The temporal relationship between LHRH release and gonadotropin secretion as well as the effects of castration on LHRH release were investigated in conscious, freely moving male rats. LHRH release was measured in hypothalamic/median eminence perfusates, while levels of pituitary gonadotropins (LH, FSH) were determined in sequential blood samples obtained via atrial catheters. Twenty-four to 26 h before experiments, rats underwent sham surgery or castration. LHRH release in push-pull perfusates from both groups was pulsatile, and nearly all identified LH pulses (83.3%) were temporally associated with LHRH pulses. Of the fewer irregular FSH pulses that were observed, only 43.7% were temporally associated with LHRH pulses. Mean LHRH pulse amplitude and mean LHRH levels were not different in intact and castrate animals. The frequency of LHRH pulses was moderately increased in castrate rats (1.30 pulses/h) compared to that in intact animals (0.83 pulses/h), and this acceleration was accompanied by a significant increase in LH pulse frequency, pulse amplitude, and mean level. It was also noted that the number of silent LHRH pulses (those not associated with LH pulses) was dramatically reduced in castrate animals. Characteristics of gonadotropin release (pulse frequency, pulse amplitude, and mean level) were not significantly different in animals undergoing push-pull perfusion/bleeding procedures from those in rats not receiving push-pull cannula implants. We conclude from these studies that 1) LH pulses show a high concordance with LHRH pulses, providing evidence that the LHRH pulse generator operates as the neural determinant of LH pulses in male rats, 2) FSH secretion is not associated with LHRH release in an obvious and consistent manner, suggesting that LHRH/FSH relationships are not easily discerned in these animals or that a FSH-releasing factor distinct from the LHRH decapeptide may regulate FSH secretion, 3) a modest increase in LHRH pulse frequency occurs 24-30 h after castration, and 4) silent LHRH pulses occur with much greater regularity in intact than in castrate rats. The latter two observations suggest that both hypothalamic and intrapituitary sequelae of castration may be critically important in the development of postcastration increases in LH secretion and the negative feedback of gonadal steroids.
For nearly a century the gold standard treatment for epiphora and nasolacrimal duct obstruction has been dacryocystorhinostomy (DCR). The definitive treatment of severe canalicular stricture remains conjunctivodacryocystorhinostomy. Although the high success rate of open external approaches continues to be confirmed in the literature, there have been promising advances for endocanalicular surgery and endonasal DCR. Despite a significant narrowing of the gap in outcomes, external DCR may hold the advantage in its ease of performance and lower economic impact. A minor controversy exists over the role of routine postoperative antibiotics. Intraoperative intravenous antibiotic dosing may be as effective as postoperative systemic antibiotics for patients at high risk of infection.
The exposure rate of porous polyethylene implants in this study (9%) was found to be comparable to published rates for hydroxyapatite implants. There were no exposures of unwrapped solid acrylic spheres. Unwrapped porous implants in pediatric patients or following trauma-related enucleation may represent an increased risk for postoperative implant exposure. Absorbable wrapping of porous implants may carry the same risk for exposure as no wrapping. Porous implants wrapped in durable material appear to be as safe as solid acrylic spheres.
In our previous studies, we found that the number of supraspinal neurons projecting to the level of tail spinal cord increases by 74% during tail regeneration and that the number of local spinal neurons with descending projections increases 233%. However, only a small fraction of the supraspinal axons (less than 4%) and half of the local spinal axons actually enter the regenerated spinal cord. We suggested that this may be the result of "synaptic capture" in which regrowing axons make synapses on denervated targets rostral to the transection, aborting further regeneration. To examine this hypothesis, morphometric analysis of electron microscope (EM) photomontages was used to test for changes in synaptic distribution on ventral horn neurons rostral to regenerating tail spinal cord. In addition, 3H-thymidine and retrograde markers were used to determine whether the regenerate axons arose from cut axons, neurogenesis, or sprouting from uninjured neurons. 3H-thymidine injections during regeneration, combined with retrograde HRP pathway tracing, did not reveal the production of new neurons in the tail spinal cord. To test whether cut axons regenerate, fluorescein isothiocyanate conjugated latex beads were applied to the exposed end of the tail spinal cord. After tail regeneration, HRP was applied to the new spinal cord in the regenerated tail. Examination of local spinal neurons (the primary source of axons that enter the regenerated tail spinal cord) revealed that 28% of the neurons contained both labels. This indicated that cut axons successfully regrew into the new tail spinal cord. The regenerated axons that fail to enter the new tail spinal cord can be found in the normal spinal cord immediately rostral to the regenerated tail. To determine whether these axons were making synaptic contacts, lamina IX ventral horn neurons were examined. EM photomontages of the spinal cord rostral to the regenerate tail revealed the following properties: (1) neurons rostral to regenerated tails are larger in area compare to non-regenerates (mean increase = 112%); (2) axosomatic contacts cover a greater percentage of the neuronal soma following regeneration compared to normal (mean increase = 23%); and (3) this increased innervation is the result of an increase in the number of synaptic boutons rather than larger boutons. The number of synaptic contacts in regenerated lizards returned to normal following lumbar transection, indicating that supraspinal and/or long descending propriospinal afferents were the major source of the increased synaptic contacts.(ABSTRACT TRUNCATED AT 400 WORDS)
During tail regeneration most lizards also regenerate the tail spinal cord. The regenerated spinal cord primarily contains neuroepithelium (i.e., the ependymal tube which forms the central canal) and descending axons. The present experiments identify the source of the axons in the regenerated spinal cord. Application of HRP to normal tail spinal cord resulted in labeled cells in the nucleus paraventricularis, the interstitial nucleus of the fasciculus longitudinalis medialis, the nucleus ruber, the medullary reticular formation (including raphe nuclei), as well as in vestibular nuclei. HRP applied to the regenerated spinal cord labeled only 4% of the cells seen in normal animals, and these were confined to rhombencephalic nuclei. The lack of labeling of more rostral nuclei was not due to the death of descending neurons. Application of HRP immediately rostral to the regenerated spinal cord resulted in the labeling of a normal, and in some cases, greater than normal, number of neurons. To quantify the origin of axons in the regenerated spinal cord, electron microscopic montages of the regenerated spinal cord were made and the number of axons counted, before and after various spinal lesions. Only lesions within one spinal segment of the regenerated spinal cord had a significant effect on the number of axons in the regenerated tail spinal cord. This indicated that most of the regenerated axons were of local spinal origin. A significant increase in the number of labeled local spinal neurons was revealed following application of HRP to a regenerated tail spinal cord. These results suggest that while various portions of the lizard central nervous system can grow axons into the regenerating tail spinal cord, the great majority of axons in the regenerate are of local origin and that some of these arise from neurons that do not normally possess descending projections. Finally, to test whether new neurons were participating in the regeneration process, 3H-thymidine was injected during the regrowth of the tail. No labeled spinal cord cells were conclusively identified as neurons. Thus, the regenerating lizard tail spinal cord exhibits robust axonal sprouting from neurons near the site of a spinal transection in a manner reminiscent of sprouting in the mammalian CNS. This sprouting can develop into descending spinal projections that extend for significant distances into the regenerated tail spinal cord and provides a unique model for exploring the requirements for successful axon growth in an adult vertebrate CNS.
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