Charlie Askew, B.A.Biological Basis of Behavior, UPENN

Email:  cha3j@virginia.edu

Paul Bonthuis, B.S. Cell and Molecular Biology,
University of Washington, Seattle
Rissman and Grant Labs

Research in Emilie Rissman's lab is focused on the study of sexually dimorphic behavior, including the involvement of neuroendocrine and genetic mechanisms. Sex chromosomes are a source of genetic variation between males and females. Using genetic mouse models, I am working toward the discovery of genes on the sex chromosomes that are both differentially expressed in the brain between the sexes, and mediate masculine and feminine behaviors. Separately, I am also working on the development of a mouse model of learned helplessness to study the effects of estrogens on resiliency to acquire depressive-like symptoms. Our aim is to find depression susceptibility and protective genes that are regulated by estrogen receptor signaling. Email: pjb4n@virginia.edu

PubMed listings for the Rissman Lab

PubMed listing for the Grant Lab

Venton Lab

Email: xb2n@virginia.edu

PubMed listings for the Venton lab

Stroke-induced damage results from the loss of a sufficient supply of metabolic substrates to the brain, which leads to the death of neuronal and non-neuronal cells. The Lee laboratory generally focuses on the cellular mechanisms of neuronal vulnerability associated with stroke. Knowledge from these basic investigations can then be utilized to develop and test specific therapeutic strategies for rescuing damaged neurons. Most therapeutic strategies for stroke target cellular degenerative mechanisms that contribute to neuronal death. My research takes a somewhat different approach by examining a novel means for enhancing the delivery of metabolic substrates during stroke. These studies utilize a novel compound, trans-sodium crocetinate (TSC), which can enhance the diffusivity of small molecules into tissue. The central goal of my research is to characterize the mechanism(s) by which TSC produces its neuroprotective effect. These studies involve assessments of microvascular function, tissue diffusivity of metabolic substrates, cerebral blood flow, and tissue oxygenation.   Email: rhc2k@virginia.edu

PubMed listings for the Lee lab

Kimberly Hillsman Cox  B.A. University of Virginia, 
M.S. UT-Austin,
Neuroscience

 Parkinson's disease (PD) is a progressive neurodegenerative disease affecting the dopaminergic neurons in the midbrain. In the Trimmer lab, we use a cellular model previously developed by the lab called a cytoplasmic hybrid ("cybrid") from PD patients. These cybrids produce Lewy bodies that match those found in PD patient's brains in both their composition and morphology. Using this model, we can study the mechanism of protein aggregation, mitochondrial respiration and axonal transport in dopaminergic cybrid neurons. Additionally, the lab has begun to investigate the use of light therapy for neurodegenerative diseases like PD. For my research, I will be using a near-infrared laser to study the effects of light therapy on a cellular model of PD. Email: enc3p@virginia.edu

PubMed listings for the Trimmer lab

Elizabeth Daubert, B.S. Zoology, North Carolina State University

Serotonergic innervation is widespread throughout the entire central nervous system and the neurotransmitter serotonin potentially modulates every circuit in the brain. However, degenerating serotonergic neurites are observed following oxidative stress, toxin administration (for example MDMA or "ecstasy"), during normal aging
and in some neurodegenerative disease states such as Parkinson's Disease and Alzheimer's Disease. Therefore, it appears that serotonergic neurons may be inherently susceptible to damage. My
research in Barry Condron's lab focuses on a novel role for serotonin itself in formation of dystrophic serotonergic neurites in the central nervous system of the fruit fly. I am using high resolution confocal imaging, electron microscopy and genetic and pharmacological techniques in order to characterize these aberrant structures and
determine the cellular and molecular mechanisms responsible for their formation.

Email: ead8g@virginia.edu 

PubMed listings for the Condron Lab 

Noel Derecki, B.A. Cognitive Science, University of Virginia

A plethora of cellular and blood-borne chemical factors-neurotransmitters, trophins, glucocorticoids and prostoglandins, to name a few-have been shown to robustly affect the pro- or anti-inflammatory and antigen-presenting characteristics of myeloid cells. In turn, factors produced by myeloid cells (macrophages and microglia, for instance) are able to potentiate changes in nervous tissue. Thus, the population of myeloid cells located in the meninges of the brain are perfectly situated to mediate interactions between the peripheral immune system and the CNS. There has been much progress made recently into the phenomenology of immune-CNS interactions, and a great deal is known about inflammation in disease states, but far less is known about these cells on the borders of both the periphery and the brain. How do they get there? When do they get there? Are they involved in CNS homeostasis, emergency response, bidirectional signaling, or all three? Questions abound, but empirical data is sparse. I am interested in characterizing these myeloid cells first from both a developmental and a mechanistic point-of-view, including the nature of the upregulation of inflammatory mediators/messengers within meninges, CSF and brain parenchyma, and concomitant changes in neuronal and glial properties in key cortical areas related to mood and cognition, such as the amygdala, cingulate gyrus, and hippocampus.  Email:ncd3z@virginia.edu

PubMed listings for the Kipnis lab 

Mike DiGruccio, B.S. Biological Sciences, UC-Irvine

Email: mrd7s@virginia.edu

 Charli Dominguez, B.S. Neuroscience, Baylor University

Email: cld2w@virginia.edu

Sara Dudgeon, B.S. Neurobiology, B.S. Zoology, University of Wisconsin, Madison

The Hill lab studies the neurophysiological, morphological, and developmental gustatory system and the plasticity that occurs within this system. The chorda tympani, greater superficial petrosal and glossopharyngeal nerves travel from the oral cavity to the nucleus of the solitary tract in the brainstem where they form terminal fields. My research focuses on how competition among the three gustatory nerves shapes development and maintenance of the terminal field morphology and seeks to understand the forces behind the large amount of plasticity seen in the system. I use a combination of anatomical, histological, electrophysiological and behavioral techniques in my research. Email: sld2r@virginia.edu  Email: sld2r@virginia.edu

PubMed listings for the Hill lab 

  Nathan Fields, B.S. Psychology, College of William and Mary

Email: nrf5a@virginia.edu 

PubMed listings for the Hussaini lab 

In the laboratory of Kevin Lee, I am working with a novel rat model of subcortical band heterotopia (SBH), the tish rat, in which a collection of misplaced neurons accumulates in the white matter beneath the normal cortex. Human patients with SBH exhibit intractable epilepsy, and the tish rat also experiences epileptic behavior. Previous evidence from our lab suggests that defects in proliferation and migration may be responsible for the phenotype in this animal model of SBH. I am interested in investigating the role of radial glia in the development of the heterotopia in the tish rat.

 Kasia Glanowska, M.A. Biotechnology, Jagiellonian University

Email: kmg5v@virginia.edu

Nicholas Hargus, B.S. Neuroscience, Lafayette College  

In the Patel lab, we use whole-cell patch-clamp electrophysiology in an intact brain slice to look at the role of sodium channels in neuronal signaling and how this plays a role in the generation of epileptic seizures.  Using electrophysiological techniques, we are comparing the sodium channel-dependent firing properties of various neurons within the rat hippocampus of control animals to those in a model of temporal lobe epilepsy (TLE).  We are also using various molecular biology techniques to look at expression patterns of these sodium channels in the epileptic animal.  Email: njh9c@virginia.edu  

PubMed listings for the Patel lab 

Geoffrey Horwitz, B.S. Biology/Psychology,
Trinity College, San Antonio

My research in the Holt Lab focuses on the identification and characterization of ion channels and conductances within the mammalian inner ear. I am specifically interested in examining the function and molecular composition of the inward rectifiers in the mammalian vestibular system. I study the physiological properties primarily using the whole cell tight seal technique, and study the expression patterns using various molecular and biochemical methods.
 

Email:  gch4f@virginia.edu 

PubMed listings for the Holt lab 

Ye Hyun Kim, B.A. Psyhcology, College of Wooster

Email:  yk2b@virginia.edu

Zofia Lasiecka, M.S. Biology,
Warsaw University 

The Winckler lab is focused on the establishment and maintenance of neuronal cell polarity. Neurons have two distinct domains, axon and dendrite, which differ in their distribution of organelles, cytoskeleton, and proteins in the plasma membrane. These distinct domains play a critical role in receiving and propagating signals. We are investigating the mechanism by which proteins are sorted and transported to specific locations in the neuronal cell, with a particular focus on trafficking of adhesion molecules from the L1 family. To address these questions we use primary hippocampal neuronal cultures, transfection, live imaging and immunocytochemistry.  I am specifically interested in the trafficking and role of cell adhesion molecules in synapse formation and function. My current project aims to answer the question whether NgCAM adhesion molecule are endocytosed and trafficked in the same organelles as the postsynaptic AMPA receptors that mediate synaptic transmission, and and plays an important role in synaptic plasticity.
Email: zml5v@virginia.edu

PubMed listings for the Winckler lab 

Michaela Levin, M.A. Education, M.A. Performance,  New York University

A myriad of ion channels are involved in the auditory and vestibular function of the inner ear. In the Holt lab my research focuses on identifying members of the potassium channel family and testing their role in hair cell function. Using molecular biology I look at developmental expression levels and potential effects of ion channel mutations on the function of the maturing hair cell. To examine the biophysical properties of these ion channels I use predominantly whole cell patch-clamp recordings.

Email: mel2u@virginia.edu

Olivia Mullins, B.A. Psychology, Boston College   

 The overall goal of the Friesen laboratory is to uncover mechanisms that underlie rhythmic behaviors. My focus is on determining the mechanisms that control swim duration, or swim maintenance in the leech swim system. At the heart of this issue is understanding how a brief sensory input can initiate a sustained behavior. The leech is an excellent model system due to its relatively simple nervous system and small repertoire of behaviors. Manipulation of the most caudal ganglion as well as gating cell 204 can alter swim duration. Using sharp electrode electrophysiology in conjunction with other techniques I am investigating the relationship between cadual ganglion cells and cells 204 to determine the neural circuitry that underlies the maintenance of leech swimming.
Email:ojm5h@virginia.edu

PubMed listings for the Friesen Lab 

Michelle Neveklovska, B.S. Biology, Syracuse University

In Scott Zeitlin's lab, we are interested in understanding the pathogenic mechanisms of Huntington's Disease (HD). HD is a dominantly inherited neurodegenerative disorder that affects some 30,000 Americans. It is caused by an expanded polyglutamine (polyQ) repeat in the huntingtin protein and is characterized by the selective loss of striatal medium spiny neurons, with some associated degeneration in the cortex. Using an inducible Cre/lox strategy, I am studying the consequences of inactivating HD gene expression in astrocytes at different developmental times. Ultimately, I am interested in understanding the role of astrocytes in HD pathology. 
Email: mmn2h@virginia.edu

PubMed listings for the Zeitlin Lab

Neurodegenerative Diseases Journal Club
http://www.healthsystem.virginia.edu/internet/
neurosci/HD_Journal_Club/home2.cfm

Justyna Pielecka, M.S. Biotechnology,
Techincal University at Lodz

PubMed listings for the Moenter lab 

Matt Rannals, B.S. Physics, Hampden-Sydney College

My research in the laboratory of Jaideep Kapur focuses on inhibitory GABAergic neurons. I use a variety of fluorescent imaging techniques along with electrophysiological recordings to study the signalling that occurs in these neurons. Classically, GABAergic signalling was thought to occur at inhibitory synapses. Recently there has been evidence shown for extrasynaptic GABA receptors playing a role in inhibition as well. Both forms of signalling may be important for homeostatic plasticity, allowing the neuron to maintain consistent responsiveness in a fluctuating environment of activity. Through my research I hope to better understand the mechanisms underlying these forms of signalling, as well as the role and targeting mechanisms of the GABAA receptor and its subunitsEmail: mdr3m@virginia.edu

PubMed listings for the Kapur lab 

Carolina Ramoa, B.A. Biology/Cognitive Science, University of Virginia

In the Kapur lab, we utilize kindling and neonatal kainate epilepsy models to study various aspects of the circuitry, the synapse, and synapse development in the brain. The lab mainly focuses on the inhibitory GABAergic neurons and understanding their role. I will be working on the development of the synapse by employing patch clamp methodology as a tool to further comprehend synapse formation and maturation.

Email:  cpr3h@virginia.edu

PubMed listings for the Kapur lab 

  Aurora Rodriguez, B.S. Biology, M.S. Computer Science, Florida Atlantic University

Email:  alr5j@virginia.edu

Victoria Sanchez, B.S. Chemistry, Frostburg State University

Email:  vs4r@virginia.edu

PubMed listings for the V. Todorovic lab 

David Sloan, B.S. Molecular Biology, Brigham Young University

Temporal lobe epilepsy involves multiple neuronal circuits that interact in complex ways. An understanding of these circuits is essential for the development of effective clinical interventions. The Bertram lab seeks to understand this circuitry in an animal model of spontaneous limbic seizures. I focus on the connectivity between the midline thalamus, the prefrontal cortex and the subiculum, and how that connectivity changes as chronic seizures develop.
Email: dms7t@virginia.edu

PubMed Listings for the Bertram lab 

Peihan Orestes (Su), B.A. Neuroscience, Rutgers University

My research in Slobo Todorovic's lab is currently focused the possible relationship between low-voltage activated calcium channels, nitrous oxide, and pain processing. I am currently doing electrophysiological recordings using transfected HEK cells, but also plan to extend this project into endogenous channels and behavioral testing.

Email: peihan@virginia.edu

PubMed listings for the S.Todorovic lab 

Lucia Tejada, B.S. Biology, La Molina National Agrarian University, Lima, Peru

Androgens, including testosterone and its metabolite dihydrotestosterone, activate androgen receptors (ARs) to exert effects on the developing and adult nervous system. Nuclear ARs are ligand-dependent transcription factors that modify the expression of androgen-responsive genes. Moreover, the AR is expressed in many hypothalamic areas that undergo sexual differentiation. Recent studies in our lab have demonstrated a role for AR in the differentiation of social preferences in mice. Using a transgenic mouse line in which cells that express AR co-express two reporter molecules (nuclear β -galactsosidase and placental alkaline phosphatase), my current research focuses in the identification of the critical period during development, puberty or adulthood when the AR plays its critical role. Email:  ldt7p@virginia.edu

PubMed listings for the Rissman lab 

Ben Thiede, B.S. Genetics, University of Wisconsin, Madison

Email:  brt7g@virginia.edu

Max Vakulenko, B.A. Biology,  Mount Sinai Graduate School of Biomedical Sciences

Winckler Lab

Email: mv2a@virginia.edu

PubMed listings for the Winckler lab 

Heidi Walsh, B.S. Neuroscience, Allegheny College
My work in Margaret Shupnik's lab focuses on how gonadotropin releasing hormone (GnRH) regulates expression of the gonadotropin subunit genes that form luteinizing hormone (LH) and follicle stimulating hormone (FSH). Specifically, I am interested in how GnRH influences the ubiquitin-proteasome pathway to exert the tight transcriptional control these genes require for fertility.
 Email:  hew8f@virginia.edu

PubMed listings for the Shupnik Lab 

Erica Young, B.A. Psychobiology,
Florida Atlantic University

 In the Williams' lab, we examine the effect of emotional arousing events on norepinephrine release in nuclei that play key roles in memory formation. My current research is examining the projections from the nucleus of the solitaire to the basolataral amygdala using in vivo microdialysis and HPLC. With in vivo microdialysis and HPLC, I am able to observe changes in norepinephrine levels in the basolateral amygdala following manipulates to upstream nuclei.   Email:ejy5m@virginia.edu

PubMed listings for the Williams lab 

Kisha Young, B.S. Biochemistry, Spelman College            MSTP

Many human mitochondrial disorders result from abnormal mtDNA and altered mitochondrial bioenergetics. A major goal of the Bennett laboratory is to study the relationship between mitochondrial genotype and the complex clinical phenotype in neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases. The other goal is to provide potential therapies for these devastating diseases by manipulating the mitochondrial genome and improving bioenergetics. Characterized pathologically by the overproduction and aggregation of b-amyloid protein and hyperphosphorylated tau, Alzheimer's disease (AD) also demonstrates reduced mitochondrial bioenergetics and increased reactive oxygen species (ROS). Using laboratory-developed cytoplasmic hybrid ("cybrid") cell lines for AD, which overproduce b-amyloid protein, I will examine the mechanism by which b-amyloid protein reduces enzyme activity and overall respiratory function. In addition, the reversibility of b-amyloid protein's toxic effects on mitochondria will be examined after pharmacologically reducing its production. Lastly, I will test the therapeutic potential of manipulating the mitochondrial genome by protein transduction to improve bioenergetics in these diseased cell lines. Since mtDNA mutations and deletions accumulate in aged and AD brains, our major aim to provide a direct causative link between mitochondrial dysfunction and AD.

Email: kjy6e@virginia.edu
 
PubMed listings for the lab