Ongoing Research Support
Title: Development of the basal telencephalic limbic system. The goal of this grant is to elucidate the genetic and cellular basis for development of the basal telencephalic limbic system encompassing the different subnuclei of the amygdala and the hypothalamus.
Title: Assembly and Function of Olfactory Circuitry from Dbx1-derived Neural Progenitors. The goal of this grant is to understand the mechanisms underlying development of genetically tagged subpopulations of accessory olfactory bulb neurons and their patterns of connectivity between the olfactory epithelium.
Title: Linking Autism genotype to executive function-social reciprocity behavioral phenotypes.
Completed Research Support (within the past 3 years)
1) NIH R01DA020140 Supplements
Title: Administrative Supplement to Development of the basal telencephalic limbic system
Awarded a total of 4 separate administrative supplements for: 1) 2) under the title “Research on Sex/Gender Differences” to provide funds for examination of both male and female mice as part of our studies under the parent grant.
2) Sage Therapeutics.
Title: Pre-clinical trials of correction of tonic inhibitory defects in the Fragile X amygdala The goal of this award was to test compounds that affect GABAergic neurotransmission to correct of amygdala inhibitory neuronal transmission deficits in the Fmr1-/y mouse model of FXS.
3) Autism Speaks, Basic and Clinical Research Award
Title: GABA transmission in the amygdala in Fmr1 mouse models of Fragile X Syndrome. The goal of this grant was to identify the pathological cellular mechanisms underlying amygdala inhibitory neurotransmission deficits in Fmr1-/y mouse model of FXS.
4) NIH NINDS R56NS53719
Title: Testing the Excitability of Inhibitory Neurons The goal of this grant was to determine the mechanism of synaptic and network dysfunction of interneurons in the Fmr1-/y mouse model of Fragile X Syndrome.
5) NIH R01GM103842
Title: Carbon monoxide exposure and anesthesia-induced neurotoxicity. The goal of this grant is to elucidate the consequences of low levels of CO exposure on neuronal viability