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WFRF:(Rorsman N. J. G.)
 

Sökning: WFRF:(Rorsman N. J. G.) > Isoform-specific re...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003643naa a2200457 4500
001oai:lup.lub.lu.se:d6069e69-5628-4ae0-8ef7-be2f4599e5be
003SwePub
008160401s2004 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/2772602 URI
0247 a https://doi.org/10.1172/JCI2004202082 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Sinnegger-Brauns, MJ4 aut
2451 0a Isoform-specific regulation of mood behavior and pancreatic beta cell and cardiovascular function by L-type Ca2+ channels
264 1c 2004
520 a Ca(v)1.2 and Ca(v)1.3 L-type Ca2+ channels (LTCCs) are believed to underlie Ca2+ currents in brain, pancreatic beta cells, and the cardiovascular system. In the CNS, neuronal LTCCs control excitation-transcription coupling and neuronal plasticity. However, the pharmacotherapeutic implications of CNS LTCC modulation are difficult to study because LTCC modulators cause card iovascular (activators and. blockers) and neurotoxic (activators) effects. We selectively eliminated high dihydropyridine (DHP) sensitivity from Ca(v)1.2 alpha1 subunits (Ca(v)1.2DHP(-/-)) without affecting function and expression. This allowed separation of the DHP effects of Ca(v)1.2 from those of Ca(v)1.3 and other LTCCs. DHP effects on pancreatic P cell LTCC currents, insulin secretion, cardiac inotropy, and arterial smooth muscle contractility were lost in Ca(v)1.2DHP(-/-) mice, which rules out a direct role of Ca(v)1.3 for these physiological processes. Using Ca(v)1.2DHP(-/-) mice, we established DHPs as mood-modifying agents: LTCC activator-induced neurotoxicity was abolished and disclosed a depression-like behavioral effect without affecting spontaneous locomotor activity. LTCC activator BayK 8644 (BayK) activated only a specific set of brain areas. In the ventral striatum, BayK-induced release of glutamate and 5-HT, but not dopamine and noradrenaline, was abolished. This animal model provides a useful tool to elucidate whether Ca(v)1.3-selective channel modulation represents a novel pharmacological approach to modify CNS function without major peripheral effects.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
7001 a Hetzenauer, A4 aut
7001 a Huber, IG4 aut
7001 a Renström, Eriku Lund University,Lunds universitet,Diabetes - öpatofysiologi,Forskargrupper vid Lunds universitet,Diabetes - Islet Patophysiology,Lund University Research Groups4 aut0 (Swepub:lu)mphy-ere
7001 a Wietzorrek, G4 aut
7001 a Berjukov, S4 aut
7001 a Cavalli, M4 aut
7001 a Walter, D4 aut
7001 a Koschak, A4 aut
7001 a Waldschutz, R4 aut
7001 a Hering, S4 aut
7001 a Bova, S4 aut
7001 a Rorsman, Patriku Lund University,Lunds universitet,Islet cell physiology,Forskargrupper vid Lunds universitet,Lund University Research Groups4 aut0 (Swepub:lu)mphy-pro
7001 a Pongs, O4 aut
7001 a Singewald, N4 aut
7001 a Striessnig, J4 aut
7102 a Diabetes - öpatofysiologib Forskargrupper vid Lunds universitet4 org
7730 t Journal of Clinical Investigationg 113:10, s. 1430-1439q 113:10<1430-1439x 0021-9738
8564 u http://dx.doi.org/10.1172/JCI200420208x freey FULLTEXT
8564 8u https://lup.lub.lu.se/record/277260
8564 8u https://doi.org/10.1172/JCI200420208

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