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High-probability grants
According to our matching algorithm, Georgia M. Alexander is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2004 — 2005 |
Alexander, Georgia M |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Epilepsy Therapy Using Metabotropic Glutamate Receptors @ Wake Forest University Health Sciences
DESCRIPTION (provided by applicant): This proposal is focused on coupling anatomical and electrophysiological techniques to answer questions of location and function of Group II metabotropic glutamate receptors (mGluRs) with the hopes of identifying a novel target for the treatment of absence epilepsy. To do this we will investigate 2 complementary aims. Aim 1 is the localization of Group II mGluRs within the thalamocortical absence circuitry in an animal model of absence (the ferret) at the light and electron microscopic level. We hypothesize that these receptors are found on presynaptic cortical terminals innervating the TRN, presynaptic TRN terminals innervating the LGN and on TRN dendrites opposing cortical terminals, thus allowing the potential for multiple functions of the Group II mGluRs in the control of cortically-evoked spike-and-wave activity. Aim 2 is directed at understanding the function of Group II mGluRs in the corticothalamic network. In this aim, we will study the influence of Group II mGluRs on corticothalamic and intra-thalamic synaptic transmission. Furthermore, we will induce absence rhythms in the in vitro slice and investigate whether modulation of Group II mGluRs will reduce these rhythms. We hypothesize that activation of Group II mGluRs will attenuate the cortically driven signal to the thalamus, and this attenuation will reduce the ability of the corticothalamic network to initiate and propagate absence rhythms.
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0.97 |
2007 — 2009 |
Alexander, Georgia M |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Single Unit Multi-Site Electrophysiological Characterization of Epileptogenesis
[unreadable] DESCRIPTION (provided by applicant): A dominant theme in limbic epilepsy research has been the "dentate gate" hypothesis which states that dentate granule cells of a normal brain limit invasion of CAS and CA1 by seizure activity from entorhinal cortex. In vivo evidence of the "dentate gate" is based upon 2-deoxyglucose imaging, hippocampal EEG, and field potential recordings of the dentate gyrus (DG) in animal models of seizures. Breakdown of the dentate gate is one mechanism thought to contribute to limbic epileptogenesis, and in vitro evidence from slices of kindled animals suggests increased penetration of excitation through DG into CAS in kindled animals. Recently, however, contrary in vitro evidence from spontaneously seizing animals has suggested that the dentate gate is intact in epileptic animals, and another direct projection from entorhinal cortex, the temporoammonic pathway (which was not studied in kindled slices) is strengthened in epilepsy. Our objective is to assess the various possibilities which lead to a strengthened entorhinal-hippocampal circuit in epilepsy by recording in vivo simultaneously from DG and hippocampal neurons of CAS and CA1 during each stage of kindling, thus eliminating fiber transaction confounds found in vitro and allowing within-animal comparison of the strength of each hippocampal pathway over the course of kindling. Therefore, in my single aim, I will use the powerful new recording technique of multisite single-unit recordings to simultaneously record tens of single units, which can be deciphered as primary neurons or interneurons, and local field potentials within DG, CAS and CA1 during epileptogenesis induced by stimulation of medial entorhinal cortex. This will permit monitoring the sequential recruitment of neurons into seizure activity within each population of neurons during epileptogenesis in the kindling model, thereby determining whether the dentate granule cells do in fact serve as a gate limiting seizure invasion of hippocampus. In sum, our study will directly test the dentate gate hypothesis at the finest resolution of neuronal activity currently available, thus building on years of research in understanding the mechanisms of epileptogenesis. Understanding the mechanisms of limbic epileptogenesis will hopefully lead to more effective treatment and ideally prevention of this disorder. [unreadable] [unreadable] [unreadable] [unreadable]
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