ORIGINAL RESEARCH article
Front. Cell. Neurosci.
Sec. Cellular Neurophysiology
Volume 19 - 2025 | doi: 10.3389/fncel.2025.1690447
Htr1b is Necessary for Normal Retinal Function in Mice
Provisionally accepted
- Baylor College of Medicine, Houston, United States
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Serotonin (5-HT) is a neurotransmitter that is involved in retinal development, retinal physiology, and vision, yet the specific contribution of individual 5-HT receptors to retinal function is poorly characterized. We have identified 5-HT receptor 1B (Htr1b) as a key regulator of serotonin-related responses in the retina. Htr1b transcript and HTR1B protein localize to RGCs and the inner retina. While histology and SD-OCT imaging show that Htr1b mutant mice have a grossly normal retinal anatomy, optomotor behavioral experiments showcased that these mice have reduced scotopic contrast sensitivity and decreased visual acuity. In vivo electroretinogram recordings show that RGCs have latency delays and show reduced sensitivity to changes in light intensity. Ex vivo multielectrode array experiments show altered RGC function and increased variability in response to exogenous 5-HT. There were distinct effects in ON and OFF RGCs; Htr1b-/- ON RGCs showed elevated basal firing rates while Htr1b-/- OFF RGCs showed reduced 5-HT responses. Overall, Htr1b plays a crucial role in retinal serotonergic signaling.
Keywords: Retina, Serotonin, 5-HT, 5-Hydroxytryptamine, Serotonin receptor 1B (HTR1B), 5-HT1B, Retinal ganglion cell (RGC)
Received: 21 Aug 2025; Accepted: 20 Oct 2025.
Copyright: © 2025 Gibson, Tao, Shen, Ma, Park, Polo-Prieto and Frankfort. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Benjamin J Frankfort, benjamin.frankfort@bcm.edu
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