bioRxiv ScienceSearch

bioRxiv · 10.1101/675702

Light responses of melanopsin-expressing ganglion cells in the foetal mammalian retina

Abstract

Sensory stimulation plays a critical role in the maturation of sensory organs and systems. For example, when deprived of light before birth, foetal mouse pups in utero exhibit altered ocular vascular development. Normal vascular development depends on light excitation of melanopsin, a non-rod, non-cone photopigment that is expressed in a subset of ganglion cells (mRGCs) in the retina. However, there is no direct evidence that mRGCs in foetal eyes are light-responsive. Very little is known about how light absorption leads to excitation in these foetal neurons. Using mRGC-specific expression of the calcium indicators GCaMP3 and GCaMP6, we report that foetal mouse mRGCs respond to light as early as 4 days before birth. Further, two distinct Gq/11-G protein family antagonists, FR9000359 and YM-254890, abolish these light responses. TTX, a blocker of voltage-activated sodium channels, reversibly represses light responses, and FPL6417 and L-cis-diltiazem, which modify L-type calcium channels, respectively increase and reduce light responses. Electrophysiological patch pipette recordings show that embryonic mRGCs respond to light of intensity as low as 2.9 x 1012 photons/cm2/s. The present findings demonstrate a heretofore unproven but postulated light sensitivity in the retinas of foetal mice and identify the transduction pathways involved. Surprisingly, mRGCs do not function as completely independent photoreceptors but are electrotonically coupled with other mRGCs. Given that melanopsin is expressed in foetal human retinas, these findings support the idea that the eyes of foetal and early preterm infants are likely to exhibit functional photosensitivity.\n\nKey pointsO_LIMelanopsin is a light-excitable photopigment expressed in a subset of ganglion cell neurons (mRGCs) in the retinas of many different species of vertebrates. In mature animals, light activation of mRGCs modulates many visual adaptive functions including pupil constriction, entrainment of circadian rhythms, mood and learning. In neonatal pups at ages prior to the developmental onset of visual signalling from rods and cones, melanopsin cells mediate photoaversive behaviour. In foetal pups, light activation of melanopsin cells accelerates maturation of the ocular vasculature. Here, we describe and physiologically characterize the light responses of melanopsin ganglion cells in the retinas of foetal pups.\nC_LIO_LIMRGCs in embryonic retinas respond to light at least four days prior to birth and exhibit responses to light of intensity as low as 3 x 1012 photons/cm2/s.\nC_LIO_LIPhototransduction mechanisms include melanopsin activation of Gq/11 - G proteins, voltage-activated sodium currents, and voltage-gated L-type calcium currents.\nC_LIO_LIMRGCs are electrotonically coupled to other mRGCs in foetal retinas.\nC_LIO_LIWe propose that melanopsin-expressing ganglion cells are excited by light while in utero and that this excitation relies, for the most part, on phototransduction pathways that have been described in postnatal retinas. Furthermore, we propose that foetal mRGCs have the requisite properties to modulate light-regulated maturation of the ocular vasculature and, perhaps, the development of visual pathways.\nC_LI

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Verweij, J., Chaney, S., Bredl, D., Vemaraju, S., Konig, G., Kostenis, E., Lang, R., Copenhagen, D.. 2019-06-20. Light responses of melanopsin-expressing ganglion cells in the foetal mammalian retina. https://doi.org/10.1101/675702

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience