Area:
neurogenetics, behavior genetics
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, David C. Airey is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2000 |
Airey, David C |
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. |
Control of Mouse Retinal Cell Populations: Rods &Cones @ University of Tennessee Health Sci Ctr
DESCRIPTION (Verbatim from applicant's abstract): The long-term objective of this application is to understand the control of normal variation in the cytoarchitecture of the major retinal cell populations in adult mice. The results of this application will describe variation in rod and cone photoreceptor number and density as well as variation in the dorsoventral fields of S-, M-, and double-pigmented cones in different strains, and will identify the quantitative trait loci (QTL) controlling these phenotypes. Photoreceptor number will be acquired with stereologically unbiased counting methods from both retina wholemounts using DIC optics and from stained cryostat-sectioned retinas. Cone subtypes will be distinguished by immunocytochemical staining. Understanding retinal development, particularly photoreceptor development, has clear health benefits, because many human diseases resulting in blindness affect photoreceptors.
|
0.948 |
2003 |
Airey, David C |
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. |
Serotonergic Regulation of Sensorimotor Gating in Mice
DESCRIPTION (provided by applicant): Animals are effectively used to model prepulse inhibition, the ability of a detectable stimulus to inhibit or gate response to a secondary startling stimulus. Deficits in prepulse inhibition are seen in persons with schizophrenia, their relatives, and persons with schizotypal disorder. This application proposes to analyze the role of variation in two genes, Htr1a and Htr1b, and their products, the G-protein coupled serotonin receptors 5-HT1A and 5-HT1B, in sensorimotor gating processes in mice. Previous analyses of pharmacologic effects and knockout mice implicate these genes and receptors in regulating prepulse inhibiton, but it is unknown if or how they might play a role in determining differences between individuals or isogenic strains. Twenty genetically and phenotypically diverse inbred mouse strains will be surveyed for variation at three levels, (i) genetic sequence, (ii) brain receptor distribution, and (iii) agonist actions on prepulse inhibition. The hypothesis that genetic variation in Htr1a and Htr1b influences sensorimotor gating processes will be evaluated by direct association of strain haplotype and behavioral phenotype. Variation in the distribution of functional receptors in the brain will be tested as a neural phenotype mediating genetic and behavioral differences.
|
1 |
2007 — 2008 |
Airey, David C |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Genetic Analysis of Htr2c Rna Editing in Amygdala
[unreadable] DESCRIPTION (provided by applicant): Htr2c RNA editing alters the potential contribution of 5-HT2C receptors to brain function by producing up to 24 receptor isoforms with different signal transduction properties. Htr2c RNA editing is an important endophenotype for serotonergic function and psychiatric disease, and understanding the genetic etiology of this variation is an important goal. Pharmacological manipulations implicate the cognate ligand serotonin (5-HT) in the regulation of RNA edited 5-HT2C receptors. Inbred mouse strain differences in both serotonin and RNA editing implicate genetic sources of variation. Two single nucleotide polymoprhisms are known to affect serotonergic function in mice. Aims 1, 2, and 3 make use of a balanced factorial table of 40 BXD recombinant inbred lines of mice that represent every two-allele combination of the SNPs Tph2:Pro447Arg and Slc6a4:Glu39Gly. Because the genetic background of the BXD RI lines has been randomized by breeding, this panel of mice in essence performs as a virtual double congenic for two important functional SNPs in the genes for tryptophan hydroxylase and the serotonin transporter. Aim 1 tests the candidacy of these SNPs as quantitative trait nucleotides (QTNs) affecting Htr2c RNA editing profiles. Aim 2 uses genome-wide QTL mapping to explore more broadly other genetic loci that may influence Htr2c RNA editing profiles. Aim 3 proposes to explore behavioral and transcriptome correlates of Htr2c RNA editing. The mouse brain region of investigation is the amygdala, which is rich in 5-HT2C receptors and plays important functional roles in stress, anxiety, fear, and emotional learning and memory. In humans, the amygdala appears to function in related psychological disorders. The serotonin 2C receptor is a focus of mental health research. This proposal aims to discover genetic causes and behavioral correlates of variation in RNA that codes for up to 24 functionally different protein isoforms of the serotonin 2C receptor. The brain region of investigation is the amygdala, which is rich in serotonin 2C receptors and plays important roles in anxiety disorders and depression. [unreadable] [unreadable]
|
1 |