Regulation of Neural Circuit Development by Cadherin-11 Provides Implications for Autism

The organ of Corti, the sensory epithelium of the mammalian auditory system, uses afferent and efferent synapses for encoding auditory signals and top-down modulation of cochlear function. During development, the final precisely ordered sensorineural circuit is established following excessive formation of afferent and efferent synapses and subsequent refinement. Here, we review the development of innervation of the mouse organ of Corti and its regulation.

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Neurotrophin, p75, and Trk Signaling Module in the Developing Nervous System of the Marine AnnelidPlatynereis dumerilii

BioMed Research International ◽

10.1155/2016/2456062 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 6

Author(s):

Antonella Lauri ◽

Paola Bertucci ◽

Detlev Arendt

Keyword(s):

Nervous System ◽

Neuronal Development ◽

Neural Circuit ◽

Circuit Development ◽

Circuit Formation ◽

Neurotrophic Signaling ◽

High Degree ◽

Developing Nervous System

In vertebrates, neurotrophic signaling plays an important role in neuronal development, neural circuit formation, and neuronal plasticity, but its evolutionary origin remains obscure. We found and validated nucleotide sequences encoding putative neurotrophic ligands (neurotrophin, NT) and receptors (Trk and p75) in two annelids,Platynereis dumerilii(Errantia) andCapitella teleta(Sedentaria, for which some sequences were found recently by Wilson, 2009). Predicted protein sequences and structures ofPlatynereisneurotrophic molecules reveal a high degree of conservation with the vertebrate counterparts; some amino acids signatures present in the annelid Trk sequences are absent in the basal chordate amphioxus, reflecting secondary loss in the cephalochordate lineage. In addition, expression analysis of NT, Trk, and p75 duringPlatynereisdevelopment by whole-mount mRNAin situhybridization supports a role of these molecules in nervous system and circuit development. These annelid data corroborate the hypothesis that the neurotrophic signaling and its involvement in shaping neural networks predate the protostome-deuterostome split and were present in bilaterian ancestors.

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Timing and Duration of Gbx2 Expression Delineates Thalamocortical and Dopaminergic Medial Forebrain Bundle Circuitry

10.1101/579664 ◽

2019 ◽

Author(s):

Elizabeth Normand ◽

Catherine Browning ◽

Mark Zervas

Keyword(s):

Gene Expression ◽

Medial Forebrain Bundle ◽

Neural Circuit ◽

Temporal Dynamics ◽

Neuronal Cell ◽

Cell Types ◽

Dopamine Neurons ◽

Genetic Lineage ◽

Thalamocortical Axons ◽

Circuit Development

SUMMARYGene expression is a dynamic process, which is highly coordinated during development to ensure the proper allocation and identity of neuronal cell types within the brain. Equally important during neurodevelopment is how cohorts of neurons establish axonal projections that innervate terminal target sites. We sought to bridge the temporal dynamics of gene expression, within a specific genetic lineage, to the establishment of neuronal circuits derived from cohorts of the lineage-specific progenitors. A central goal was to be able to accomplish genetic inducible circuit mapping non-invasively and with commonly available CreER/loxP technology. Specifically, we genetically marked thalamic neuron progenitors that expressed the transcription factor Gbx2 at an early embryonic stage and tracked the formation of lineage-derived thalamocortical axons during embryogenesis. We then assessed the neural circuitry at an early postnatal stage. We show that the temporal specificity of lineage marking provides a high degree of clarity for following neural circuit development. We also determined that the onset and duration of gene expression can delineate subsets of neural circuits derived from a common lineage. For example, we uncovered a novel contribution of Gbx2-expressing progenitors to midbrain dopamine neurons and dopaminergic axons of the medial forebrain bundle. We anticipate that this system can be instructive in elucidating changes in neural circuit development in both normal development and in mutant mice in which neural circuit formation is altered.

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