Recent advances in the expression profiling and manipulation of developmental patterning genes and in the visualization of neuronal activity has begun to shed light on how genes direct the patterning and functional development of neuronal circuits in the brainstem and cerebellum. In this research topic, we present new insights into the formation of specific sensory, sensorimotor, and motor regulatory circuits in these vital parts of the vertebrate brain during embryonic, fetal and early postnatal life. Topics include how patterning genes specify neuron identities and regulate axon pathfinding and synaptic targeting, how activity patterns develop and become sculpted into circuit-specific interactions, and how genes and activity may interact to provide ongoing consolidation and plasticity during circuit use and modification. These topics are approached through the use of cutting edge technologies for assessing gene expression and regulation in identified neuron populations, optical mapping of circuit function, behavioral testing, and genetic manipulation to test the role of specific genes and epigenetic mechanisms. In the case of some circuits, several animal models are included, providing a degree of comparative analysis that also sheds light on the evolutionary underpinnings governing the molecular genetics of neuronal circuit formation.
Systems included:
Auditory
Vestibular
Trigeminal
Serotonergic
Respiration
Precerebellar
Cerebellar
Animal models included:
Mouse
Chicken
Frog
Recent advances in the expression profiling and manipulation of developmental patterning genes and in the visualization of neuronal activity has begun to shed light on how genes direct the patterning and functional development of neuronal circuits in the brainstem and cerebellum. In this research topic, we present new insights into the formation of specific sensory, sensorimotor, and motor regulatory circuits in these vital parts of the vertebrate brain during embryonic, fetal and early postnatal life. Topics include how patterning genes specify neuron identities and regulate axon pathfinding and synaptic targeting, how activity patterns develop and become sculpted into circuit-specific interactions, and how genes and activity may interact to provide ongoing consolidation and plasticity during circuit use and modification. These topics are approached through the use of cutting edge technologies for assessing gene expression and regulation in identified neuron populations, optical mapping of circuit function, behavioral testing, and genetic manipulation to test the role of specific genes and epigenetic mechanisms. In the case of some circuits, several animal models are included, providing a degree of comparative analysis that also sheds light on the evolutionary underpinnings governing the molecular genetics of neuronal circuit formation.
Systems included:
Auditory
Vestibular
Trigeminal
Serotonergic
Respiration
Precerebellar
Cerebellar
Animal models included:
Mouse
Chicken
Frog
![Retraction of spontaneous activity (SA) over developmental time. (A) Initiation and propagation of an event at E11.5. Images taken at the indicated times show an event initiating at the initiation zone (InZ; *), which propagates rostrally and laterally. Colored circles indicate regions of interest (ROIs, at 0.0 s) positioned rostrocaudally along the midline (orange, red, brown) and mediolaterally from the InZ (red, green, blue). Scale bar: 100 μm. (B) Representative [Ca]i traces recorded at E11.5 (left), E13.5 (middle) and E15.5 (right) in r2, showing rostrocaudal (top) and mediolateral (bottom) propagation. Traces are stacked for clarity and the color corresponds to the position of ROIs shown in (A). The event from the images in (A) is marked with gray vertical bar. Scale bar = 5 F/F, 1 min. (C) At E11.5, SA encompasses the entire hindbrain. Intensity of [Ca]i signal is higher at the midline (dark orange) compared with the lateral regions (light orange). The region of [Ca]i imaging shown in (A,B) is indicated by gray rectangle, marked “r2”. By E13.5 the propagation has retracted from lateral and caudal regions middle image. SA disappears by E15.5 (right image). Circles indicating sites of patch clamp recordings shown in (D,E), with gray indicating InZ (r2) site, blue is caudal midline site, and red is lateral site. Some parts of the figure are adapted and modified from Hunt et al. (2006a) and Watari et al. (2013). Scale bar: 1 mm. (D) Examples of current clamp recordings at different sites and stages, showing SA events in midline (black, blue) and gradual hyperpolarization over time. (E) Averaged data from all stages, showing hyperpolarization first in lateral (red) regions, followed by caudal midline (blue) and finally by r2 (InZ) midline cells.](https://www.frontiersin.org/_rtmag/_next/image?url=https%3A%2F%2Fwww.frontiersin.org%2Ffiles%2FArticles%2F236054%2Ffncir-10-00110-HTML%2Fimage_m%2Ffncir-10-00110-g001.jpg&w=3840&q=75)
