PT  - JOURNAL ARTICLE
AU  - Maynard, Kristen R.
AU  - Kardian, Alisha
AU  - Hill, Julia L.
AU  - Mai, Yishan
AU  - Barry, Brianna
AU  - Hallock, Henry L.
AU  - Jaffe, Andrew E.
AU  - Martinowich, Keri
TI  - TrkB Signaling Influences Gene Expression in Cortistatin-Expressing Interneurons
AID  - 10.1523/ENEURO.0310-19.2019
DP  - 2020 Jan 01
TA  - eneuro
PG  - ENEURO.0310-19.2019
VI  - 7
IP  - 1
4099  - http://www.eneuro.org/content/7/1/ENEURO.0310-19.2019.short
4100  - http://www.eneuro.org/content/7/1/ENEURO.0310-19.2019.full
SO  - eNeuro2020 Jan 01; 7
AB  - Brain-derived neurotrophic factor (BDNF) signals through its cognate receptor tropomyosin receptor kinase B (TrkB) to promote the function of several classes of inhibitory interneurons. We previously reported that loss of BDNF–TrkB signaling in cortistatin (Cort)-expressing interneurons leads to behavioral hyperactivity and spontaneous seizures in mice. We performed bulk RNA sequencing (RNA-seq) from the cortex of mice with disruption of BDNF–TrkB signaling in cortistatin interneurons, and identified differential expression of genes important for excitatory neuron function. Using translating ribosome affinity purification and RNA-seq, we define a molecular profile for Cort-expressing inhibitory neurons and subsequently compare the translatome of normal and TrkB-depleted Cort neurons, revealing alterations in calcium signaling and axon development. Several of the genes enriched in Cort neurons and differentially expressed in TrkB-depleted neurons are also implicated in autism and epilepsy. Our findings highlight TrkB-dependent molecular pathways as critical for the maturation of inhibitory interneurons and support the hypothesis that loss of BDNF signaling in Cort interneurons leads to altered excitatory/inhibitory balance.