The Role of Mitochondrial Channels in Programmed Cell Death: This laboratory is examining the translocation of proteins across membranes. The role of mitochondrial channels in programmed cell death is examined with electrophysiological techniques as well as a variety of additional approaches including microinjection and microsurgery of single cells, time-lapse video microscopy (fluorescence and phase), and flow cytometry. Understanding the cell death process will facilitate development of therapies that enable activation of this cascade to control the growth of malignancies and blockade of the pathway to reduce the volume of cell death after ischemic injury, e.g., stroke or heart attack.

The main focus of my lab is to identify cellular, genetic and biochemical processes affecting the mineralization of dental enamel. My research combines molecular biology, genetics and morphology to identify growth processes of this tissue. My current research focuses on the analysis of calcium transport mechanisms by enamel cells and in particular the role of the endoplasmic reticulum in this process. Calcium is critical to the development of enamel but how exactly calcium enters enamel cells and how it is then moved into the extracellular compartment where crystals grow, remains obscure. I focus this work on the analysis of CRAC channel proteins STIM and ORAI. Mutations to these genes may result in ectodermal dysplasia and amelogenesis imperfecta.  I am also interested in mechanism of facial growth. In particular I am interested in the processes mediating the growth of the maxillary complex, using animal models and the hominin fossil record to better understand constrains and plasticity of rostral form.

The Llinas lab research pertains mostly to neuroscience from the molecular to the cognitive level. They focus on the intrinsic electrophysiological properties of mammalian neurons in vitro, where they correlate ionic conductances with the different molecular structures (channels) responsible for them.

Dr. Morley's current research interests focus on determining the molecular mechanisms responsible for cardiac arrhythmias. One major area of interest includes studies determining the arrhythmogenic role of dysregulation of cardiac gap junctions. A second area of interest involves determining the mechanisms that are responsible for the developmental changes in impulse initiation and conduction within the sinus node and atria.

In order to better guide the development of medications for the treatment of dependence on cocaine or amphetamines, it is important to increase our understanding of the targets for these compounds, and one important target is the dopamine transporter (DAT). Thus, much of the research in the Reith lab deals with the structure, function, and regulation of DAT. The link between drug reward and natural reward is intriguing and suggests that treatments for drug abuse could also be effective as treatments of eating disorders.

Research in Dr. Rice's laboratory is focused on regulation of dopamine, a key transmitter in motor and reward pathways in the brain. Current research is centered on a novel finding from the Rice group that hydrogen peroxide (H2O2), produced by mitochondrial respiration, is an endogenous regulator of synaptic and somatodendritic dopamine release, as well as dopamine neuron activity in the substantia nigra. The Rice group also studies regulation of axonal dopamine release by glutamate, GABA, calcium, cannabinoids and caffeine, the mechanism and regulation of somatodendritic dopamine release, and dopamine dysfunction in transgenic mouse models of dystonia and PD.

Using C. elegans as a model system, the Ringstad lab seeks to identify genes that function in neurochemical signaling pathways, specifically in neuropeptide signaling and in biogenic amine signaling pathways. Such genes might encode new targets for therapeutics in the treatment of psychiatric and neurological illnesses that are associated with defects in neurochemical signaling, such as major depression, Parkinson's disease and schizophrenia.

The Rudy lab studies K+ channels, which regulate the excitability level of neurons and play a major role in determining their firing patterns, and thus significantly contribute to neuronal integration. A special focus of their research are channels expressed in thalamic relay neurons, the cells that process all sensory information before transmitting it to the cortex, as well as in the cortical neurons that receive and process this information.

The Salzer laboratory is investigating the complex, reciprocal interactions between axons and myelinating glia, i.e. Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. Their current studies examine the role of the neuregulin-1 family of neuronal growth factors, they are developing strategies to identify neuronal signals that promote myelination and they investigate mechanisms by which axons become organized into distinct longitudinal domains (e.g. the node of Ranvier).

Dr Skolnik's lab studies the Ca2+-activated K+ channel, KCa3.1, which is required for Ca2+ influx and the subsequent activation of B and T cells. They identified several new signaling molecules that are critical for regulating KCa3.1 channel activity in human CD4+ T cells. These studies have the potential to uncover novel pathways that regulate T cell activation and may identify new mechanisms whereby aberrant activation of these pathways can contribute to autoimmune diseases.