Abstract
Abstract
The transient receptor potential cation channel subfamily V member 1 (Trpv1) is a polymodal sensor of noxious stimuli, including heat and pain. However, its contribution to mammalian reproductive physiology remains incompletely understood. Here, we evaluated reproductive phenotypes and transcriptomic responses in a Trpv1-knockout mouse model under normal and heat-stress conditions. Vaginal-smear profiling showed altered estrous cyclicity in Trpv1-deficient females. Bulk RNA-seq and Smart-seq2 analyses identified tissue- and condition-dependent gene-expression changes associated with Trpv1 deficiency, including extracellular-matrix-related transcriptional signatures in heat-stressed oocytes. In males, Trpv1 deficiency was associated with altered sperm-motility measurements under heat stress, changes in steroidogenesis-related transcripts, and testicular stress-response signatures. These findings identify candidate molecular pathways associated with Trpv1 deficiency and thermal challenge. Further studies, including mating, fertilization, embryo-development, protein-level, and cellular functional assays, are required to determine the consequences for gamete competence and fertility.