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The authors have used monoclonal estrophilin antibodies and the peroxidase antiperoxidase technique to characterize the distribution of estrogen receptor in the human vagina, uterus, and fallopian tubes. Exclusively nuclear localization of estrogen receptor was observed in epithelial cells, stromal cells of the lamina propria, and smooth muscle cells with both immunohistologic studies and immunoelectron-microscopy studies. The endometrium in various regions of the uterus (uterine isthmus, corpus, and fundus) was stained for estrogen receptor, with similar staining intensities in each of the respective cell types. There was no systematic regional variation in the staining intensity or distribution of cells with stained nuclei. The functionalis ofthe endometrium showed distinctive variation in the intensity ofthe staining for estrogen receptor with the menstrual cycle. The staining intensity of both endometrial epithelium and THE PRODUCTION of tritiated hexestrol1 and tritiated estradiol2 of high specific activity has provided a means of studying the tissue distribution and metabolism of estrogens.3 The uterus takes up and retains larger amounts of estradiol than any other organ.3 This ability to concentrate estradiol against a concentration gradient is mediated by a specific estrogen receptor protein, estrophilin.4'5 The cellular distribution of estrogen receptor has been characterized with autoradiography using radioactive estrogens, initially in rat6-8 and subsequently in human9 reproductive tissues. These studies showed that 3H-estradiol was localized over the nuclei of epithelial cells, of underlying "connective tissues (substantia propria)," and of muscularis in the rat vagina, uterus, and oviduct. stroma was greatly reduced in the functionalis during the secretory phase. The vaginal epithelium did show some variation with the menstrual cycle, but it was much less than that observed in the functionalis ofthe endometrium. The basal cells ofthe vaginal stratified squamous epithelium, strongly stained during the proliferative phase, were less strongly stained during the secretory phase. No variation in the staining intensity for estrogen receptor was observed in different regions of the fallopian tube (isthmus, ampulla, and infundibulum), and the staining intensity varied only minimally with the menstrual cycle. The serosa ofthe female reproductive tract, connective tissues in the muscularis and in the vicinity of blood vessels, as well as neutrophils, eosinophils, mast cells, and lymphoid cells in the female genital tract were not stained for estrogen receptor. (Am J Pathol 1986, 123:280-292) steroid hormones may be difficult to immobilize in tissue, making autoradiograms with low background difficult to obtain; fixed estophilin does not bind estrogen, necessitating administration to viable tissue; the relatively low specific activity of tritiated estrogens requires months of storage for adequate exposure of the autoradiographic emulsion. In addition, it is not the estrophilin which is identified with this ...

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Calcitonin gene-related peptide (CGRP) is a neuropeptide that has been implicated in the transmission and modulation of primary afferent nociceptive stimuli. In this study, we describe the light microscopic distribution of CGRP immunoreactivity (IR) within the feline trigeminal ganglion and trigeminal nucleus of normal adult subjects and in subjects 10 and 30 days following complete retrogasserian rhizotomy. Within the trigeminal ganglion of normal subjects, cell bodies and fibers showed CGRP-IR, whereas immunoreactive fibers were rare in the central root region. Within the normal spinal trigeminal and main sensory nuclei, CGRP-IR was seen to form a reproducible pattern that varied between the different nuclei. Following rhizotomy, most, but not all, of the CGRP-IR was lost from the spinal trigeminal and main sensory nuclei, except in regions where the upper cervical roots and cranial nerves VII, IX and X project into the trigeminal nucleus. The pattern seen at 10 days contained more CGRP-IR than that seen at 30 days and suggests that degenerating fibers still show CGRP-IR. In contrast to the decrease seen in the nuclei after rhizotomy, examination of the central root that was still attached to the trigeminal ganglion showed an increase in CGRP-IR within fibers, some of which ended in growth conelike enlargements. Rhizotomy induced a dramatic increase in CGRP-IR within trigeminal motoneurons and their fibers, which was strongest 10 days after rhizotomy and weaker at 30 days, which was still stronger than normal. These results indicate that the majority of CGRP-IR found in the trigeminal nucleus originates from trigeminal primary afferents and that an upregulation of CGRP-IR occurs in trigeminal motoneurons and in regenerating fibers in the part of the central root that was still attached to the ganglion. In addition, the persistence of CGRP-IR fibers in the trigeminal nucleus provides one possible explanation for the preservation of pain in humans following trigeminal rhizotomy.