Browsing Cumming School of Medicine by Department "Cell Biology & Anatomy"
Now showing 1 - 4 of 4
Results Per Page
- ItemOpen AccessThe innervation of the human acetabular labrum and hip joint: an anatomic study(BioMed Central, 2014-02-14) Abdullah Alzaharan; Bali, Kamal; Gudena, Ravi; Railton, Pamela; Ponjevic, Dragana; Matyas, John R.; Powell, James N.
- ItemOpen AccessMercury-induced toxicity of rat cortical neurons is mediated through N-Methyl-D-Aspartate receptors(BioMed Central Ltd., 2012-09-14) Xu, Fenglian; Farkas, Svetlana; Kortbeek, Simone; Chen, Lina; Zhang, Fangxiong; Zamponi, Gerald W.; Syed, Naweed I.Mercury is a well-known neurotoxin implicated in a wide range of neurological or psychiatric disorders including autism spectrum disorders, Alzheimer's disease, Parkinson's disease, epilepsy, depression, mood disorders and tremor. Mercury-induced neuronal degeneration is thought to invoke glutamate-mediated excitotoxicity, however, the underlying mechanisms remain poorly understood. Here, we examine the effects of various mercury concentrations (including pathological levels present in human plasma or cerebrospinal fluid) on cultured, rat cortical neurons.
- ItemOpen AccessSignaling complexes of voltage-gated calcium channels(Taylor and Francis, 2011-09) Turner, Ray W.; Anderson, Dustin M.; Zamponi, Gerald W.Voltage gated calcium channels are key mediators of depolarization induced calcium entry into electrically excitable cells. There is increasing evidence that voltage gated calcium channels, like many other types of ionic channels, do not operate in isolation, but instead forms signaling complexes with signaling molecules, G protein coupled receptors, and other types of ion channels. Furthermore, there appears to be bidirectional signaling within these protein complexes, thus allowing not only for efficient translation of calcium signals into cellular responses, but also for tight control of calcium entry per se. In this review, we will focus predominantly on signaling complexes between G protein-coupled receptors and high voltage activated calcium channels, and on complexes of voltage-gated calcium channels and members of the potassium channel superfamily.
- ItemOpen AccessUse 'em and lose 'em-activity-induced removal of calcium channels from the plasma membrane(Elsevier Inc., 2007-08-16) Varela, Diego L.; Zamponi, Gerald W.Calcium influx via L-type (Cav1.2 and Cav1.3) calcium channels is tightly regulated to ensure optimal intracellular calcium levels. Although much is known about acute modulation of these channels by second messengers, the mechanisms that control their trafficking to and from the plasma membrane remain poorly understood. In this issue of Neuron, Green and colleagues demonstrate that the opening of L-type calcium channels results in negative feedback regulation due to their calcium-dependent internalization.