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Suzuki, Yuko; Takeda, Masako; Farbman, Albert I.
doi: 10.1002/(SICI)1096-9861(19961223)376:4<509::AID-CNE1>3.0.CO;2-5pmid: 8978466
Macrophages are known to be phagocytes in the olfactory epithelium of adult rats. The participation of other cell types in phagocytosis in association with the cell death process was examined in the olfactory epithelium after unilateral bulbectomy of neonatal mice. The terminal deoxynucleotidyl transferase (TdT)‐mediated biotinylated dUTP nick end‐labeling (TUNEL) method revealed that the process of olfactory cell death consists of acute and chronic periods. The number of apoptotic cell profiles on the operated side peaked at 1 day, and the percentage of labeled cell profiles was 13.6%. The number of dying cells rapidly decreased at 3 days and decreased further at 5 days. Only 3% of the cells were labeled at 5 days. The percentage of dying cells increased again at the end of first postoperative week and remained two‐ to four‐fold higher than control values for 2 months (4.7–5.3%). Electron micrographs of sections from early postbulbectomy stages (1–7 days) showed that as many as 30% of supporting cell profiles contained apoptotic bodies, cellular debris, and phagosomes in the cytoplasm. The number of supporting cell profiles containing phagosomes declined to a plateau 2 weeks following bulbectomy and remained at 8–12% of the supporting cell population for 2 months. The results indicate that supporting cells in the olfactory epithelium play a significant role in phagocytosis in both acute and chronic periods of cell death after bulbectomy in newborn mice. However, supporting cells are not the exclusive phagocytic cell type in the bulbectomized epithelium; a small number of macrophages was also observed. Moreover, the phagocytosis by supporting cells was observed in unperturbed epithelium in the early stages during postnatal development. © 1996 Wiley‐Liss, Inc.
doi: 10.1002/(SICI)1096-9861(19961223)376:4<518::AID-CNE2>3.0.CO;2-4pmid: 8978467
Reciprocal projections between cortical areas have been subdivided into two functionally distinct components, “feedforward” and “feedback” (for review, see Felleman and Van Essen [1991] Cereb. Cortex 1:1–47). Some anatomical evidence, such as differences in the laminar distribution of the neurons of origin and of the terminations of their axons, has supported this division. However, very little is actually known about the distribution and morphology of the neurons of the feedback projections. In order to contribute further to our understanding of these two components of the corticocortical projections, I studied the distribution and morphology of a feedback projection, the reciprocal projection from the posterior medial lateral suprasylvian sulcus (PMLS), to primary visual cortex (area 17). Retrograde transport of horseradish peroxidase and fluorescent tracers in vivo combined with intracellular dye injections in lightly fixed cortical slices revealed many similarities between the feedforward and feedback projections: 1) They both emanate from all layers but layer 1; 2) each layer of origin contains a wide variety of standard and/or inverted pyramidal neurons; and 3) all of these, with the exception of a rare, large layer 5 neuron, have dendritic fields restricted principally to their layers of origin. There was, however, one major difference between the feedforward and feedback projections: In contrast to the projection from area 17 to PMLS, the projection from PMLS had a dense projection from layer 6 that comprised a striking abundance of spiny fusiform and inverted pyramidal neurons. These were morphologically distinct from other layer 6 neurons that project to the thalamus. Taken together, these data suggest that the reciprocal projections between area 17 and area PMLS, although not completely equivalent, share essential features that form a distinct population of neurons differing in morphology from corticothalamic projection neurons. © 1996 Wiley‐Liss, Inc.
Steiner, Heinz; Gerfen, Charles R.
doi: 10.1002/(SICI)1096-9861(19961223)376:4<530::AID-CNE3>3.0.CO;2-2pmid: 8978468
Dynorphin, an endogenous kappa opioid receptor ligand, acts in the striatum to regulate the response of striatonigral neurons to D1 dopamine receptor stimulation. We investigated the relative contributions of both presynaptic kappa receptors on dopamine terminals and postsynaptic kappa receptors on striatal neurons by analyzing opioid regulation of D1 effects in the absence of presynaptic kappa receptors, after 6‐hydroxydopamine depletion of striatal dopamine. D1‐receptor‐mediated immediate‐early gene induction was measured by using in situ hybridization histochemistry. First, repeated treatment with the D1‐receptor agonist SKF‐38393 (2 mg/kg/day, 3–14 days) was used to increase dynorphin levels in rats with dopamine depletions. In the nucleus accumbens, increased dynorphin expression was accompanied by reduced induction of the immediate‐early genes c‐fos and zif 268 by SKF‐38393. In contrast, in dorsal/lateral aspects of the dopamine‐depleted striatum, this D1 response was sustained despite a large increase in dynorphin expression. These results are consistent with a requirement of dopamine terminals (presynaptic kappa receptors) for the inhibitory action of dynorphin in the dorsal/lateral striatum, but not in the ventral striatum. Second, the kappa receptor agonist spiradoline (1–10 mg/kg) reduced c‐fos and zif 268 induction by SKF‐38393 (2.5 mg/kg) preferentially in ventral parts of the dopamine‐depleted striatum, which contain higher levels of kappa receptor mRNA and binding. These results also indicate that postsynaptic kappa receptors contribute to the inhibition of the D1 response at least in the ventral striatum. Together, these results indicate that dynorphin in the striatum functions to regulate dopamine input to striatonigral neurons, acting at both pre‐ and postsynaptic sites, and that the relative contributions of these mechanisms differ between dorsal and ventral striatal regions. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, in the public domain in the United States of America.
Noble, L.J.; Mautes, A.E.M.; Hall, J.J.
doi: 10.1002/(SICI)1096-9861(19961223)376:4<542::AID-CNE4>3.0.CO;2-1pmid: 8978469
The glycocalyx of microvasculature in normal and injured spinal cord was characterized by using cationized ferritin to define anionic sites and the lectins concanavalin agglutinin (Con A) and Ricinus communis agglutinin I (RCA) to delineate carbohydrate moities. Binding of cationized ferritin was evaluated at the ultrastructural level in control animals and at 3 hours after spinal cord injury. Horseradish peroxidase (HRP) was administered intravenously before euthanasia. In control spinal cord, there was continuous even binding of cationized ferritin along the luminal front of microvasculature and no evidence of barrier permeability to HRP. After spinal cord injury, there was a reduction in binding of cationized ferritin in those regions of spinal cord that exhibited barrier breakdown to HRP.
Johnson, Brett A.; Leon, Michael
doi: 10.1002/(SICI)1096-9861(19961223)376:4<557::AID-CNE5>3.0.CO;2-0pmid: 8978470
Previous work has shown that odors induce focal uptake of [14C]2‐deoxyglucose (2‐DG) within the glomerular layer of the main olfactory bulb and that the amount of 2‐DG accumulated in these foci increases after early odor learning. To determine if learning‐associated changes in 2‐DG uptake occur across the entire glomerular layer, we have mapped uptake throughout that layer at fixed angles in coronal sections through the bulb. Resulting arrays for individual bulbs were corrected for differing bulb size and averaged across experimental groups to address the spatial distribution of uptake. The average arrays revealed at least three discrete fields of uptake in naive, peppermint‐exposed rats at postnatal day 19 that were not seen in air‐exposed littermates. In agreement with previous studies, early preference training with peppermint odor given on postnatal days 1–18 increased 2‐DG uptake at postnatal day 19 within odor‐dependent patches of uptake in the posterior half of the midlateral bulb, whereas odor‐dependent, ventrolateral patches of uptake did not increase to the same extent. In addition, early preference learning was associated with significantly increased 2‐DG uptake averaged over the entire analyzed glomerular layer. These increases were smaller than those within odor‐dependent foci and were distributed widely across the glomerular layer, showing low overlap between trained and control rats in anterior regions where peppermint odor did not stimulate 2‐DG uptake. The widely distributed increases in 2‐DG uptake after learning may reflect changed activity of centrifugal projections that diffusely innervate the glomerular layer. © 1996 Wiley‐Liss, Inc.
Kashon, Michael L.; Arbogast, Jonathan A.; Sisk, Cheryl L.
doi: 10.1002/(SICI)1096-9861(19961223)376:4<567::AID-CNE6>3.0.CO;2-#pmid: 8978471
The distribution and hormonal regulation of androgen‐receptor‐immunoreactive (AR‐ir) cells in the male European ferret forebrain were examined. AR‐ir cells were found in many limbic and hypothalamic structures, and their distribution was similar to that reported for cells that either bind androgen or contain AR protein or mRNA in other species. Regulation of brain AR immunoreactivity by gonadal steroids was brain‐region dependent. In most regions examined, including the preoptic area, amygdala, and several hypothalamic nuclei, castration reduced the density of AR‐ir profiles and the intensity of immunocytochemical staining, and long‐term (days) androgen, but not estrogen, replacement restored these parameters of AR immunoreactivity. Other areas, such as the bed nucleus of the stria terminalis, appeared to be relatively resistant to modulation of AR immunoreactivity by castration and long‐term androgen treatment. The ability of testosterone to increase AR‐ir profile density is not a simple consequence of translocation of AR from the cytoplasm to the nucleus, because short‐term (hours) treatment with testosterone did not result in an increase in AR‐ir profile density equivalent to that seen after 10 days of testosterone treatment. Thus, androgens appear to be able to increase AR levels within certain brain cell groups, thereby altering target tissue responsiveness to their own action. © 1996 Wiley‐Liss, Inc.
Nosrat, Christopher A.; Ebendal, Ted; Olson, Lars
doi: 10.1002/(SICI)1096-9861(19961223)376:4<587::AID-CNE7>3.0.CO;2-Ypmid: 8978472
Although many studies have demonstrated the dependency of taste bud function and/or survival on intact innervation, relatively few have dealt with the development of taste bud innervation. Using in situ hybridization histochemistry, we show that brain‐derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) mRNA are expressed in a specific pattern in the taste buds, tongue papillae, and lingual epithelium during development and that expression persists into adulthood. BDNF mRNA is expressed in a fraction of the taste cells of the developing and adult taste buds in rats, showing different labeling intensities among the labeled cells. NT3 mRNA seems to be located in areas other than those where BDNF mRNA is expressed, mainly in the superior epithelial surfaces of circumvallate papillae, the outer surface epithelium of foliate papilae, the superior surface and the lateral epithelium of the fungiform papillae, and the epithelium of the filiform papillae. NT3 mRNA labeling is also observed among muscle and connective tissue of the tongue. The morphological appearance, expression of NT3 mRNA, and ramification of nerve fibers in defined epithelial structures in the posterior wall of the anterior filiform papillae suggest the existence of a mechanosensory apparatus in these papillae. Nerve growth factor and neurotrophin 4 probes did not give rise to selective labeling in tongue, although their presence cannot be totally excluded. Based on present and prior studies, we suggest that BDNF is needed during initiation and for maintenance of gustatory innervation of taste buds and gustatory papillae and that NT3 is mainly needed for somatosensory innervation of the tongue. © 1996 Wiley‐Liss, Inc.
Miyazono, Masayuki; Nowell, Peter C.; Finan, Janet L.; Lee, Virginia M.‐Y.; Trojanowski, John Q.
doi: 10.1002/(SICI)1096-9861(19961223)376:4<603::AID-CNE8>3.0.CO;2-5pmid: 8978473
NTera‐2 (NT2) cells are a human embryonal carcinoma (EC) cell line derived from a teratocarcinoma that differentiate exclusively into postmitotic neurons in vitro following retinoic acid (RA) treatment. Like other EC cell lines, NT2 cells rapidly form lethal tumors following transplantation into peripheral sites or many regions of the brain. However, when grafts are confined to the caudoputamen (CP), the NT2 cells differentiate into postmitotic neuronlike cells and do not form lethal tumors. To examine the long‐term fate of such grafts, we studied NT2 cell transplants in the CP of nude mice that survived for > 1 year. NT2 cells in these grafts acquired molecular markers of fully mature neurons including the low, middle, and high molecular weight neurofilament proteins, microtubule‐associated protein 2, tau, and synaptophysin. Furthermore, neuronlike cells in long‐term CP grafts formed synaptic structures, and their processes became myelinated, whereas tyrosine hydroxylase (TH)‐positive neuronlike cells in the grafts increased with progressively longer postimplantation survival times. Soluble extracts of the adult mouse CP augmented TH expression in RA‐treated NT2 cells in vitro. These data suggest that the adult mouse CP is a source of factor(s) that inhibits tumor formation and induce a catecholaminergic neuronal phenotype in these human NT2 cells in vivo and in vitro. Identification of these factors could accelerate efforts to elucidate mechanisms that regulate progenitor cell fate and the commitment of neurons to specific neurotransmitter phenotypes. © 1996 Wiley‐Liss, Inc.
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