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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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| 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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| 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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| 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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| | 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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| Isabel Parada |
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| expert histologist & microscopist |
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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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| Catherine Christian |
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| postdoctoral fellow |
| Research Topic |
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| I'm working on two projects, but they are top secret so I can't tell you about them yet. |
| Contact Catherine |
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| | Chris Dulla |
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| postdoctoral fellow |
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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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