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PLoS One. 2013 Dec 31;8(12):e83974. doi: 10.1371/journal.pone.0083974. eCollection 2013.

Glutamatergic neurotransmission from melanopsin retinal ganglion cells is required for neonatal photoaversion but not adult pupillary light reflex.

Author information

1
Department of Ophthalmology, University of California San Francisco, San Francisco, California, United States of America.
2
Department of Anatomy, University of California San Francisco, San Francisco, California United States of America.
3
Department of Ophthalmology, University of California San Francisco, San Francisco, California, United States of America ; Department of Anatomy, University of California San Francisco, San Francisco, California United States of America.
4
Department of Physiology, University of California San Francisco, San Francisco, California, United States of America ; Department of Neurology, University of California, San Francisco San Francisco, California, United States of America.
5
Department of Neurology, University of California, San Francisco San Francisco, California, United States of America ; Department of Neurosciences, University of California San Diego, San Diego, California, United States of America.
6
Department of Ophthalmology, University of California San Francisco, San Francisco, California, United States of America ; Department of Physiology, University of California San Francisco, San Francisco, California, United States of America.

Abstract

Melanopsin-expressing retinal ganglion cells (mRGCs) in the eye play an important role in many light-activated non-image-forming functions including neonatal photoaversion and the adult pupillary light reflex (PLR). MRGCs rely on glutamate and possibly PACAP (pituitary adenylate cyclase-activating polypeptide) to relay visual signals to the brain. However, the role of these neurotransmitters for individual non-image-forming responses remains poorly understood. To clarify the role of glutamatergic signaling from mRGCs in neonatal aversion to light and in adult PLR, we conditionally deleted vesicular glutamate transporter (VGLUT2) selectively from mRGCs in mice. We found that deletion of VGLUT2 in mRGCs abolished negative phototaxis and light-induced distress vocalizations in neonatal mice, underscoring a necessary role for glutamatergic signaling. In adult mice, loss of VGLUT2 in mRGCs resulted in a slow and an incomplete PLR. We conclude that glutamatergic neurotransmission from mRGCs is required for neonatal photoaversion but is complemented by another non-glutamatergic signaling mechanism for the pupillary light reflex in adult mice. We speculate that this complementary signaling might be due to PACAP neurotransmission from mRGCs.

PMID:
24391855
PMCID:
PMC3877098
DOI:
10.1371/journal.pone.0083974
[Indexed for MEDLINE]
Free PMC Article
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