Universität zu Köln

Albanna, Walid ORCID: 0000-0001-9986-8739, Neumaier, Felix ORCID: 0000-0002-6376-6391, Lueke, Jan Niklas, Kotliar, Konstantin, Conzen, Catharina, Lindauer, Ute, Hescheler, Juergen, Clusmann, Hans, Schneider, Toni and Schubert, Gerrit Alexander ORCID: 0000-0001-9135-6042 (2018). Unconjugated bilirubin modulates neuronal signaling only in wild-type mice, but not after ablation of the R-type/Ca(v)2.3 voltage-gated calcium channel. CNS Neurosci. Ther., 24 (3). S. 222 - 231. HOBOKEN: WILEY. ISSN 1755-5949

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Abstract

IntroductionThe relationship between blood metabolites and hemoglobin degradation products (BMHDPs) formed in the cerebrospinal fluid and the development of vasospasm and delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) has been the focus of several previous studies, but their molecular and cellular targets remain to be elucidated. MethodsBecause BMHDP-induced changes in Ca(v)2.3 channel function are thought to contribute to DCI after aSAH, we studied their modulation by unconjugated bilirubin (UCB) in an organotypical neuronal network from wild-type (WT) and Ca(v)2.3-deficient animals (KO). Murine retinae were isolated from WT and KO and superfused with nutrient solution. Electroretinograms were recorded before, during, and after superfusion with UCB. Transretinal signaling was analyzed as b-wave, implicit time, and area under the curve (AUC). ResultsSuperfusion of UCB significantly attenuated the b-wave amplitude in the isolated retina from wild-type mice by 14.9% (P<0.05), followed by gradual partial recovery (P=0.09). Correspondingly, AUC decreased significantly with superfusion of UCB (P<0.05). During washout, the b-wave amplitude returned to baseline (P=0.2839). The effects of UCB were absent in Ca(v)2.3-deficient mice, lacking the expression of Ca(v)2.3 as proofed on the biochemical level. ConclusionsEx vivo neuronal recording in the murine retina is able to detect transient impairment of transretinal signaling by UCB in WT, but not in KO. This new model may be useful to further clarify the role of calcium channels in neuronal signal alteration in the presence of BHMDPs.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Albanna, Walid UNSPECIFIED orcid.org/0000-0001-9986-8739 UNSPECIFIED Neumaier, Felix UNSPECIFIED orcid.org/0000-0002-6376-6391 UNSPECIFIED Lueke, Jan Niklas UNSPECIFIED UNSPECIFIED UNSPECIFIED Kotliar, Konstantin UNSPECIFIED UNSPECIFIED UNSPECIFIED Conzen, Catharina UNSPECIFIED UNSPECIFIED UNSPECIFIED Lindauer, Ute UNSPECIFIED UNSPECIFIED UNSPECIFIED Hescheler, Juergen UNSPECIFIED UNSPECIFIED UNSPECIFIED Clusmann, Hans UNSPECIFIED UNSPECIFIED UNSPECIFIED Schneider, Toni UNSPECIFIED UNSPECIFIED UNSPECIFIED Schubert, Gerrit Alexander UNSPECIFIED orcid.org/0000-0001-9135-6042 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-195388
DOI:	10.1111/cns.12791
Journal or Publication Title:	CNS Neurosci. Ther.
Volume:	24
Number:	3
Page Range:	S. 222 - 231
Date:	2018
Publisher:	WILEY
Place of Publication:	HOBOKEN
ISSN:	1755-5949
Language:	English
Faculty:	Faculty of Mathematics and Natural Sciences
Divisions:	Faculty of Medicine > Physiologie und Pathophysiologie > Institut für Neurophysiologie
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language ROD BIPOLAR CELLS; SUBARACHNOID HEMORRHAGE; CEREBRAL VASOSPASM; CA2+ CHANNELS; RAT RETINA; PLASMA-MEMBRANE; AMACRINE CELLS; SERUM-ALBUMIN; MURINE RETINA; OXIDATION Multiple languages Neurosciences; Pharmacology & Pharmacy Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/19538