| First Author | Maynard KR | Year | 2020 |
| Journal | eNeuro | Volume | 7 |
| Issue | 1 | PubMed ID | 31941661 |
| Mgi Jnum | J:288436 | Mgi Id | MGI:6432192 |
| Doi | 10.1523/ENEURO.0310-19.2019 | Citation | Maynard KR, et al. (2020) TrkB Signaling Influences Gene Expression in Cortistatin-Expressing Interneurons. eNeuro 7(1):ENEURO.0310-19.2019 |
| abstractText | 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. |
