Graduate Students Research Heading link
|I work with the unique model system known as the naked mole rat (NMR). My lab found that adult NMRs have the ability to live in/withstand lower concentrations of oxygen compared to similar laboratory animals. When most mammals are exposed to low oxygen concentrations, they show severe if not lethal characteristics compared to the NMR. I use in vivo techniques including Electroencephalography (EEG), Electromyography (EMG) and Electrocardiography (EKG) to see how the brain, muscles, and heart respond to oxygen deprivation. Additional in vitro studies are used to look at cell death in the brain to understand the damage caused in these animals at a cellular level.
|My lab discovered a novel protein in drosophila that plays a role in glutamate receptor subunit translation. I am currently characterizing the protein to better understand how it interacts with glutamate receptor mRNA as well as looking at its role in drosophila development. Drosophila is an ideal model organism for studying synaptic biology due to its easily accessible neuromuscular junctions in the larval stage. Characterizing the protein in drosophila could also help us understand the human homolog which has been implicated in several neurological disorders
|I am interested in characterizing developmental pathways in the Naked Mole Rat. My research uses behavioral markers in conjunction with fMRI, electrophysiology, and various molecular techniques to establish developmental milestones and understand how manipulation of key developmental receptors effects an animal’s ability to reach these milestones.
|My research focuses on the roles that glial cells play in the function of the nervous system. In addition to maintaining stable extracellular ion concentrations and removing neurotransmitters released by neurons, recent research has suggested that glial cells may directly modulate neuronal signals. My work explores the molecular mechanisms by which glial cells may modulate neuronal activity within the nervous system.
|In humans, the mis-regulation of ionotropic glutamate receptors (iGluRs) has been linked to various neurological disorders including autism, schizophrenia, migraine, bipolar disorder, and anxiety. Proper iGluR subunit production, trafficking, and assembly are required for normal brain development, function, and plasticity. Our lab has recently identified a novel protein in Drosophila associated with iGluR regulation. I am interested in studying the uncharacterized homolog in mouse. My work focuses on determining the spatial-temporal gene and protein expression during mouse development and examining the protein’s relationship with mammalian iGluRs. This work aims to provide insight into a potential novel mammalian iGluR regulatory mechanism.
|I work in Dr. Liang-wei Gong’s lab and our general research interest is the mechanisms of synaptic transmission in neurons and neuroendocrine chromaffin cells. Currently, my work is to understand the molecular mechanisms of endocytosis in chromaffin cells, utilizing patch clamping technique.
|I am using a mouse model to study the mechanism of endocytosis. Specifically, our lab found a particular TRP channel, a non-selective cation channel, which plays a critical role in regulating endocytosis by allowing Ca2+ flowing through it. My project is to examine the function of this channel in endocytosis using pHluorin-based live imaging combined with molecular biological techniques.
|I study synaptic transmission in C. elegans and Drosophila using a variety of techniques, primarily high pressure freeze electron microscopy. This technique allows for nanometer resolution at the synapse to characterize ultrastructural phenotypes and is supported by behavioral and electrophysiological assays. Coupled with genetics and other imaging techniques, I examine the influence of various molecular pathways on synaptic remodeling and the vesicle cycle.
|My research is focused on investigating the differential role of a basic helix-loop-helix transcription factor, hlh-3, in the differentiation and function of sex-specific and “core” neurons of Caenorhabditis elegans. A fundamental behavior in every species is reproduction. It is essential that organisms efficiently execute reproductive behaviors to successfully propagate. In males, HLH-3 has already been implicated in the specification of the male linker cell involved in proper development of the somatic gonad. In addition to exhibiting abnormal somatic gonads, mutant males are also defective in specific steps of male-mating behavior. They exhibit abnormal turning behavior and are inefficient at detecting hermaphrodite secreted pheromones. This suggests that hlh-3 has a function in regulating the differentiation or function of “core” and/or male-specific neurons implicated in mediating such behaviors. We have found that these neurons are abnormal in hlh-3 mutant males.
|Glutamate is the most abundant neurotransmitter in the vertebrate nervous system. Up to 80% of synapses in the mammalian brain are glutamatergic, and changes in glutamate signaling form the basis of learning and memory. Ambient extracellular glutamate levels in the mammalian brain are approximately 0.5-5 µm. This concentration is high enough to cause constitutive desensitization of most glutamate receptors. Thus, ambient extracellular glutamate may be a key regulator of synaptic signaling. In the Featherstone lab, I use the mouse CA3-CA1 hippocampal synapse as a model to study the effects of decreased ambient extracellular glutamate on synaptic transmission and neural signaling. Through electrophysiology and imaging techniques, I hope to decipher the mechanism by which a reduction in hippocampal extracellular glutamate leads to increases in both synaptic strength and glutamate receptor abundance at my model synapse.
|The Alfonso Lab has shown that hlh-3 is required for the differentiation of hermaphrodite specific neurons in the egg laying circuitry. In the absence of hlh-3 function hermaphrodites fail to lay eggs normally. We also have evidence that mutant males have defects in specific mating steps and neurons involved in these behaviors appear to be defective in their differentiation and function. Although it is clear that the protein encoded by this gene is required for the identity of neurons that are unique to each sex, as well as some that are shared by both sexes, we do not yet know about the targets of the HLH-3 transcription factor. My research is focused on identifying target genes of the HLH-3 transcription factor in order to understand how the protein regulates acquisition of neuronal cell fate.
|I am interested in the modulation of synaptic transmission. Specifically I am studying the relationship between SNARE proteins, seratonin and G beta gamma. Seratonin inhibits synaptic transmission by interacting with a G protein coupled receptor. The G beta gamma subunit then interacts with SNARE proteins resulting in inhibition of synaptic transmission. We believe the change in synaptic activity can be attributed to a change in the mode of vesicular fusion. I use electrophysiology and imaging techniques in the lamprey spinal cord to examine what's happening at a cellular and subcellular level during this inhibition. I am utilizing mutant proteins to elucidate the binding patterns of the proteins involved in this interaction.
|Dendrites of many sensory neurons have an extensively branched but neuron type specific morphology. Specific branching pattern of dendrites is essential for a neuron to receive inputs only from its specific receptive field which in turn ensures the proper functioning of a neuron in its neuronal circuit. How do dendrites achieve its complex yet specific branched morphology? My research interest lies in unraveling the cellular and molecular mechanism underlying dendritic arborization. I am using C.elegans as a model system. PVD, a sensory neuron in C. elegans, has a stereotypical highly branched dendritic structure which covers almost entire body of the animal. Currently, I am trying to understand how dendrites of this sensory neuron achieve a stereotypical branched structure.
|Left-right differences in anatomical structures and functions of the central nervous system are present throughout the animal kingdom. Left-right asymmetry has been implicated as an important aspect of normal brain development and function in humans. The Amphid Wing ‘C’ (AWC) neurons of the C. elegans olfactory system is a good model to elucidate genes and mechanisms underline neuron asymmetry. I study the mechanisms of how this pair of AWC neurons are bilaterally symmetric in their morphological and anatomical features, but develop asymmetrically at the molecular and functional level.