Area:
neurogenetics, neuroendocrinology, depression, stress
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High-probability grants
According to our matching algorithm, Jennifer S. Wilcoxon is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2001 — 2003 |
Wilcoxon, Jennifer S |
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.). |
Fetal Alcohol, Thyroid Hormone Affected Genes &Behavior @ Northwestern University
Fetal alcohol exposure (FAE) in humans leads to hyperactivity, learning deficits, response inhibition and higher prevalence of depression. I would like to find the mechanism(s) responsible for these outcomes in an animal model, in order to facilitate the prevention or treatment of FAE- related behavioral deficits in humans. In our animal model of FAE, we found a hypothyroid state in both the mother and fetus at gestation day 22. Since congenital hypothyroidism results in learning impairments and hyperactivity in children, one of the mechanisms by which the FAE behavioral impairments could be related to the congenital hypothyroidism of the FAE fetus. Preliminary data show increased depressive behavior in both male and female adult FAE offspring in the forced swim test (FST) compared to their pair-fed controls. Thyroid hormone receptor beta (TRbeta) knockout mice show decreased immobility in the FST compared to controls. In addition, using cDNA microarray technology, we have found altered expression in the FAE male amygdala/hypothalamic region on E19 of 80 genes, several of which are thyroid hormone regulated. In order to elucidate the role of thyroid abnormalities in the FAE-induced behavior, first I plan to confirm the results found from the microarray data using real-time quantitative RT-PCR and in situ hybridization. Then I will treat these animals with thyroid hormones prenatally, to correct for the fetal hypothyroid state, to alleviate hyperactivity, learning deficit and increased depressive behavior and changes in thyroid hormone-related gene expression found in these FAE offspring. Finally, I will treat these animals by early postnatal thyroid replacement to determine if this reverses any of the behavioral deficits and/or alterations in gene expression. If any of these thyroid hormone administration paradigms lead to attenuation of behavioral deficits in the FAE offspring, the could become treatments for FAE children.
|
1 |
2006 — 2007 |
Wilcoxon, Jennifer S |
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. |
Specific Role of Fgf8 and Fgf17 in Cortical Patterning
[unreadable] DESCRIPTION (provided by applicant): Altering FGF8/17 signaling in the embryonic cortex causes a rearrangement of the cortical area map. Depending on the exact experimental condition, individual areas and regions can be shrunken or expanded, shifted or duplicated following FGF8/17 manipulations. Nonetheless, initial morphology of individual areas appears normal; moreover, correct thalamic axons find their repositioned targets. We now plan to examine the long-term effects of rearranging the cortical area map. Our overall hypothesis is that alterations in cortical anatomy and function will emerge over time as a result of early changes in the area map. We expect that our findings will help to shed light on how basic organization of cerebral cortical function is set up in development. We plan to generate a series of mouse lines in which progressive loss of FGF8/17 signaling leads to a progressive decrease in anterior cortex. These findings should further characterize the role of FGF8/17 signaling in anterior-posterior (A/P) patterning of the cortex. We will then determine which receptors are involved in Fgf8/17 signaling by conditionally deleting floxed Fgf receptor genes in the cortical primoridum. Our prediction is that loss of two or more Fgf receptors will phenocopy reduction of Fgf8. Finally, we will cross mutant mouse lines to delete, sequentially, one or both alleles of the genes encoding Emx2, Fgf8, Fgf17. Findings should help identify interactions between telencephalic Fgf8 and some of the transcription factors implicated in area patterning. [unreadable] [unreadable]
|
0.948 |