Morphine modulates IL-1 activation of fos in the rat hypothalamus
By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few...
Ausführliche Beschreibung
Gespeichert in:
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1994 |
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| Reproduktion: |
Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 |
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| Übergeordnetes Werk: |
in: Regulatory Peptides - Amsterdam : Elsevier, 53(1994), Seite S265-S266 |
| Übergeordnetes Werk: |
volume:53 ; year:1994 ; pages:S265-S266 |
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| 520 | |a By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. | ||
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(DE-627)NLEJ186792964 (DE-599)GBVNLZ186792964 DE-627 ger DE-627 rakwb eng Morphine modulates IL-1 activation of fos in the rat hypothalamus 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Chang, S.L. oth Zadina, J.E. oth Niu, Y.F. oth Thompson, J. oth in Regulatory Peptides Amsterdam : Elsevier 53(1994), Seite S265-S266 (DE-627)NLEJ186750862 (DE-600)1498712-0 0167-0115 nnns volume:53 year:1994 pages:S265-S266 http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90341-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 53 1994 S265-S266 |
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(DE-627)NLEJ186792964 (DE-599)GBVNLZ186792964 DE-627 ger DE-627 rakwb eng Morphine modulates IL-1 activation of fos in the rat hypothalamus 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Chang, S.L. oth Zadina, J.E. oth Niu, Y.F. oth Thompson, J. oth in Regulatory Peptides Amsterdam : Elsevier 53(1994), Seite S265-S266 (DE-627)NLEJ186750862 (DE-600)1498712-0 0167-0115 nnns volume:53 year:1994 pages:S265-S266 http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90341-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 53 1994 S265-S266 |
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(DE-627)NLEJ186792964 (DE-599)GBVNLZ186792964 DE-627 ger DE-627 rakwb eng Morphine modulates IL-1 activation of fos in the rat hypothalamus 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Chang, S.L. oth Zadina, J.E. oth Niu, Y.F. oth Thompson, J. oth in Regulatory Peptides Amsterdam : Elsevier 53(1994), Seite S265-S266 (DE-627)NLEJ186750862 (DE-600)1498712-0 0167-0115 nnns volume:53 year:1994 pages:S265-S266 http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90341-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 53 1994 S265-S266 |
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(DE-627)NLEJ186792964 (DE-599)GBVNLZ186792964 DE-627 ger DE-627 rakwb eng Morphine modulates IL-1 activation of fos in the rat hypothalamus 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Chang, S.L. oth Zadina, J.E. oth Niu, Y.F. oth Thompson, J. oth in Regulatory Peptides Amsterdam : Elsevier 53(1994), Seite S265-S266 (DE-627)NLEJ186750862 (DE-600)1498712-0 0167-0115 nnns volume:53 year:1994 pages:S265-S266 http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90341-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 53 1994 S265-S266 |
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(DE-627)NLEJ186792964 (DE-599)GBVNLZ186792964 DE-627 ger DE-627 rakwb eng Morphine modulates IL-1 activation of fos in the rat hypothalamus 1994 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Chang, S.L. oth Zadina, J.E. oth Niu, Y.F. oth Thompson, J. oth in Regulatory Peptides Amsterdam : Elsevier 53(1994), Seite S265-S266 (DE-627)NLEJ186750862 (DE-600)1498712-0 0167-0115 nnns volume:53 year:1994 pages:S265-S266 http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90341-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 53 1994 S265-S266 |
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Morphine modulates IL-1 activation of fos in the rat hypothalamus |
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By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. |
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By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. |
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By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ186792964</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707060404.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070506s1994 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ186792964</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVNLZ186792964</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Morphine modulates IL-1 activation of fos in the rat hypothalamus</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1994</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">By using FOS proto-oncogene protein as a marker for neuronal activity induced by an extracellular stimulus, we have shown that several hypothalamic nuclei are sites of action for interleukin-1 (IL-1). These nuclei, including the paraventricular (PVN) and supraoptic (SON) nuclei, have relatively few IL-1 receptors. One of the possibilities for this dysjunction may be that IL-1 acts on receptors other than currently defined IL-1 receptors to induce FOS activation. Acute subcutaneous morphine treatment also increased FOS immunoreactivity in several hypothalamic nuclei including PVN and SON. Taken together, these results suggest the possibility of an interaction between morphine and IL-1 in the hypothalamic PVN and SON. The PVN and SON have been suggested to be involved in a neuroendocrine-immune axis. In this study we examined the effects of chronic morphine on IL-1 activation of FOS. The chronic morphine pretreatment consisted of 2 pellets on the 1st day and 4 pellets on the 2nd day, 75 mg morphine sulfate/pellet. This regimen has been shown to induce a high degree of tolerance and dependence, and it markedly decreased IL-1 activation of c-fos mRNA in the hypothalamus and FOS immunoreactivity in the hypothalamic PVN and SON nuclei. These data suggest that attenuation of IL-1 activation of FOS expression in the hypothalamus may be a mechanism by which morphine tolerance and dependence affects the neuro-endocrine-immune axis.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Elsevier Journal Backfiles on ScienceDirect 1907 - 2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chang, S.L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zadina, J.E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Niu, Y.F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Thompson, J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Regulatory Peptides</subfield><subfield code="d">Amsterdam : Elsevier</subfield><subfield code="g">53(1994), Seite S265-S266</subfield><subfield code="w">(DE-627)NLEJ186750862</subfield><subfield code="w">(DE-600)1498712-0</subfield><subfield code="x">0167-0115</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:53</subfield><subfield code="g">year:1994</subfield><subfield code="g">pages:S265-S266</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90341-7</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_H</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SDJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">53</subfield><subfield code="j">1994</subfield><subfield code="h">S265-S266</subfield></datafield></record></collection>
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