English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  The mammalian amygdala is composed of two primary functional subdivisions, classified according to whether the major output projection of each nucleus is excitatory or inhibitory. The posterior dorsal and ventral subdivisions of the medial amygdala, which primarily contain inhibitory output neurons, modulate specific aspects of innate socio-sexual and aggressive behaviors. However, the development of the neuronal diversity of this complex and important structure remains to be fully elucidated.    Results  Using a combination of genetic fate-mapping and loss-of-function analyses, we examined the contribution and function of  Sonic hedgehog  ( Shh )-expressing and  Shh -responsive ( Nkx2-1  +  and  Gli1  + ) neurons in the medial amygdala. Specifically, we found that  Shh-  and  Nkx2-1- lineage cells contribute differentially to the dorsal and ventral subdivisions of the postnatal medial amygdala. These  Shh - and  Nkx2-1 -lineage neurons express overlapping and non-overlapping inhibitory neuronal markers, such as Calbindin, FoxP2, nNOS and Somatostatin, revealing diverse fate contributions in discrete medial amygdala nuclear subdivisions. Electrophysiological analysis of the  Shh -derived neurons additionally reveals an important functional diversity within this lineage in the medial amygdala. Moreover, inducible  Gli1 CreER(T2)   temporal fate mapping shows that early-generated progenitors that respond to  Shh  signaling also contribute to medial amygdala neuronal diversity. Lastly, analysis of  Nkx2-1  mutant mice demonstrates a genetic requirement for  Nkx2-1  in inhibitory neuronal specification in the medial amygdala distinct from the requirement for  Nkx2-1  in cerebral cortical development.    Conclusions  Taken together, these data reveal a differential contribution of  Shh- expressing and  Shh -responding cells to medial amygdala neuronal diversity as well as the function of  Nkx2-1  in the development of this important limbic system structure.

Sonic hedgehogexpressing and responding cells generate neuronal diversity in the medial amygdala