The retinal basis of light aversion in neonatal mice

• Autores: Caval Holme, Franklin S.; Aranda, Marcos L.; Chen, Andy Q.; Tiriac, Alexandre; Zhang, Yizhen; Smith, Benjamin; Birnbaumer, Lutz; Schmidt, Tiffany M.; Feller, Marla B.
• Año de publicación: 2022
• Idioma: inglés
• Tipo de recurso: artículo
• Fuente: The Journal of Neuroscience. Vol.42, No.20, 4101-4115, 2022
• Materia: RETINA; DESARROLLO; ENUCLEACION; CORRIENTE FOTOELECTRICA; FOTOFOBIA
• Institución: Pontificia Universidad Católica Argentina

Fil: Caval Holme, Franklin S. University of California Berkeley. Helen Wills Neuroscience Institute; Estados Unidos
Fil: Aranda, Marcos L. Northwestern University. Department of Neurobiology; Estados Unidos
Fil: Chen, Andy Q. University of California Berkeley. Department of Molecular and Cell Biology; Estados Unidos
Fil: Tiriac, Alexandre. University of California Berkeley. Department of Molecular and Cell Biology; Estados Unidos
Fil: Zhang, Yizhen. University of California Berkeley. Department of Molecular and Cell Biology; Estados Unidos
Fil: Smith, Benjamin. University of California Berkeley. School of Optometry; Estados Unidos
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina; Argentina
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. National Institutes of Health. Signal Transduction Laboratory; Estados Unidos
Fil: Schmidt, Tiffany M. Northwestern University. Department of Neurobiology; Estados Unidos
Fil: Schmidt, Tiffany M. Northwestern University Feinberg School of Medicine. Department of Ophthalmology; Estados Unidos
Fil: Feller, Marla B. University of California Berkeley. Helen Wills Neuroscience Institute; Estados Unidos
Fil: Feller, Marla B. University of California Berkeley. Department of Molecular and Cell Biology; Estados Unidos
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 before 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. Here, 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 Ca21 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 Brn3bnegative 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...