This renewal application is focused on the study of the development of the basolateral complex and medial nucleus of the amygdala. Collectively these nuclei regulate major aspects of limbic system function. Our previous studies have identified distinct progenitor pools in the developing telencephalon that contribute to postnatal neuronal cell diversity in these amygdala subdivisions. Based on this work, in this project we will test two hypotheses. First, we will test the hypothesis that embryonic transcriptional factor expression diversity within amygdala progenitor pools underlies differential postnatal amygdala neuronal subtype fate and patterns of axonal connectivity. Second, we will test the hypothesis that key transcription factors that are expressed in these progenitor domains are required for the development and/or connectivity of postnatal amygdala neurons that are derived from these populations. Testing of these hypotheses will be accomplished using a combination cutting edge approaches including genetic fate mapping, electrophysiology, axonal tracing and conditional loss of function.
The mammalian amygdala is a central structure of the brain's limbic system, a brain circuit that coordinates appropriate behavioral responses to stimuli with emotional and motivational salience. Amygdala dysfunction is associated with numerous brain disorders including addictive behavior and developmental disorders such as autism spectrum disorders. This proposal is directed toward understanding the genetic and cellular basis of amygdala development, and thus will provide valuable insight into human disorders in which amygdala function is altered.
|Jones, Kevin S; Corbin, Joshua G; Huntsman, Molly M (2014) Neonatal NMDA receptor blockade disrupts spike timing and glutamatergic synapses in fast spiking interneurons in a NMDA receptor hypofunction model of schizophrenia. PLoS One 9:e109303|
|Vislay, Rebecca L; Martin, Brandon S; Olmos-Serrano, Jose Luis et al. (2013) Homeostatic responses fail to correct defective amygdala inhibitory circuit maturation in fragile X syndrome. J Neurosci 33:7548-58|
|Cocas, Laura A; Georgala, Petrina A; Mangin, Jean-Marie et al. (2011) Pax6 is required at the telencephalic pallial-subpallial boundary for the generation of neuronal diversity in the postnatal limbic system. J Neurosci 31:5313-24|
|Olmos-Serrano, Jose Luis; Paluszkiewicz, Scott M; Martin, Brandon S et al. (2010) Defective GABAergic neurotransmission and pharmacological rescue of neuronal hyperexcitability in the amygdala in a mouse model of fragile X syndrome. J Neurosci 30:9929-38|
|Gray, Paul A; Hayes, John A; Ling, Guang Y et al. (2010) Developmental origin of preBotzinger complex respiratory neurons. J Neurosci 30:14883-95|
|Carney, Rosalind S E; Cocas, Laura A; Hirata, Tsutomu et al. (2009) Differential regulation of telencephalic pallial-subpallial boundary patterning by Pax6 and Gsh2. Cereb Cortex 19:745-59|
|Hirata, Tsutomu; Li, Peijun; Lanuza, Guillermo M et al. (2009) Identification of distinct telencephalic progenitor pools for neuronal diversity in the amygdala. Nat Neurosci 12:141-9|
|Corbin, Joshua G; Haydar, Tarik F (2007) Quantum dots for neuroscience research: new tools for old problems? Nanomedicine (Lond) 2:579-81|
|Slotkin, Jonathan R; Chakrabarti, Lina; Dai, Hai Ning et al. (2007) In vivo quantum dot labeling of mammalian stem and progenitor cells. Dev Dyn 236:3393-401|
|Carney, Rosalind S E; Alfonso, Teresa B; Cohen, Daniela et al. (2006) Cell migration along the lateral cortical stream to the developing basal telencephalic limbic system. J Neurosci 26:11562-74|
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