In situ hybridization histochemistry and immunocytochemistry were used to study the prenatal expression of luteinizing hormone-releasing hormone (LHRH) cells in the mouse. Cells expressing LHRH mRNA and peptide product were first detected on embryonic day 11.5 (E11.5) in the olfactory pit. On E12.5, the majority of LURH cells were located on "tracks" extending from the olfactory pit to the base of the telencephalon. From E12.5 to E15. toradiography was used to determine when LHRH cells left the mitotic cycle. We show that LHRH neurons exhibit a discrete time of birth, suggesting that they arise as a single neuronal population between E10.0 and E11.0. Postnatal LHRH neurons were "birth-dated" shortly after differentiation of the olfactory placode and before LHRH mRNA was expressed in cells in the olfactory pit. Taken together, these studies support the hypothesis that all LHRH cells in the central nervous system arise from a discrete group of progenitor cells in the olfactory placode and that a subpopulation of these cells migrate into forebrain areas where they subsequently establish an adult-like distribution.It has been proposed (1, 2) that luteinizing hormone-releasing hormone (LHRH) neurons in the mouse originate in the olfactory placode and migrate into forebrain areas during prenatal development. Prior to this hypothesis, it had been assumed that forebrain LHRH cells had multiple embryonic origins, since the anatomical distribution of forebrain LHRH cells in postnatal animals spanned neuronal areas that normally develop from different regions of the neuroepithelium (3). The "olfactory placode" hypothesis for the ontogeny of mouse forebrain LHRH neurons was largely based on the observations that immunopositive cells were first detected in the olfactory pit and that the spatiotemporal distribution of LHRH cells progressed from nasal regions into the forebrain during embryonic development (1, 2). The latter studies used antibodies directed against LHRH (1, 2) and the gonadotropin-releasing hormone-associated peptide (1).In this study, we use in situ hybridization histochemistry for LHRH mRNA as well as immunocytochemistry for the LHRH peptide to study the prenatal expression of the LHRH gene in cells in the embryonic mouse. The use of oligonucleotide probes for mRNA eliminates misidentification by possible antibody crossreactivity with non-LHRH epitopes. In addition, by using in situ hybridization histochemistry, it is possible to determine if embryonic forebrain areas, which are known to contain LHRH cells postnatally, have LHRH mRNA-containing cells that are LHRH peptide deficient. If such cells exist, it would suggest that forebrain LHRH cells, which may be delayed in peptide synthesis or processing, could originate in the brain itself. Alternatively, if cells expressing LHRH mRNA show the same onset and spatiotemporal distribution as previously reported for immunopositive cells (1, 2), then the hypothesis (1, 2, 4) that all LHRH cells found in the brain originate in the olfactory placode would be ...

The origin of GnRH-1 cells and olfactory ensheathing cells (OECs) has been controversial. Genetic Cre-lox lineage tracing of the neural crest (NC) versus ectodermal contribution to the developing nasal placode was performed using two complementary mouse models, the NC specific Wnt1Cre mouse line and an ectodermal specific Crect mouse line. Using these lines we prove that the NC give rise to the olfactory ensheathing cells and subpopulations of GnRH-1 neurons, olfactory and vomeronasal cells. These data demonstrate that Schwann cells and olfactory ensheathing cells share a common developmental origin. Furthermore, the results indicate that certain conditions that impact olfaction and sexual development, such as Kallmann Syndrome, may be in part neurocristopathies.

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Gonadotrophin‐releasing hormone‐1 (GnRH‐1) is essential for mammalian reproduction, controlling release of gonadotrophins from the anterior pituitary. GnRH‐1 neurones migrate from the nasal placode into the forebrain during development. Although first located within the nasal placode, the embryonic origin/lineage of GnRH‐1 neurones is still unclear. The migration of GnRH‐1 cells is the best characterised example of neurophilic/axophilic migration, with the cells using a subset of olfactory‐derived vomeronasal axons as their pathway and numerous molecules to guide their movement into the forebrain. Exciting work in this area is beginning to identify intersecting pathways that orchestrate the movement of these critical neuroendocrine cells into the central nervous system, both spatially and temporally, through a diverse and changing terrain. Once within the forebrain, little is known about how the axons target the median eminence and ultimately secrete GnRH‐1 in a pulsatile fashion.