Light Aversion in Neonatal Mice
These datasets were generated to study the neural mechanisms of light aversion in neonatal mice. For further details, see the abstract below and the publication at biorxiv (DOI: https://doi.org/10.1101/2022.01.20.477130) or Journal of Neuroscience (DOI: https://doi.org/10.1523/JNEUROSCI.0151-22.2022). There are two types of data: Behavioral tracking of neonatal mice during a light aversion assay Two-photon calcium imaging of ganglion cells in acutely dissected neonatal mouse retinas Each data type has associated summary spreadsheets containing metadata and sets of minimally preprocessed data pertaining to individual behavioral trials or calcium imaging sessions. Code used to analyze the dataset can be found at https://github.com/FellerLabCodeShare Abstract: Aversive responses to bright light (photoaversion) require signaling from the eye to the brain. Melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) encode absolute light intensity and are thought to provide the light signals for photoaversion. Consistent with this, neonatal mice exhibit photoaversion prior to the developmental onset of image vision, and melanopsin deletion abolishes photoaversion in neonates. It is not well understood how the population of ipRGCs, which constitutes multiple physiologically distinct types (denoted M1-M6 in mouse), encodes light stimuli to produce an aversive response. We provide several lines of evidence that M1 ipRGCs that lack the Brn3b transcription factor drive photoaversion in neonatal mice. First, neonatal mice lacking TRPC6 and TRPC7 ion channels failed to turn away from bright light, while two photon Ca2+ imaging of their acutely isolated retinas revealed reduced photosensitivity in M1 ipRGCs, but not other ipRGC types. Second, mice in which all ipRGC types except for Brn3b-negative M1 ipRGCs are ablated, exhibited normal photoaversion. Third, pharmacological blockade or genetic knockout of gap junction channels expressed by ipRGCs, which reduces the light sensitivity of M2-M6 ipRGCs in the neonatal retina, had small effects on photoaversion only at the brightest light intensities. Finally, M1s were not strongly depolarized by spontaneous retinal waves, a robust source of activity in the developing retina that depolarizes all other ipRGC types. M1s therefore constitute a separate information channel between the neonatal retina and brain that could ensure behavioral responses to light but not spontaneous retinal waves.