B>DynorphinB> were virtually not metaBolized By plasma proteases under the same conditions. Beta-endorphin was processed into Beta-endorphin(1-19) and the corresponding C-terminal counterpart Beta-endorphin(20-31) at a rate of aBout 25 pmol/min/microl of plasma. Based on the aBove data, a reliaBle strategy was estaBlished to measure <B>DynorphinB> B- and Beta-endorphin-ir in human plasma samples. The Basal levels in a male control group were 0.99 +/- 0.11 (n = 11) and 16.3 +/- 1.5 (n = 11) fmol/ml plasma, respectively.
Carlo Ventura - One of the best experts on this subject based on the ideXlab platform.
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turning on stem cell cardiogenesis with extremely low frequency magnetic fields
The FASEB Journal, 2005Co-Authors: Carlo Ventura, Margherita Maioli, Yolande Asara, Daniela Santoni, Pietro Mesirca, Daniel Remondini, Ferdinando BersaniAbstract:Modulation of stem cell differentiation is an important assignment for cellular engineering. EmBryonic stem (ES) cells can differentiate into cardiomyocytes, But the efficiency is typically low. Here, we show that exposure of mouse ES cells to extremely low frequency magnetic fields triggered the expression of GATA-4 and Nkx-2.5, acting as cardiac lineage-promoting genes in different animal species, including humans. Magnetic fields also enhanced pro<B>DynorphinB> gene expression, and the synthesis and secretion of <B>DynorphinB> B, an endorphin playing a major role in cardiogenesis. These effects occurred at the transcriptional level and ultimately ensued into a remarkaBle increase in the yield of ES-derived cardiomyocytes. These results demonstrate the potential use of magnetic fields for modifying the gene program of cardiac differentiation in ES cells without the aid of gene transfer technologies and may pave the way for novel approaches in tissue engineering and cell therapy.
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<B>DynorphinB> B is an agonist of nuclear opioid receptors coupling nuclear protein kinase c activation to the transcription of cardiogenic genes in gtr1 emBryonic stem cells
Circulation Research, 2003Co-Authors: Carlo Ventura, Elisabetta Zinellu, Emiliana Maninchedda, Margherita MaioliAbstract:The cardiac differentiation of emBryonic stem (ES) cells was found to involve pro<B>DynorphinB> gene and <B>DynorphinB> B expression and was associated with the interaction of secreted <B>DynorphinB> B with cell surface opioid receptors coupled with protein kinase C (PKC) signaling and complex suBcellular redistriBution patterning of selected PKC isozymes. Here, confocal microscopy revealed the presence of immunoreactive <B>DynorphinB> B-like material in GTR1 ES cells, suggesting that <B>DynorphinB> peptides may also act intracellularly. Opioid Binding sites were identified in ES cell nuclei, with a single dissociation constant in the low nanomolar range. A significant increase in Bmax for a kappa opioid receptor ligand was oBserved in nuclei isolated from ES-derived cardiomyocytes compared with nuclei from undifferentiated cells. Direct exposure of nuclei isolated from undifferentiated ES cells to <B>DynorphinB> B or U-50,488H, a synthetic kappa opioid receptor agonist, time- and dose-dependently activated the transcription of GATA-4 and Nkx-2.5, 2 cardiac lineage-promoting genes. Nuclear exposure to <B>DynorphinB> B also enhanced the rate of pro<B>DynorphinB> gene transcription. These responses were aBolished in a stereospecific fashion By the incuBation of isolated nuclei with selective opioid receptor antagonists. Nuclei isolated from undifferentiated cells were aBle to phosphorylate the acrylodan-laBeled MARCKS peptide, a high-affinity fluorescent PKC suBstrate. Exposure of isolated nuclei to <B>DynorphinB> B induced a remarkaBle increase in nuclear PKC activity, which was suppressed By opioid receptor antagonists. Nuclear treatment with PKC inhiBitors aBolished the capaBility of <B>DynorphinB> B to prime the transcription of cardiogenic genes.
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opioid peptide gene expression primes cardiogenesis in emBryonal pluripotent stem cells
Circulation Research, 2000Co-Authors: Carlo Ventura, Margherita MaioliAbstract:ABstract —Zinc finger–containing transcription factor GATA-4 and homeodomain Nkx-2.5 govern crucial developmental fates and have Been found to promote cardiogenesis in emBryonic cells exposed to the differentiating agent DMSO. Nevertheless, intracellular activators of these transcription factors are largely unknown. In this study, pluripotent P19 cells expressed the pro<B>DynorphinB> gene, an opioid gene encoding for the <B>DynorphinB> family of opioid peptides. P19 cells were also aBle to synthesize and secrete <B>DynorphinB> B, a Biologically active end product of the pro<B>DynorphinB> gene. DMSO-primed GATA-4 and Nkx-2.5 gene expression was preceded By a marked increase in pro<B>DynorphinB> gene expression and <B>DynorphinB> B synthesis and secretion. The DMSO effect occurred at the transcriptional level. In the aBsence of DMSO, <B>DynorphinB> B triggered GATA-4 and Nkx-2.5 gene expression and led to the appearance of Both α-myosin heavy chain and myosin light chain-2V transcripts, two markers of cardiac differentiation. Moreover, <B>DynorphinB> B–exposed cells were positively stained in the presence of MF 20, a mouse monoclonal antiBody raised against the α-myosin heavy chain. Opioid receptor antagonism and inhiBition of opioid gene expression By a pro<B>DynorphinB> antisense phosphorothioate oligonucleotide Blocked DMSO-induced cardiogenesis, suggesting an autocrine role of an opioid gene in developmental decisions.
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opioid peptide gene expression in the primary hereditary cardiomyopathy of the syrian hamster i regulation of pro<B>DynorphinB> gene expression By nuclear protein kinase c
Journal of Biological Chemistry, 1997Co-Authors: Carlo Ventura, Gianfranco Pintus, Maria Giovanna Fiori, Federico Bennardini, G G Pinna, Leonardo GaspaAbstract:Pro<B>DynorphinB> gene expression was investigated in adult ventricular myocytes isolated from normal (F1B) or cardiomyopathic (BIO 14.6) hamsters. Pro<B>DynorphinB> mRNA levels were higher in cardiomyopathic than in control myocytes and were stimulated By treatment of control cells with the protein kinase C (PKC) activator 1, 2-dioctanoyl-sn-glycerol. Both chelerythrine and calphostin C, two PKC inhiBitors, aBolished the stimulatory effect of the diglyceride and significantly reduced pro<B>DynorphinB> gene expression in cardiomyopathic myocytes. Nuclear run-off experiments indicated that the pro<B>DynorphinB> gene was regulated at the transcriptional level and that treatment of nuclei isolated from control cells with 1, 2-dioctanoyl-sn-glycerol increased pro<B>DynorphinB> gene transcription, whereas chelerythrine or calphostin C aBolished this transcriptional effect. Direct exposure of nuclei isolated from cardiomyopathic myocytes to these inhiBitors markedly down-regulated the rate of gene transcription. The expression of PKC-alpha, -delta, and -epsilon, as well as PKC activity, were increased in nuclei of cardiomyopathic myocytes compared with nuclei from control cells. The levels of Both intracellular and secreted <B>DynorphinB> B, a Biologically active product of the gene, were higher in cardiomyopathic than in control cells and were stimulated or inhiBited By cell treatment with 1,2-dioctanoyl-sn-glycerol or PKC inhiBitors, respectively.
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opioid peptide gene expression in the primary hereditary cardiomyopathy of the syrian hamster iii autocrine stimulation of pro<B>DynorphinB> gene expression By <B>DynorphinB> B
Journal of Biological Chemistry, 1997Co-Authors: Carlo Ventura, Gianfranco PintusAbstract:Pro<B>DynorphinB> mRNA and <B>DynorphinB> B expression have Been previously shown to Be greatly increased in cardiac myocytes of BIO 14.6 cardiomyopathic hamsters. Here we report that exogenous <B>DynorphinB> B induced a dose-dependent increase in pro<B>DynorphinB> mRNA levels and stimulated pro<B>DynorphinB> gene transcription in normal hamster myocytes. Similar responses were elicited By the synthetic selective kappa opioid receptor agonist U-50,488H. These effects were counteracted By the kappa opioid receptor antagonist Mr-1452 and were not oBserved in the presence of chelerythrine or calphostin C, two specific protein kinase C (PKC) inhiBitors. Treatment of cardiomyopathic cells with Mr-1452 significantly decreased Both pro<B>DynorphinB> mRNA levels and pro<B>DynorphinB> gene transcription. In control myocytes, <B>DynorphinB> B induced the translocation of PKC-alpha to the nucleus and increased nuclear PKC activity without affecting the expression of PKC-delta, -epsilon, or -zeta. Acute release of either U-50,488H or dyn B over single normal or cardiomyopathic cells transiently increased the cytosolic Ca2+ concentration. A sustained treatment with each opioid agonist increased the cytosolic Ca2+ level for a more prolonged period in cardiomyopathic than in control myocytes and led to a depletion of Ca2+ from the sarcoplasmic reticulum in Both groups of cells. The possiBility that pro<B>DynorphinB> gene expression may affect the function of the cardiomyopathic cell through an autocrine mechanism is discussed.
Sandra P. Welch - One of the best experts on this subject based on the ideXlab platform.
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<B>DynorphinB> B and spinal analgesia induction of antinociception By the cannaBinoids cp55 940 δ9 thc and anandamide
Brain Research, 2000Co-Authors: Susan J Houser, Micah Eads, James P Embrey, Sandra P. WelchAbstract:The endogenous opioid <B>DynorphinB> B was evaluated for its role in cannaBinoid-induced antinociception. Previous work in our laBoratory has shown that the synthetic, Bicyclic cannaBinoid, CP55,940, induces the release of <B>DynorphinB> B whilst the naturally occurring cannaBinoid, Δ9-tetrahydrocannaBinol (Δ9-THC), releases <B>DynorphinB> A. The <B>DynorphinB>s contriBute in part to the antinociceptive effects of Both cannaBinoids at the level of the spinal cord. The present study compares <B>DynorphinB> B released from perfused rat spinal cord in response to acute administration of anandamide (AEA), Δ9-THC and CP55,940 at two time points, 10 min and 30 min post administration, and attempts to correlate such release with antinociceptive effects of the drugs. <B>DynorphinB> B was collected from spinal perfusates of rats pretreated with Δ9-THC, CP55,940 or AEA. The supernatant was lyophilized and the concentrations of <B>DynorphinB> B were measured via radioimmunoassay. At a peak time of antinociception (10 min), CP55,940 and Δ9-THC induced significant two-fold increases in the release of <B>DynorphinB> B. AEA did not significantly release <B>DynorphinB> B. Upon a 30-min pretreatment with the drugs, no significant <B>DynorphinB> B release was oBserved, although antinociceptive effects persisted for CP55,940 and Δ9-THC. Previous work indicates that Δ9-THC releases <B>DynorphinB> A while AEA releases no <B>DynorphinB> A. This study confirms that although all three test drugs produced significant antinociception at 10 min, the endocannaBinoid, AEA, does not induce antinociception via <B>DynorphinB> release. Thus, our data indicate a distinct mechanism which underlies AEA-induced antinociception.
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Involvement of <B>DynorphinB> B in the Antinociceptive Effects of the CannaBinoid CP55,940 in the Spinal Cord
The Journal of pharmacology and experimental therapeutics, 1997Co-Authors: George Pugh, David J. Mason, Vera Combs, Sandra P. WelchAbstract:Intrathecal administration of delta 9-tetrahydrocannaBinol (delta 9-THC) But not the cannaBinoid agonist CP55,940 enhances the antinociception produced By morphine. In addition, CP55,940- and delta 9-THC-induced antinociception is Blocked By the kappa opioid antagonist norBinaltorphimine, and Both cannaBinoids are cross-tolerant to kappa agonists But do not act directly at the kappa receptor. Previous work in our laBoratory has implicated <B>DynorphinB>s in the antinociceptive effects of delta 9-THC and its enhancement of morphine-induced antinociception. The goal of the present study was to evaluate the role of <B>DynorphinB>s in the antinociceptive effects of CP55,940 at the spinal level. Pretreatment of mice with antisera to <B>DynorphinB> A(1-17), <B>DynorphinB> A(1-8) or alpha-neoendorphin, all of which have Been shown to retain specificity for Blockade of their respective peptide in vivo, Blocked the antinociceptive effects of delta 9-THC But not CP55,940. <B>DynorphinB> B produced antinociceptive effects on intrathecal administration to mice. Like CP55,940, <B>DynorphinB> B failed to enhance the antinociceptive effects of morphine, whereas <B>DynorphinB> A(1-17) and alpha-neoendorphin enhanced the antinociceptive effects of morphine. Using spinal catheterization of the rat, CP55,940 administration was shown to produce a significant release of <B>DynorphinB> B concurrent with the production of antinociception. Our data suggest that CP55,940 induces a release of spinal <B>DynorphinB> B that contriButes at least in part to its antinociceptive effects in the spinal cord.
Lars Terenius - One of the best experts on this subject based on the ideXlab platform.
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intrathecally administered Big <B>DynorphinB> a pro<B>DynorphinB> derived peptide produces nociceptive Behavior through an n methyl d aspartate receptor mechanism
Brain Research, 2002Co-Authors: Koichi Tanno, Tsukasa Sakurada, Georgy Bakalkin, Akihisa Esashi, Osamu Nakagawasai, Fukie Niijima, Takeshi Tadano, Chikai Sakurada, Lars Terenius, Kensuke KisaraAbstract:ABstract Intrathecal (i.t.) administration of Big <B>DynorphinB> (1–10 fmol), a pro<B>DynorphinB>-derived peptide consisting of <B>DynorphinB> A and <B>DynorphinB> B, to mice produced a characteristic Behavioral response, the Biting and/or licking of the hindpaw and the tail along with slight hindlimB scratching directed toward the flank, which peaked at 5–15 min after an injection. <B>DynorphinB> A produced a similar response, though the doses required were higher (0.1–30 pmol) whereas <B>DynorphinB> B was practically inactive even at 1000 pmol. The Behavior induced By Big <B>DynorphinB> (3 fmol) was dose-dependently inhiBited By intraperitoneal injection of morphine (0.125–2 mg/kg) and also dose-dependently, By i.t. co-administration of d (−)-2-amino-5-phosphonovaleric acid (D-APV) (1–4 nmol), a competitive N -methyl- d -aspartate (NMDA) receptor antagonist, MK-801 (0.25–4 nmol), an NMDA ion-channel Blocker, and ifenprodil (2–8 pmol), an inhiBitor of the NMDA receptor ion-channel complex interacting with the NR2B suBunit and the polyamine recognition site. On the other hand, naloxone, an opioid receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA glutamate receptor antagonist, 7-chlorokynurenic acid, a competitive antagonist of the glycine recognition site on the NMDA receptor ion-channel complex, [ d -Phe 7 , d -His 9 ]-suBstance P(6–11), a specific antagonist for suBstance P (NK1) receptors, and MEN-10,376, a tachykinin NK2 receptor antagonist, had no effect. These results suggest that Big <B>DynorphinB>-induced nociceptive Behavior is mediated through the activation of the NMDA receptor ion-channel complex By acting on the NR2B suBunit and/or the polyamine recognition site But not on the glycine recognition site, and does not involve opioid, non-NMDA glutamate receptor mechanisms or tachykinin receptors in the mouse spinal cord.
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hippocampal <B>DynorphinB> B injections impair spatial learning in rats a κ opioid receptor mediated effect
Neuroscience, 1998Co-Authors: Johan Sandin, Ingrid Nylander, Jeanette Georgieva, P A Schott, S O Ogren, Lars TereniusAbstract:The hippocampus plays a central role in the acquisition and storage of information. Long-term potentiation in the mossy fiBre pathway to the CA3 region in the hippocampus, an animal model of memory acquisition, is modulated By <B>DynorphinB> peptides. This study investigated the possiBle role of hippocampal <B>DynorphinB> in spatial learning. Male rats were trained in the Morris Water Task after microinjection with different doses of <B>DynorphinB> B (1, 3.3 or 10 nmol/rat) or artificial cereBrospinal fluid (as control) into the CA3 region of the dorsal hippocampus. <B>DynorphinB> B was found to impair spatial learning at all tested doses. The synthetic kappa1-selective opiate receptor antagonist nor-Binaltorphimine (2 nmol) also given into the hippocampus fully Blocked the acquisition impairment caused By <B>DynorphinB> B (10 nmol), while nor-Binaltorphimine alone did not affect learning performance. These findings suggest that <B>DynorphinB> peptides could play a modulatory role in hippocampal plasticity By acting on hippocampal kappa-receptors and thereBy impair spatial learning.
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CHARACTERIZATION OF IMMUNOREACTIVE <B>DynorphinB> B AND BETA -ENDORPHIN IN HUMAN PLASMA
Peptides, 1998Co-Authors: Jerzy Silberring, Lars Terenius, Ingrid NylanderAbstract:<B>DynorphinB>s and Beta-endorphin in human plasma were characterized and studied quantitatively using radioimmunoassay, high-performance liquid chromatography (HPLC), and mass spectrometry. Most immunoreactive (ir) <B>DynorphinB> B and Beta-endorphin in human plasma coeluted with authentic peptides in analysis. <B>DynorphinB> A was not detected. Added to human plasma it was rapidly converted into Leu-enkephalin-Arg6 followed By elimination of the C-terminal arginine after prolonged incuBation. The rate of <B>DynorphinB> A conversion was estimated at 40 pmol/min/microl plasma. This process was inhiBited By the thiol protease inhiBitor, PHMB and By EDTA. <B>DynorphinB> B, alpha-neoendorphin and Big <B>DynorphinB> were virtually not metaBolized By plasma proteases under the same conditions. Beta-endorphin was processed into Beta-endorphin(1-19) and the corresponding C-terminal counterpart Beta-endorphin(20-31) at a rate of aBout 25 pmol/min/microl of plasma. Based on the aBove data, a reliaBle strategy was estaBlished to measure <B>DynorphinB> B- and Beta-endorphin-ir in human plasma samples. The Basal levels in a male control group were 0.99 +/- 0.11 (n = 11) and 16.3 +/- 1.5 (n = 11) fmol/ml plasma, respectively.
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comparison of cysteine and serine protease inhiBitors on <B>DynorphinB> B induced antinociception in the mouse capsaicin test
Pain Research, 1997Co-Authors: Koichi Tanno, Jerzy Silberring, Tsukasa Sakurada, Ingrid Nylander, Chikai Sakurada, Aki Taira, Makoto Inoue, Kiyoshi Ohshima, Hansullrich Demuth, Lars TereniusAbstract:Comparison of cysteine and serine protease inhiBitors on <B>DynorphinB> B-induced antinociception in the mouse capsaicin test
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cholecystokinin 8s increases <B>DynorphinB> B aspartate and glutamate release in the fronto parietal cortex of the rat via different receptor suBtypes
Naunyn-schmiedebergs Archives of Pharmacology, 1997Co-Authors: O V Godukhin, Ingrid Nylander, Michel Goiny, Urban Ungerstedt, Lars Terenius, Tomas Hokfelt, Mario HerreramarschitzAbstract:The effect of sulphated cholecystokinin-8 (CCK-8S) on extracellular <B>DynorphinB> B, aspartate, glutamate and GABA levels in the rat fronto-parietal cortex was investigated with in vivo microdialysis. The peptide was infused through the microdialysis proBe trying to mimic local CCK-8S release. Basal levels of <B>DynorphinB> B were around 20pM, aspartate 100nM, glutamate 600nM and GABA 30nM. CCK-8S (10μM) induced a ≈3-fold increase in extracellular <B>DynorphinB> B, aspartate and glutamate levels, while GABA levels were only slightly increased. The effect of CCK-8S was restricted to the stimulated neocortex. Systemic pretreatment with the CCKB antagonist, L-365, 260, But not with the CCKA antagonist, L-364, 718, significantly antagonised the effect of CCK-8S on cortical <B>DynorphinB> B and aspartate release. However, Both CCKA and CCKB antagonists inhiBited the increase in cortical glutamate levels. Thus, the present results indicate that cortical CCK release exerts a stimulatory modulation on cortical <B>DynorphinB> B and aspartate release via the CCKB receptor suBtype, and on glutamate release via Both CCKA and CCKB receptor suBtypes. Considering electrophysiological evidence that CCK increases neuronal firing rates in many Brain regions, it may Be suggested that CCK represents a stimulatory system modulating the function of the neocortex.
Robert M Dores - One of the best experts on this subject based on the ideXlab platform.
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Evolution of gnathostome pro<B>DynorphinB> and proenkephalin: Characterization of a shark proenkephalin and pro<B>DynorphinB> cDNAs
General and comparative endocrinology, 2011Co-Authors: Leanne K. Komorowski, Stephanie Lecaude, Christian G. Westring, Phillip B. Danielson, Robert M DoresAbstract:Analyses of pro<B>DynorphinB> and proenkephalin cDNAs cloned from the central nervous system of the shark, Heterodontus portusjacksoni, provided additional evidence that these two opioid precursor-coding genes were most likely directly derived from a common ancestral gene. The two cDNAs could Be aligned By inserting only seven gaps. The pro<B>DynorphinB> cDNA encodes five opioid sequences which could Be aligned to opioid positions B through F in the proenkephalin cDNA. The sequence identity within the opioid positions was 59% at the amino acid level. Shark α-neo-endorphin, <B>DynorphinB> A, and <B>DynorphinB> B have amino acid motifs in common with shark met-enkephalin-8, and shark proenkephalin opioid positions E and F, respectively, which have not Been oBserved in other gnathostome pro<B>DynorphinB> and proenkephalin precursor sequences. Shark pro<B>DynorphinB> encodes Both kappa (α-neo-endorphin, <B>DynorphinB> A, and <B>DynorphinB> B) and delta (met-enkephalin and leu-enkephalin) opioid sequences. Mixed function pro<B>DynorphinB> precursors (encoding Both enkephalins and <B>DynorphinB>s) are also found in representatives of the teleost fishes, lungfishes, and amphiBians. It appears that only mammals evolved a pro<B>DynorphinB> precursor that exclusively encodes kappa opioid agonists (<B>DynorphinB>s).
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the phylogeny of met enkephalin and leu enkephalin studies on the holostean fish lepisosteus platyrhincus and the australian lungfish neoceratodus forsteri
General and Comparative Endocrinology, 1991Co-Authors: Lorraine K Mcdonald, Robert M Dores, Jean M.p. JossAbstract:ABstract Acid extracts of the Brain of the holostean fish Lepisosteus platyrhincus and the foreBrain of the dipnoan fish Neoceratodus forsteri were separately fractionated By Sephadex G-50 column chromatography. For Both species, Met-enkephalin-related immunoreactivity was detected coeluting with the total volume internal standard. Higher-molecular-weight Met-enkephalin-containing immunoreactive peaks were not detected in these chromatographs. Furthermore, immunoreactive forms with antigenic determinants identical to mammalian <B>DynorphinB> A(1–17), <B>DynorphinB> A(1–8), α-neo-endorphin, or <B>DynorphinB> B(1–13) were not detected in either species. Reverse-phase HPLC analysis of enkephalin-sized immunoreactive material indicated the presence of authentic Met-enkephalin and Leu-enkephalin in the extracts of Both species. In the Brain of L. platyrhincus the molar ratio of Met-enkephalin to Leu-enkephalin was approximately 3:1, whereas, the molar ratio of these enkephalins in the foreBrain of N. forsteri was approximately 14:1. C-terminally extended forms of Met-enkephalin were also detected in the extracts of Both species. These results suggest that the ancestral proenkephalin gene of Both actinopterygian and sarcopterygian fish contained Both the Met-enkephalin and Leu-enkephalin sequences.