| Leo Faria |
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| postdoctoral fellow |
| Research Topic |
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| Damage in the cerebral cortex produces alterations in the synaptic responses of local circuits that can promote the later development of seizures and epilepsy. In the hyperexcited brain, the mechanisms responsible for maintaining the thin balance between excitation and inhibition are disrupted. The "undercut" or "cortical island" model reproduces many features of human post traumatic epilepsy. My current project uses whole cell patch clamp to investigate alterations in the inhibitory postsynaptic currents in the cortex of rodents with epilepsy |
| Leo Factoids |
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| Every weekend, early in the morning, a noisy squirrel wakes me up. He, certainly, does not know what I do for a living. |
| Contact Leo |
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| | Xiaoming Jin |
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| postdoctoral fellow |
| Research Topic |
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| It has been shown that structural reorganization such as axonal sprouting and enhanced excitatory synaptic connectivity occur in the cortical layer V pyramidal neurons after traumatic injury, and may be associated with epileptogenesis. How inhibitory synaptic connectivity changes and its role in epileptogenesis are still unclear. Currently, I use a combination of whole cell patch clamp recording, laser scanning photostimulation, and morphological techniques to map inhibitory and excitatory input to GFP-expressing fast-spiking interneurons, and inhibitory input to pyramidal neurons in layer V of the cortex. The studies are carried out in two animal models of epileptogenesis: the posttramatic injury model of the partial cortical isolation ("undercut") and the cortical dysplasia model of freeze lesion. |
| Xiaoming Factoids |
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| I practice "TaiChi golf", which I have invented (...but haven't yet patented it) |
| Contact Xiaoming |
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| Alex Goddard |
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| postdoctoral fellow |
| Research Topic |
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| I'm working on the role of acetylcholine in modulating the gain of sensory circuits. To address this, I'm using whole-cell patch clamp recordings combined with local application of cholinergic agonists and antagonists in acute slices from the avian brain, as well as anatomical techniques. |
| Alex Factoids |
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In my spare time, I play in a guitar in a local san francisco band, am a taster for Toast Connoisseur magazine, and am a
regular in the pro-am full-contact knitting circuit. |
| Contact Alex |
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| | Trent Anderson |
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| postdoctoral fellow |
| Research Topic |
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| The primary use of ATP in neuronal tissue is to drive the Na+-K+ ATPase which maintains ionic gradients and responds to periods of high cellular activity. The Na+-K+ ATPase is ubiquitously expressed in all neuronal cell types, including both excitatory and inhibitory neurons. Inhibition of the Na+-K+ ATPase plays an important role in the development of numerous CNS insults including epilepsy. This is due in part to decreases in GABA release and changes in the balance of excitatory versus inhibitory function. We are using whole cell recordings in slice to examine the differential sensitivity of excitatory pyramidal and inhibitory fast-spiking neurons to blockade of the Na+-K+ ATPase. Differences in Na+-K+ ATPase activity may have more generalized roles in the capacity of excitatory and inhibitory neurons at rest and during periods of high cellular activity, as well as more subtle contributions at the synaptic level. |
| Trent Factoids |
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| Winter driving in California can be worse then Canada! |
| Contact Trent |
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| | Max Kleiman-Weiner |
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| undergraduate researcher |
| Research Topic |
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| I am interested in intracellular calcium signaling mediated by voltage gated calcium channels and NMDA receptors during thalamocortical oscillations. Through extracellular multiunit recordings, pharmacological manipulations and computational modeling, I am investigating the contribution of calcium dependent potassium channels to both spindle and epileptic-like oscillations. In addition, I am looking at how neurotransmitter demand during heightened activity affects the duration of oscillatory activity. |
| Max Factoids |
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| “In Soviet Russia neurons patch you!” |
| Contact Max |
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| | Hiro Tani |
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| postdoctoral fellow |
| Research Topic |
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| I am interested in determining how neurons and astrocytes work together to maintain constant supply of the excitatory transmitter glutamate during seizures. Using a combination of molecular biology, pharmacology, electrophysiology and real-time imaging on rodent cortical slices, I am defining key molecular components that are rate-limiting to the production and recycling of glutamate and how these are altered in an injured cortex that display epileptiform activity. |
| Hiro Factoids |
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| When I grow up, I want to be like Takeru Kobayashi! |
| Contact Hiro |
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| | Mark Beenhakker |
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| postdoctoral fellow |
| Research Topic |
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Epilepsy is a neurological disorder that results from neural hyperexcitability, which in turn, results when the balance of inhibition and excitation within neural networks is compromised. This basic tenet has motivated the search for genetic mutations in ion channels – the fundamental units that define the excitability of a neuron – that may underlie the congenital epilepsies. One such candidate gene that has been associated with certain inherited human generalized epilepsies, including absence epilepsy, encodes the chloride channel subtype CLCN2.
While it remains unknown how mutations in a chloride channel subtype can lead to epilepsy, altered neuronal excitability within substructures of the thalamus, particularly the reticular thalamic nucleus (RT), can promote neural activity patterns characteristic of absence epilepsy. We, therefore, have started to explore the mechanisms that may link chloride channel dysfunction in the thalamus to absence epilepsy. This study employs several approaches ranging from anatomical localization of CLCN2, including co-localization with other proteins, to electrophysiological techniques that provide clues into the function of CLCN2 in regulating thalamic neuron excitability.
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| Mark Factoids |
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| Mark once managed a pygmy elephant reserve. |
| Contact Mark |
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| Claude Schofield |
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| postdoctoral fellow |
| Research Topic |
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| I use whole cell patch clamp techniques to study synaptic inhibition in the rodent brain. My current projects focus on the kinetics, pharmacology and modulation of GABA-A receptors in the thalamus, and I'm also interested in wide range of topics pertaining to ion channel function and neuropharmacology. I strive to one day elucidate molecular processes underlying synaptic transmission, their correlative behaviors, and pathologies related to human disease. |
| Claude Factoids |
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| I enjoy swimming at Avery Aquatic Center, hanging out in the Haight, and commuting to lab on 280 in my fuel efficient Toyota. |
| Contact Claude |
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| | Carolyn Lacey |
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| postdoctoral fellow |
| Research Topic |
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| Absence seizures, characterized by a brief loss of consciousness accompanied by cessation of normal behavior, arise from disturbances of the circuitry connecting the excitatory neurons of the cortex and dorsal thalamus and the inhibitory neurons of the thalamic reticular nucleus (RT). Excitation, from the cortex or the dorsal thalamus, recruits inhibition within the RT, which leads to network oscillations associated with normal activity and communication within this loop. Currently my project focuses on the role of AMPA receptors, and their trafficking molecules, in the generation of absence seizures. By taking advantage of mouse models of absence epilepsy, such as the Stargazer mouse, that lack the AMPA receptor trafficking molecule Stargazin, we can begin to identify the effect of disrupting the excitation of inhibitory cells within the thalamic circuitry. In order to understand this fully, I am taking a multidisciplinary approach using electrophysiological and anatomical techniques to dissect the normal and pathological interactions of neurons within, and between, the cortex, thalamus and reticular nucleus. |
| Carolyn Factoids |
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| I came to work in California all the way from the UK to get some much needed sunlight…only to find myself working in a windowless basement! |
| Contact Carolyn |
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| | Chris Dulla |
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| postdoctoral fellow |
| Research Topic |
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| My studies are focused on detecting glutamate release from brain slices. New FRET-based glutamate nanosensors allow detection of glutamate with unprecedented temporal and spatial precision. We are implementing this technology in the brain slice preparation to study glutamate release and reuptake during normal and epileptiform neural activity in the cortex and thalamus. We are also extremely interested in how glutamate supply is maintained during times of heightened neuronal activation and how disturbing glutamate production may aid in aborting or terminating epileptiform network activity. |
| Chris Factoids |
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| I can throw a tennis ball with my toes. |
| Contact Chris |
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| Isabel Parada |
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| expert histologist & microscopist |
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| | Julia Brill |
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| postdoctoral fellow |
| Research Topic |
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| My project focuses on the expression of AMPA receptor subunits during development and in hyperexcitable ('epileptic') tissue. I use electrophysiology, pharmacology and immunohistochemistry to distinguish calcium permeable (GluR2-lacking) from calcium impermeable (GluR2-containing) AMPA receptors. I am investigating electrophysiological differences between synaptic and extrasynaptic receptors, as well as connectivity mapping using glutamate uncaging/laser scanning photostimulation. By comparing results from control neocortex to those from hyperexcitable cortical tissue, I hope to gain insights into the mechanisms underlying focal epilepsies. |
| Julia Factoids |
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One late night in the lab, I tattooed a dot on my ankle to see if that
ink was really permanent. It is.
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| Contact Julia |
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