Analyses of signal transduction cascades in rat pinealocytes reveal a switch in cholinergic signaling during postnatal development
In the rat pineal gland, norepinephrine activates α 1- and β-adrenergic receptors and triggers melatonin production through an increase in the intracellular calcium concentration ([Ca 2+] i ) and stimulation of the cAMP/cAMP responsive element-binding protein (CREB) cascade. VIP and PACAP also eleva...
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| Veröffentlicht in: | Brain research 1999-06, Vol.833 (1), p.39-50 |
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| creator | Schomerus, Christof Laedtke, Elke Korf, Horst-Werner |
| description | In the rat pineal gland, norepinephrine activates α
1- and β-adrenergic receptors and triggers melatonin production through an increase in the intracellular calcium concentration ([Ca
2+]
i
) and stimulation of the cAMP/cAMP responsive element-binding protein (CREB) cascade. VIP and PACAP also elevate the intracellular cAMP level and promote melatonin formation. Finally, ACh antagonizes the norepinephrine-induced hormone synthesis via nicotinic acetylcholine receptors and subsequent activation of voltage-gated calcium channels. By immuno(cyto)chemical demonstration of phosphorylated CREB and calcium imaging we have investigated the temporal relationship between the maturation of these signaling pathways and the rhythmic onset of melatonin biosynthesis in developing rat pinealocytes. Norepinephrine-regulated calcium signaling and phosphorylation of CREB are already fully developed at birth, i.e., prior to ingrowth of the sympathetic innervation into the pineal parenchyma, and appear to develop in an innervation-independent manner. VIP- and PACAP-induced CREB phosphorylation is restricted to subpopulations of neonatal cells and thus also displays an adult pattern. Cholinergic calcium signaling exhibits a developmental switch within the first three postnatal weeks. In neonatal pinealocytes, acetylcholine elevates [Ca
2+]
i
via muscarinic rather than nicotinic acetylcholine receptors. In the second postnatal week, pinealocytes gain responsiveness to nicotine and gradually lose responsiveness to muscarinic cholinergic stimuli. Voltage-gated calcium channels are absent in neonatal cells and develop during the first postnatal days. ACh-evoked cellular events may be diversified depending on the functional subclass of receptor that is present. The transient existence of muscarinic acetylcholine receptors and the subsequent switch to nicotinic receptors would permit ACh to elicit temporary effects in early pineal development. |
| doi_str_mv | 10.1016/S0006-8993(99)01533-4 |
| format | Article |
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1- and β-adrenergic receptors and triggers melatonin production through an increase in the intracellular calcium concentration ([Ca
2+]
i
) and stimulation of the cAMP/cAMP responsive element-binding protein (CREB) cascade. VIP and PACAP also elevate the intracellular cAMP level and promote melatonin formation. Finally, ACh antagonizes the norepinephrine-induced hormone synthesis via nicotinic acetylcholine receptors and subsequent activation of voltage-gated calcium channels. By immuno(cyto)chemical demonstration of phosphorylated CREB and calcium imaging we have investigated the temporal relationship between the maturation of these signaling pathways and the rhythmic onset of melatonin biosynthesis in developing rat pinealocytes. Norepinephrine-regulated calcium signaling and phosphorylation of CREB are already fully developed at birth, i.e., prior to ingrowth of the sympathetic innervation into the pineal parenchyma, and appear to develop in an innervation-independent manner. VIP- and PACAP-induced CREB phosphorylation is restricted to subpopulations of neonatal cells and thus also displays an adult pattern. Cholinergic calcium signaling exhibits a developmental switch within the first three postnatal weeks. In neonatal pinealocytes, acetylcholine elevates [Ca
2+]
i
via muscarinic rather than nicotinic acetylcholine receptors. In the second postnatal week, pinealocytes gain responsiveness to nicotine and gradually lose responsiveness to muscarinic cholinergic stimuli. Voltage-gated calcium channels are absent in neonatal cells and develop during the first postnatal days. ACh-evoked cellular events may be diversified depending on the functional subclass of receptor that is present. The transient existence of muscarinic acetylcholine receptors and the subsequent switch to nicotinic receptors would permit ACh to elicit temporary effects in early pineal development.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(99)01533-4</identifier><identifier>PMID: 10375675</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Acetylcholine ; Acetylcholine - pharmacology ; Aging - physiology ; Animals ; Animals, Newborn - growth & development ; Animals, Newborn - physiology ; Biological and medical sciences ; Calcium ; Calcium Signaling - physiology ; CREB ; Cyclic AMP Response Element-Binding Protein - metabolism ; Fundamental and applied biological sciences. Psychology ; Hormones and neuropeptides. Regulation ; Hypothalamus. Hypophysis. Epiphysis. Urophysis ; Male ; Neuropeptides - pharmacology ; Norepinephrine ; Norepinephrine - pharmacology ; Ontogeny ; Phosphorylation ; Pineal Gland - cytology ; Pineal Gland - drug effects ; Pineal Gland - physiology ; Pituitary Adenylate Cyclase-Activating Polypeptide ; Rats ; Receptors, Cholinergic - physiology ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Vasoactive intestinal peptide ; Vasoactive Intestinal Peptide - pharmacology ; Vertebrates: endocrinology</subject><ispartof>Brain research, 1999-06, Vol.833 (1), p.39-50</ispartof><rights>1999 Elsevier Science B.V.</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1999 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-548693fc379fdea38ebae572717df44cf293cee1d3446875e004246d8e2b89883</citedby><cites>FETCH-LOGICAL-c421t-548693fc379fdea38ebae572717df44cf293cee1d3446875e004246d8e2b89883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(99)01533-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1874641$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10375675$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schomerus, Christof</creatorcontrib><creatorcontrib>Laedtke, Elke</creatorcontrib><creatorcontrib>Korf, Horst-Werner</creatorcontrib><title>Analyses of signal transduction cascades in rat pinealocytes reveal a switch in cholinergic signaling during postnatal development</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>In the rat pineal gland, norepinephrine activates α
1- and β-adrenergic receptors and triggers melatonin production through an increase in the intracellular calcium concentration ([Ca
2+]
i
) and stimulation of the cAMP/cAMP responsive element-binding protein (CREB) cascade. VIP and PACAP also elevate the intracellular cAMP level and promote melatonin formation. Finally, ACh antagonizes the norepinephrine-induced hormone synthesis via nicotinic acetylcholine receptors and subsequent activation of voltage-gated calcium channels. By immuno(cyto)chemical demonstration of phosphorylated CREB and calcium imaging we have investigated the temporal relationship between the maturation of these signaling pathways and the rhythmic onset of melatonin biosynthesis in developing rat pinealocytes. Norepinephrine-regulated calcium signaling and phosphorylation of CREB are already fully developed at birth, i.e., prior to ingrowth of the sympathetic innervation into the pineal parenchyma, and appear to develop in an innervation-independent manner. VIP- and PACAP-induced CREB phosphorylation is restricted to subpopulations of neonatal cells and thus also displays an adult pattern. Cholinergic calcium signaling exhibits a developmental switch within the first three postnatal weeks. In neonatal pinealocytes, acetylcholine elevates [Ca
2+]
i
via muscarinic rather than nicotinic acetylcholine receptors. In the second postnatal week, pinealocytes gain responsiveness to nicotine and gradually lose responsiveness to muscarinic cholinergic stimuli. Voltage-gated calcium channels are absent in neonatal cells and develop during the first postnatal days. ACh-evoked cellular events may be diversified depending on the functional subclass of receptor that is present. The transient existence of muscarinic acetylcholine receptors and the subsequent switch to nicotinic receptors would permit ACh to elicit temporary effects in early pineal development.</description><subject>Acetylcholine</subject><subject>Acetylcholine - pharmacology</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Animals, Newborn - growth & development</subject><subject>Animals, Newborn - physiology</subject><subject>Biological and medical sciences</subject><subject>Calcium</subject><subject>Calcium Signaling - physiology</subject><subject>CREB</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hormones and neuropeptides. Regulation</subject><subject>Hypothalamus. Hypophysis. Epiphysis. Urophysis</subject><subject>Male</subject><subject>Neuropeptides - pharmacology</subject><subject>Norepinephrine</subject><subject>Norepinephrine - pharmacology</subject><subject>Ontogeny</subject><subject>Phosphorylation</subject><subject>Pineal Gland - cytology</subject><subject>Pineal Gland - drug effects</subject><subject>Pineal Gland - physiology</subject><subject>Pituitary Adenylate Cyclase-Activating Polypeptide</subject><subject>Rats</subject><subject>Receptors, Cholinergic - physiology</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Vasoactive intestinal peptide</subject><subject>Vasoactive Intestinal Peptide - pharmacology</subject><subject>Vertebrates: endocrinology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2PFCEQhonRuOPqT9BwMEYPrdDQfJw2m41fySYe1DNhoHoW0wMt0Gvm6i-X3pmotz1VXniq3kq9CD2n5C0lVLz7SggRndKavdb6DaEDYx1_gDZUyb4TPScP0eYvcoaelPKjScY0eYzOKGFyEHLYoN-X0U6HAgWnEZewawrXbGPxi6shRexscda3_xBxthXPIYKdkjvU9pbhtglscfkVqrtZGXeTpobkXXCneSHusF_yWuZUarS1tfjWOaV5D7E-RY9GOxV4dqrn6PuH99-uPnXXXz5-vrq87hzvae0GroRmo2NSjx4sU7C1MMheUulHzt3Ya-YAqGecCyUHIIT3XHgF_VZppdg5enWcO-f0c4FSzT4UB9NkI6SlGKEVp_3A7wWpbFaK0AYOR9DlVEqG0cw57G0-GErMmpK5S8msERitzV1KZjV4cTJYtnvw_3UdY2nAyxOwXn8aWyAulH-cklzw1f_iiEE7222AbIoLEB34kMFV41O4Z5M_seWw-A</recordid><startdate>19990626</startdate><enddate>19990626</enddate><creator>Schomerus, Christof</creator><creator>Laedtke, Elke</creator><creator>Korf, Horst-Werner</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19990626</creationdate><title>Analyses of signal transduction cascades in rat pinealocytes reveal a switch in cholinergic signaling during postnatal development</title><author>Schomerus, Christof ; Laedtke, Elke ; Korf, Horst-Werner</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-548693fc379fdea38ebae572717df44cf293cee1d3446875e004246d8e2b89883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Acetylcholine</topic><topic>Acetylcholine - pharmacology</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Animals, Newborn - growth & development</topic><topic>Animals, Newborn - physiology</topic><topic>Biological and medical sciences</topic><topic>Calcium</topic><topic>Calcium Signaling - physiology</topic><topic>CREB</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hormones and neuropeptides. Regulation</topic><topic>Hypothalamus. Hypophysis. Epiphysis. Urophysis</topic><topic>Male</topic><topic>Neuropeptides - pharmacology</topic><topic>Norepinephrine</topic><topic>Norepinephrine - pharmacology</topic><topic>Ontogeny</topic><topic>Phosphorylation</topic><topic>Pineal Gland - cytology</topic><topic>Pineal Gland - drug effects</topic><topic>Pineal Gland - physiology</topic><topic>Pituitary Adenylate Cyclase-Activating Polypeptide</topic><topic>Rats</topic><topic>Receptors, Cholinergic - physiology</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Vasoactive intestinal peptide</topic><topic>Vasoactive Intestinal Peptide - pharmacology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schomerus, Christof</creatorcontrib><creatorcontrib>Laedtke, Elke</creatorcontrib><creatorcontrib>Korf, Horst-Werner</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schomerus, Christof</au><au>Laedtke, Elke</au><au>Korf, Horst-Werner</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analyses of signal transduction cascades in rat pinealocytes reveal a switch in cholinergic signaling during postnatal development</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1999-06-26</date><risdate>1999</risdate><volume>833</volume><issue>1</issue><spage>39</spage><epage>50</epage><pages>39-50</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>In the rat pineal gland, norepinephrine activates α
1- and β-adrenergic receptors and triggers melatonin production through an increase in the intracellular calcium concentration ([Ca
2+]
i
) and stimulation of the cAMP/cAMP responsive element-binding protein (CREB) cascade. VIP and PACAP also elevate the intracellular cAMP level and promote melatonin formation. Finally, ACh antagonizes the norepinephrine-induced hormone synthesis via nicotinic acetylcholine receptors and subsequent activation of voltage-gated calcium channels. By immuno(cyto)chemical demonstration of phosphorylated CREB and calcium imaging we have investigated the temporal relationship between the maturation of these signaling pathways and the rhythmic onset of melatonin biosynthesis in developing rat pinealocytes. Norepinephrine-regulated calcium signaling and phosphorylation of CREB are already fully developed at birth, i.e., prior to ingrowth of the sympathetic innervation into the pineal parenchyma, and appear to develop in an innervation-independent manner. VIP- and PACAP-induced CREB phosphorylation is restricted to subpopulations of neonatal cells and thus also displays an adult pattern. Cholinergic calcium signaling exhibits a developmental switch within the first three postnatal weeks. In neonatal pinealocytes, acetylcholine elevates [Ca
2+]
i
via muscarinic rather than nicotinic acetylcholine receptors. In the second postnatal week, pinealocytes gain responsiveness to nicotine and gradually lose responsiveness to muscarinic cholinergic stimuli. Voltage-gated calcium channels are absent in neonatal cells and develop during the first postnatal days. ACh-evoked cellular events may be diversified depending on the functional subclass of receptor that is present. The transient existence of muscarinic acetylcholine receptors and the subsequent switch to nicotinic receptors would permit ACh to elicit temporary effects in early pineal development.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>10375675</pmid><doi>10.1016/S0006-8993(99)01533-4</doi><tpages>12</tpages></addata></record> |
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| ispartof | Brain research, 1999-06, Vol.833 (1), p.39-50 |
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| subjects | Acetylcholine Acetylcholine - pharmacology Aging - physiology Animals Animals, Newborn - growth & development Animals, Newborn - physiology Biological and medical sciences Calcium Calcium Signaling - physiology CREB Cyclic AMP Response Element-Binding Protein - metabolism Fundamental and applied biological sciences. Psychology Hormones and neuropeptides. Regulation Hypothalamus. Hypophysis. Epiphysis. Urophysis Male Neuropeptides - pharmacology Norepinephrine Norepinephrine - pharmacology Ontogeny Phosphorylation Pineal Gland - cytology Pineal Gland - drug effects Pineal Gland - physiology Pituitary Adenylate Cyclase-Activating Polypeptide Rats Receptors, Cholinergic - physiology Signal Transduction - drug effects Signal Transduction - physiology Vasoactive intestinal peptide Vasoactive Intestinal Peptide - pharmacology Vertebrates: endocrinology |
| title | Analyses of signal transduction cascades in rat pinealocytes reveal a switch in cholinergic signaling during postnatal development |
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