Relaxed selective pressure on an essential component of pheromone transduction in primate evolution.
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The vomeronasal organ (VNO) detects pheromones in many vertebrate species but is likely to be vestigial in humans. TRPC2(TRP2), a gene that is essential for VNO function in the mouse, is a pseudogene in humans. Because TRPC2 is expressed only in the VNO, the loss of selective pressure on this gene can serve as a molecular marker for the time at which the VNO became vestigial. By analyzing sequence data from the TRPC2 gene of 15 extant primate species, we provide evidence that the VNO was most likely functional in the common ancestor of New World monkeys and Old World monkeys and apes, but then became vestigial in the common ancestor of Old World monkeys and apes. We propose that, at this point in evolution, other modalities, notably the development of color vision, may have largely replaced signaling by pheromones. (+info)
Sex and the MHC.
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Major histocompatibility complex class Ib molecules may play a surprising role in pheromone detection in mammals. (+info)
Regulation by voltage and adenine nucleotides of a Ca2+-activated cation channel from hamster vomeronasal sensory neurons.
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Bipolar sensory neurons within the vomeronasal organ (VNO) are thought to mediate the detection of pheromones in vertebrates. In the mouse, VNO neurons respond to pheromones with a rise in intracellular Ca2+ that accompanies a depolarization of the cell. Transduction of the pheromone appears to occur through the activation of a phosphatidylinositol signalling pathway, but the ion channels that respond to this signalling pathway have not been identified. In this report patch-clamp recording from hamster vomeronasal sensory neurons was used to identify second-messenger-gated channels that might play a role in transduction. The results demonstrate that VNO neurons show abundant expression of a Ca2+-activated non-selective (CaNS) cation channel. The CaNS channel does not discriminate between Na+ and K+ and has a slope conductance of 22 pS. Half-activation of the channel occurs at a Ca2+ concentration of 0.5 mM (at -80 mV). The probability of opening (Po) of the channel is further augmented at positive potentials, and shows an e-fold voltage dependence per 37 mV. The channel exhibits rapid rundown following patch excision with Po decreasing from near 1.0 to near 0. The adenine nucleotides ATP and cAMP block the channel with an apparent affinity of 3 and 42 microM, respectively (-80 mV). Both the activation of the channel by Ca2+ and the block of the channel by adenine nucleotides show a mild voltage dependence, which can be accounted for by the voltage dependence of Po. The properties of this channel make it a candidate to either directly mediate vomeronasal sensory transduction, or to amplify the primary sensory response. (+info)
Vomeronasal organ: pheromone recognition with a twist.
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Pheromones are detected by the vomeronasal organ using members of two receptor superfamilies: the V1Rs and V2Rs. New studies show that MHC class I molecules are co-expressed in particular combinations with specific V2Rs in the vomeronasal organ. The role of these MHC molecules is unknown, but they may be of considerable biological significance. (+info)
Pre-exposure to female chemosignals or intracerebral GnRH restores mating behavior in naive male hamsters with vomeronasal organ lesions.
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Chemosensory input is essential for mating in male hamsters and the vomeronasal organ is critical to mating in naive males. In studies to investigate the convergence of vomeronasal chemosensory input and the neurohormone gonadotrophin releasing hormone (GnRH), we have unexpectedly found that pre-exposure to pheromone-containing chemosignals from female hamsters will also eliminate mating deficits normally seen in naive male hamsters with vomeronasal organs removed (VNX). In the present studies, naive-intact and naive-VNX male hamsters were given intracerebroventricular injections of GnRH or saline and exposed to female pheromones found in hamster vaginal fluid (HVF) or to water 40 min prior to a 5 min mating test. VNX males given saline injections and exposed to water had severe mating deficits, but VNX males given saline injections and exposed to HVF mated normally. As shown previously, males given GnRH injections and exposed to water also mated normally. HVF exposure prior to a mating test apparently acted to compensate for the lack of vomeronasal input in these males. (+info)
Expression of Hes6 and NeuroD in the olfactory epithelium, vomeronasal organ and non-sensory patches.
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Basic helix-loop-helix transcription factors NeuroD and Hes6 promote neuronal differentiation. The expression of their genes in the olfactory epithelium (OE), vomeronasal organ (VNO) and the non-sensory patches of the posterior nasal cavity of mice was examined. As detected by in situ hybridization, Hes6 was expressed in a basal progenitor layer of the embryonic OE. After birth, the expression of Hes6 was detected in a cell layer above the basement membrane, globose basal cells (GBCs). Expression of NeuroD in the embryonic OE was in agreement with that previously described; and in the postnatal OE, it was detected in cells of GBC layer and cells upper to GBCs. In the VNO, Hes6 was expressed throughout the sensory epithelium (S-VNO) at embryonic day 12, and later became restricted to a single layer of cells in the basal region of the S-VNO, where Hes5-expressing undifferentiated cells were present. NeuroD was expressed throughout the S-VNO during the embryonic stage. After birth, Hes6 and NeuroD expressions were observed in the border between the S-VNO and non-sensory VNO. Immunohistochemistry using anti-NeuroD antibody revealed that NeuroD-positive cells were still present not only at the edges but also in the center of the S-VNO until P3. These findings suggest that Hes6 and NeuroD are expressed in progenitors of chemoreceptor neurons and that the expression of Hes6 precedes that of NEUROD: Moreover, in the regenerating VNO of bulbectomized mice, NeuroD-positive cells were observed both at the edges and in the center of the S-VNO, suggesting that neuronal turnover occurred in both regions. Moreover, in the dorsal fossa of the posterior nasal cavity, several non-sensory patches are formed between postnatal (P) days 10 and 21 because of programmed death of ORNs and GBCs. During embryonic stages, the expression of Hes6 and NeuroD in the OE showed no regional differences. At P3-P7, expression of NeuroD and Hes6 disappeared in the region corresponding to the presumptive non-sensory patches. The loss of these genes may stop the differentiation and may cause apoptosis of GBCs and ORNs. (+info)
Histochemical characterization of the lectin-binding sites in the equine vomeronasal organ.
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The binding specificities of various lectins, such as the Dolichos biflorus agglutinin (DBA), soybean agglutinin (SBA), and the Bandeiraea simplicifolia BS-1 (Isolectin B4), Triticum vulgaris (WGA), Arachis hypogaea (PNA), and Ulex europaeus (UEA-I) lectins, were studied in the vomeronasal organ of the horse. The microvilli of the vomeronasal sensory epithelium were positive for DBA, SBA, Isolectin B4, WGA, PNA, and UEA-I. The receptor cells showed intense reactivity for DBA and WGA. Lectins were not detected in the supporting cells or basal cells. The Jacobson's glands were positive for WGA and UEA-I, but lectins were absent from the nerve bundles. From these results, we postulate that several lectin-binding carbohydrates on the microvilli and neurosensory cells are associated with chemoreception in the horse. In addition, the differential lectin-binding patterns in the horse suggest that the carbohydrates present in this particular sense organ are species-specific. (+info)
Evolutionary deterioration of the vomeronasal pheromone transduction pathway in catarrhine primates.
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Pheromones are water-soluble chemicals released and sensed by individuals of the same species to elicit social and reproductive behaviors or physiological changes; they are perceived primarily by the vomeronasal organ (VNO) in terrestrial vertebrates. Humans and some related primates possess only vestigial VNOs and have no or significantly reduced ability to detect pheromones, a phenomenon not well understood at the molecular level. Here we show that genes encoding the TRP2 ion channel and V1R pheromone receptors, two components of the vomeronasal pheromone signal transduction pathway, have been impaired and removed from functional constraints since shortly before the separation of hominoids and Old World monkeys approximately 23 million years ago, and that the random inactivation of pheromone receptor genes is an ongoing process even in present-day humans. The phylogenetic distribution of vomeronasal pheromone insensitivity is concordant with those of conspicuous female sexual swelling and male trichromatic color vision, suggesting that a vision-based signaling-sensory mechanism may have in part replaced the VNO-mediated chemical-based system in the social/reproductive activities of hominoids and Old World monkeys (catarrhines). (+info)