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.

ABSTRACT:

Introduction

The 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.

Methods

Because 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, a

SUBMITTER: Albanna W 

PROVIDER: S-EPMC6489700 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature