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PubMed2006

Platelet-activating factor in the enteric nervous system of the guinea pig small intestine.

Platelet-activating factor (PAF) is a proinflammatory mediator that may influence neuronal activity in the enteric nervous system (ENS). Electrophysiology, immunofluorescence, Western blot analysis, and RT-PCR were used to study the action of PAF and the expression of PAF receptor (PAFR) in the ENS. PAFR immunoreactivity (IR) was expressed by 6.9% of the neurons in the myenteric plexus and 14.5% of the neurons in the submucosal plexus in all segments of the guinea pig intestinal tract as determined by double staining with anti-human neuronal protein antibody. PAFR IR was found in 6.1% of the neurons with IR for calbindin, 35.8% of the neurons with IR for neuropeptide Y (NPY), 30.6% of the neurons with IR for choline acetyltransferase (ChAT), and 1.96% of the neurons with IR for vasoactive intestinal peptide (VIP) in the submucosal plexus. PAFR IR was also found in 1.5% of the neurons with IR for calbindin, 51.1% of the neurons with IR for NPY, and 32.9% of the neurons with IR for ChAT in the myenteric plexus. In the submucosal plexus, exposure to PAF (200-600 nM) evoked depolarizing responses (8.2 +/- 3.8 mV) in 12.4% of the neurons with S-type electrophysiological behavior and uniaxonal morphology and in 12.5% of the neurons with AH-type electrophysiological behavior and Dogiel II morphology, whereas in the myenteric preparations, depolarizing responses were elicited by a similar concentration of PAF in 9.5% of the neurons with S-type electrophysiological behavior and uniaxonal morphology and in 12.0% of the neurons with AH-type electrophysiological behavior and Dogiel II morphology. The results suggest that subgroups of secreto- and musculomotor neurons in the submucosal and myenteric plexuses express PAFR. Coexpression of PAFR IR with ChAT IR in the myenteric plexus and ChAT IR and VIP IR in the submucosal plexus suggests that PAF, after release in the inflamed bowel, might act to elevate the excitability of submucosal secretomotor and myenteric musculomotor neurons. Enhanced excitability of motor neurons might lead to a state of neurogenic secretory diarrhea.

Animals↗
PubMed1997

Purinergic Ca2+ signaling in myenteric neurons via P2 purinoceptors.

Fura 2 microfluorimetry was used to test the hypothesis that ATP acts at P1 and P2 purinoceptors to elevate cytosolic free Ca2+ concentrations [Ca2+]i) in calbindin-immunoreactive cultured myenteric neurons from adult guinea pig small intestine. Local "micro-puff" application of ATP or ATP(gamma)S caused an increase in [Ca2+]i in 99% of 200 multipolar neurons. The potency profile of agonists for the rise in [Ca2+]i was ATP(gamma)S = ATP >> ADP >> AMP, adenosine, 5'-(N-ethylcarboxamido)adenosine, and 2-chloro-N(6)-cyclopentyladenosine. Tetrodotoxin-sensitive synaptic transmission could contribute as much as 25% to the ATP response. The P1 antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked 50% of the peakATP Ca2+ response. P2 antagonists blocked the ATP response: pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid > reactive blue 2 > suramin. Suramin enhanced the ATP response in 27.5% of neurons. Some neurons (<15%) displayed distinct multiphasic Ca2+ signatures. About 54% of ATP-responsive neurons expressed calbindin. The data support the following hypotheses: 1) two distinct P2 purinoceptors are linked to the rise in [Ca2+]i in myenteric neurons; 2) purinergic Ca2+ signaling is not restricted to one neuronal phenotype; and 3) intraneuronal Ca2+ is not involved in adenosinergic hyperpolarization in AH/type 2 neurons.

Adenosine↗
PubMed2001

Localization of thiazide-sensitive Na(+)-Cl(-) cotransport and associated gene products in mouse DCT.

The mammalian distal nephron develops a complex assembly of specialized cell types to accomplish the fine adjustment of urinary electrolyte composition. The epithelia of the distal convoluted tubule (DCT), the connecting tubule (CNT), and the cortical collecting duct (CCD) show an axial structural heterogeneity that has been functionally elucidated by the localization of proteins involved in transepithelial ion transport. We compared the distribution of the thiazide-sensitive Na(+)-Cl(-) cotransporter (TSC), basolateral Na(+)/Ca(2+) exchanger (Na/Ca), cytosolic calcium-binding proteins calbindin D(28K) and parvalbumin, and the key enzyme for selective aldosterone actions, 11 beta-hydroxysteroid-dehydrogenase 2 (11HSD2), in the distal convolutions of the mouse. In the mouse, as opposed to the rat, we found no clear subsegmentation of the DCT into a proximal (DCT1) and a distal (DCT2) portion. The TSC was expressed along the entire DCT. Na/Ca and calbindin D(28K) were similarly expressed along most of the DCT, with minor exceptions in the initial portion of the DCT. Both were also present in the CNT. Parvalbumin was found in the entire DCT, with an occasional absence from short end portions of the DCT, and was not present in CNT. 11HSD2 was predominantly located in the CNT and CCD. Short end portions of DCT only occasionally showed the 11HSD2 signal. We also observed an overlap of 11HSD2 immunoreactivity and mRNA staining. Our observations will have implications in understanding the physiological effects of gene disruption and targeting experiments in the mouse.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1998

Effect of 26,26,26,27,27,27-Hexafluoro-1,25-dihydroxyvitamin D3 on the expression of vitamin-D-responsive genes in vitamin-D-deficient mice.

26,26,26,27,27,27-Hexafluoro-1,25-dihydroxyvitamin D3 (ST-630) is a newly developed agent to maintain the levels of calcium and phosphorus in blood. Herein, we investigated the effect of this compound on the expression of vitamin-D-responsive genes in vitamin-D-deficient mice. ST-630 was more effective than 1, 25-dihydroxyvitamin D3 [1,25(OH)2D3] with respect to the induction of Cyp24 and calbindin-D9k mRNAs in the kidney and in the small intestine. Moreover, the increase in mRNA levels of vitamin-D-responsive genes induced by ST-630 lasted longer than that induced by 1,25(OH)2D3. These results indicate that ST-630 was more effective in inducing Cyp24 and calbindin-D9k gene expression than 1, 25(OH)2D3 when both compounds were injected into vitamin-D-deficient mice.

Animals↗
PubMed2003

Neurogenesis in the hippocampus of an adult marsupial.

In the adult eutherian brain, stem cells in the dentate gyrus continually divide throughout adult life and into old age producing new granule cells. However, it was not known whether this is also the case for marsupials. Previously, in fact, it was thought that marsupials did not have continued neurogenesis in the mature brain. Here we examined neurogenesis in the adult brain of a small marsupial, the fat-tailed dunnart, using 3H-thymidine to label newly generated cells. We showed that neurogenesis takes place in the adult dentate gyrus along its inner margin, as seen in eutherian mammals. Control animals had similar numbers of labeled cells 24 h and 1 month after 3H-thymidine injection. An enriched environment resulted in similar numbers of cells being generated as controls. However, there was a significant decline in the number of labeled cells one month later. Stress and old age resulted in significantly lower numbers of new cells being generated. In immunohistochemically treated control brains, 3H-thymidine-labeled cells at the early stage were sometimes GFAP positive, were not calbindin positive at either stage examined and at the later stage were PSA-NCAM positive. We hypothesize that, as seen in eutherian mammals, the new cells progressed from being GFAP positive at stem cell stage to PSA-NCAM positive during outgrowth of mossy fibers 1 month later, to calbindin positive when mature. It is possible that maturity of these cells was not reached by 1 month as marsupials have a slower metabolic rate and this species also undergoes daily periods of torpor.

Aging↗
PubMed1988

Immunocytochemical studies on parafollicular cells of various mammals.

Using specific antisera, calcitonin, calcitonin gene-related peptide (CGRP), somatostatin as well as neuron-specific enolase, chromogranin, secretory peptide I and calbindin (vitamin D-dependent calcium-binding protein) were looked for in parafollicular cells of rats, Syrian hamsters, Mongolian gerbils, mice, guinea pigs, rabbits and pigs. Calcitonin and CGRP were most invariably present in various species. Somatostatin was absent in mice and Mongolian gerbils and present in variable amounts in the remaining species. Neuron-specific enolase could not be detected in rabbits, while in the pigs and the Mongolian gerbils it could be demonstrated only in some parafollicular cells. Calbindin was present exclusively in parafollicular cells of guinea pigs. Chromogranin and secretory protein-I were present only in some animal species.

Animals↗
PubMed1991

Vitamin D receptors and compensatory tissue growth in spontaneously diabetic BB rats.

Untreated diabetic (BB) rats exhibited compensatory intestinal growth which was associated with hyperplasia and was accompanied by an increase in unoccupied vitamin D receptors. Although vitamin D receptors were increased, low circulating 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] prevented amplification of the action of 1,25(OH)2D3, as evidenced by reductions in calbindin D-9K and alkaline phosphatase activity in the BB rat intestine compared to control. In the kidney, a lesser degree of compensatory growth was observed which was not associated with hyperplasia, and no significant effect of diabetes on vitamin D receptors or calbindin D-28K was observed. These studies suggest tissue-specific changes in 1,25(OH)2D3 metabolism during spontaneous diabetes which may be related to the hyperplasia which occurs during compensatory tissue growth.

Animals↗
PubMed2003

Limitation of anatomical integration between subretinal transplants and the host retina.

PURPOSE: In previous studies of subretinal transplantation in rabbits, the host photoreceptor layer seemed to prevent the bridging of neuronal fibers between the graft and the host retina. The current study was undertaken to determine whether the same phenomenon occurs in transplants to the subretinal space of the vascularized retina of rats. Bridging of fibers was examined in transplants to animals of different genetic backgrounds (normal versus dystrophic rats), of different ages, and after different survival times. METHODS: Sprague-Dawley (SD) rat retinal tissue from embryonic day (E)18 was subretinally grafted to adult (60-day-old) normal SD rats, to RCS rats (32 and 73 days old), and to adult (60-day-old) transgenic P23H rats. After various survival times (28-183 days), transplanted retinas were processed for routine histology and immunocytochemistry. Antibodies against calbindin, neuronal nitric oxide synthase (NOS), and protein kinase C (PKC) were used to identify specific retinal cell types and their processes. RESULTS: The shape and position of the immunoreactive cell bodies indicated that the expected neuronal populations were labeled within the grafts and in the host retina. Labeled neuronal processes were also observed. In each case, NOS-, calbindin-, and PKC-immunolabeled fibers formed bridges between the graft and the host tissues. However, regardless of the extent of host photoreceptor cell loss, the age of the recipient, or the genetic background, bridging fibers were observed only in areas where the host photoreceptor layer was discontinuous or completely missing. CONCLUSIONS: The present study demonstrates that the host photoreceptor layer plays a role in limiting graft-host anatomical integration.

Animals↗
PubMed2005

A developmental switch in the expression of aquaporin-4 and Kir4.1 from horizontal to Müller cells in mouse retina.

PURPOSE: In adult retina, aquaporin-4 (AQP4) and inwardly rectifying K(+) (Kir4.1) channels localize to astrocyte and Müller cell membranes facing vascular and vitreous compartments, optimizing clearance of extracellular K(+) and water from the synaptic layers. However, it is unknown whether these channels are expressed at early developmental stages, before gliogenesis or angiogenesis take place in the neural retina. This study was conducted to determine the presence of AQP4 and Kir4.1 proteins in the developing mouse retina. METHODS: Simultaneous AQP4 and Kir4.1 immunodetection was performed in postnatal mice 1, 9, 15, and 30 days of age. Confocal microscopy was used to identify the cellular distribution of AQP4 and Kir4.1 proteins, as well as their coexpression with the cell-selective immunomarkers Prox-1, calbindin, and neurofilament. RESULTS: AQP4 and Kir4.1 proteins were coexpressed in calbindin- and Prox1-expressing retinal neurons at birth. These neurons were identified as horizontal cells based on their position and morphology. By P15, when vision starts, AQP4 and Kir4.1 localization coordinately switched from horizontal cells to Müller glial cells. CONCLUSIONS: The findings showed that AQP4 and Kir4.1 protein expression is confined to differentiating horizontal cells before its expression in Müller cells. The finding of AQP4 in neurons is novel, since AQP4 expression within the central nervous system is restricted to glia. Also, the results demonstrated that AQP4 is a horizontal cell-specific immunomarker in neonatal retina. The transitory coexpression of AQP4 and Kir4.1 proteins by differentiating horizontal interneurons suggests that these cells mediate K(+) and water transcellular uptake until the initiation of phototransduction, when glial cells assume these functions.

Animals↗
PubMed1998

Hyperresponsiveness of vitamin D receptor gene expression to 1,25-dihydroxyvitamin D3. A new characteristic of genetic hypercalciuric stone-forming rats.

Hypercalciuria in genetic hypercalciuric stone-forming (GHS) rats is accompanied by intestinal Ca hyperabsorption with normal serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels, elevation of intestinal, kidney, and bone vitamin D receptor (VDR) content, and greater 1,25(OH)2D3-induced bone resorption in vitro. To test the hypothesis that hyperresponsiveness of VDR gene expression to 1,25(OH)2D3 may mediate these observations, male GHS and wild-type Sprague- Dawley normocalciuric control rats were fed a normal Ca diet (0.6% Ca) and received a single intraperitoneal injection of either 1,25(OH)2D3 (10-200 ng/100 g body wt) or vehicle. Total RNAs were isolated from both duodenum and kidney cortex, and the VDR and calbindin mRNA levels were determined by Northern blot hybridization using specific cDNA probes. Under basal conditions, VDR mRNA levels in GHS rats were lower in duodenum and higher in kidney compared with wild-type controls. Administration of 1,25(OH)2D3 increased VDR gene expression significantly in GHS but not normocalciuric animals, in a time- and dose-dependent manner. In vivo half-life of VDR mRNA was similar in GHS and control rats in both duodenum and kidney, and was prolonged significantly (from 4-5 to > 8 h) by 1,25(OH)2D3 administration. Neither inhibition of gene transcription by actinomycin D nor inhibition of de novo protein synthesis with cycloheximide blocked the upregulation of VDR gene expression stimulated by 1,25(OH)2D3 administration. No alteration or mutation was detected in the sequence of duodenal VDR mRNA from GHS rats compared with wild-type animals. Furthermore, 1,25(OH)2D3 administration also led to an increase in duodenal and renal calbindin mRNA levels in GHS rats, whereas they were either suppressed or unchanged in wild-type animals. The results suggest that GHS rats hyperrespond to minimal doses of 1,25(OH)2D3 by an upregulation of VDR gene expression. This hyperresponsiveness of GHS rats to 1,25(OH)2D3 (a) occurs through an increase in VDR mRNA stability without involving alteration in gene transcription, de novo protein synthesis, or mRNA sequence; and (b) is likely of functional significance, and affects VDR-responsive genes in 1, 25(OH)2D3 target tissues. This unique characteristic suggests that GHS rats may be susceptible to minimal fluctuations in serum 1, 25(OH)2D3, resulting in increased VDR and VDR-responsive events, which in turn may pathologically amplify the actions of 1,25(OH)2D3 on Ca metabolism that thus contribute to the hypercalciuria and stone formation.

Animals↗
PubMedDate not supplied

Organization and histochemical phenotype of human fetal cerebellar cells following transplantation into the cerebellum of nude mice.

Previous rodent studies have demonstrated the capacity of cerebellar transplants to organize into trilaminar cell layers typically observed in the normal cerebellum. In Purkinje Cell (PC)-deficient animals, PCs will migrate into the host and form synaptic connections. Recently, fetal cerebellar grafts transplanted into the Purkinje cell degeneration (pcd) mutant mouse were shown to result in an improvement of motor behaviors. These studies indicate the potential therapeutic use of neural transplantation in patients with cerebellar degeneration. In the present study, human fetal cerebellar tissue (8.5 wk postconception) was dissociated and transplanted into the normal cerebellum of nude mice. Six months following transplantation, histological analysis revealed donor cells in recipient mice. Immunostaining for the 28 kDa calcium-binding protein (calbindin) revealed the presence of donor PCs that were organized in discrete cellular layers within the transplant neuropil. In most cases the dendritic processes were oriented in a planar fashion perpendicular to the transplant cell layer. Human neurofilament immunostaining revealed bundles of donor fibers within the core of the transplant and/or at the periphery. These bundles were found to be calbindin positive (PC fibers). Three animals provided evidence of donor PC axon growth ventrally into host white matter, and in one case, this ventral migration reached the deep cerebellar nuclei. Most notable was the development of a pronounced folia-like organization by the implanted cell suspensions. Glial processes within the grafts were aligned perpendicular to the long axis of the transplant folia. These results demonstrate the capacity of human fetal cerebellar cell suspension to reorganize into cell layers typical of the normal cerebellum following transplantation into the rodent cerebellum, and develop an organotypic folia-like organization.

Animals↗
PubMed2003

Calcium transporter 1 and epithelial calcium channel messenger ribonucleic acid are differentially regulated by 1,25 dihydroxyvitamin D3 in the intestine and kidney of mice.

We examined the expression of calcium transporter 1 (CaT1) and epithelial calcium channel (ECaC) mRNA in the duodenum and kidney of mice. Intestinal CaT1 mRNA level increased 30-fold at weaning, coincident with the induction of calbindin-D(9k) expression. In contrast, renal CaT1 and ECaC mRNA expression was equal until weaning when ECaC mRNA is induced and CaT1 mRNA levels fall 70%. Long- and short-term adaptation to changes in dietary calcium (Ca) level and 1,25 dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] injection strongly regulated duodenal calbindin D(9k) and CaT1 mRNA. Following a single dose of 1,25(OH)(2)D(3), induction of CaT1 mRNA occurred rapidly (within 3 h, peak at 6 h of 9.6 +/- 0.8-fold) and preceded the induction of intestinal Ca absorption (significantly increased at 6 h, peak at 9 h). Neither renal CaT1 nor ECaC mRNA were strongly regulated by dietary calcium level or 1,25(OH)(2)D(3) injection. Our data indicate that CaT1 and ECaC mRNA levels are differentially regulated by 1,25(OH)(2)D(3) in kidney and intestine and that there may be a specialized role for CaT1 in kidney in fetal and neonatal development. The rapid induction of intestinal CaT1 mRNA expression by 1,25(OH)(2)D(3), and the marked induction at weaning, suggest that CaT1 is critical for 1,25(OH)(2)D(3)-mediated intestinal Ca absorption.

Animal Feed↗
PubMed2006

Transient transcription of the somatostatin gene at the time of estrogen-dependent organization of the sexually dimorphic nucleus of the rat preoptic area.

In situ hybridization detected a transient, sex-specific transcription of somatostatin gene in the central part of the rat medial preoptic nucleus, which coincides with the sexually dimorphic nucleus of the preoptic area (SDN-POA), during, but not after, the establishment of sex difference. On postnatal d 1 (day of birth), somatostatin mRNA was detected in the SDN-POA of both sexes. On d 8 through 35, the area of somatostatin mRNA-positive cells was significantly larger in males than in females. In males the area attained its maximum size on d 15 and diminished gradually thereafter. In females the area did not change in size during this period. On d 60 expression of somatostatin mRNA was low and not different between sexes. Throughout the observed period, Nissl staining and calbindin immunohistochemistry enabled visualization of the typical SDN-POA in the same region. As with Nissl staining and calbindin immunohistochemistry, somatostatin mRNA hybridization on d 15 revealed a reversal of the sexual dimorphism in the size of the SDN-POA in males that had been neonatally orchidectomized or females given estrogen as pups, showing that sex steroid milieu during the organizational period determines the area occupied by somatostatin mRNA-positive cells. Sex-specific, transient transcription of the somatostatin gene may causally relate to the estrogen-dependent organization of the SDN-POA.

Animals↗
PubMed1994

Growth hormone and parathyroid hormone stimulate intestinal calcium absorption in aged female rats.

Aged (16-month-old) female rats (n = 8/treatment) were injected for 12 days with GH (100 micrograms/100 g x day), PTH (8 micrograms/100 g x day), GH plus PTH, or vehicle (V) in an experiment designed to determine the effects of these hormones on intestinal mineral absorption in senescent rats. PTH and GH increased fractional net calcium absorption to a similar extent (PTH, 1.6-fold; GH, 1.4-fold) even though PTH increased serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] 3.7-fold, and GH had no significant effect. GH plus PTH caused no further increase in serum 1,25-(OH)2D3 above that caused by PTH alone, but resulted in an additive effect on net calcium absorption (2.3-fold increase). PTH and GH also had statistically independent effects on phosphate absorption; magnesium absorption was elevated only by PTH. Duodenal calbindin-D9k levels were increased by GH (from 3.79 +/- 0.72 to 6.98 +/- 0.73 micrograms/mg protein) and PTH (from 3.23 +/- 0.46 to 7.55 +/- 0.75 micrograms/mg protein); PTH plus GH treatment resulted in an additive effect on calbindin-D9k levels. Additional in vitro transport studies in the human intestinal cell line Caco-2 showed that 72 h of pretreatment with the local mediator of GH action, insulin-like growth factor-I (at 10 and 100 ng/ml), stimulated transcellular calcium transport (22% and 44%, respectively) regardless of concomitant 1 nM 1,25-(OH)2D3 pretreatment (80% increase). Our findings suggest a 1,25-(OH)2D3-mediated mechanism for PTH-induced changes in calcium and phosphorus absorption. In contrast, the effects of GH in the senescent rat are independent of changes in circulating 1,25-(OH)2D3 and our data suggest that these effects may be mediated by insulin-like growth factor-I.

Aging↗
PubMed1998

Reduced immunoreactivity to calcium-binding proteins in Purkinje cells precedes onset of ataxia in spinocerebellar ataxia-1 transgenic mice.

Earlier we have shown alterations in immunoreactivity (IR) to the calcium-binding proteins parvalbumin (PV) and calbindin D-28k (CaB) in surviving Purkinje cells of patients with spinocerebellar ataxia-1 (SCA-1). In the present study we determined PV and CaB expression (by immunohistochemical and immunoblot analyses) in Purkinje cells of transgenic mice (TM) expressing the human SCA-1 gene with an expanded (line B05) and normal (line A02) CAG tract, as well as in age-matched nontransgenic mice (nTM). Heterozygotes in the B05 line develop progressive ataxia beginning around 12 weeks of age. A02 animals are phenotypically indistinguishable from wild-type (nontransgenic) animals. In the cerebella of 8-, 9-, and 12-week-old TM-B05 there was a progressive decrease in PV IR in Purkinje cells compared with nTM and TM-A02. Parvalbumin immunostaining in interneurons was well preserved in all groups. A progressive decrease was also observed in CaB IR in Purkinje cells of 8-, 9-, and 12-week-old TM-B05. Cerebellar Purkinje cells of 6-week-old TM-B05, which exhibit no ataxia and even lack demonstrable Purkinje cell loss, also revealed reduction in PV IR. This change was matched by a significant decrease in the amount of cerebellar PV in 6-week-old TM-B05 as determined by Western blot analysis. Calbindin D-28K immunohistochemistry did not detect any marked changes in CaB IR within Purkinje cells at 4 weeks. However, at 6 weeks immunostaining and immunoblot analysis revealed a significant decrease in CaB in TM-B05 compared with controls. These data suggest that decreased levels of calcium-binding proteins in Purkinje cells in SCA-1 transgenic mice may cause alteration in Ca2+ homeostasis.

Alleles↗
PubMed1995

Morphologic study of the laryngeal taste buds in the cat.

The distribution of laryngeal taste buds (TBs) and their neutral components in the cat were investigated by immunohistochemistry and electron microscopy. The antisera used in this study were against cytokeratin, protein gene product 9.5 (PGP9.5), neuron-specific enolase (NSE), S-100 protein, calbindin D, calcitonin gene-related peptide (CGRP), and substance P (SP). Taste bud cells were specifically immunoreactive to the antibodies of human cytokeratin subtypes 8 and 18 (CAM5.2). On observation with CAM5.2, TBs were seen distributed on the laryngeal surface of the epiglottis and spread caudally along the aryepiglottic folds, reaching peak density at the laryngeal side of the arytenoid tubercle. The PGP9.5 and NSE immunoreactivities were recognized in TB cells and nerve fibers, both within the TBs and in the subepithelial connective tissue. S-100 protein immunoreactivities were not found in any of the cells in the TBs but were found exclusively in the subepithelial neural elements. The calbindin-D, CGRP, and SP immunoreactivities were confined to a part of the neural elements that was very thin. Taste pores, taste villi, neuronal varicosity, and synapselike structures were observed by scanning and transmission electron microscopic study. From these results it is considered that the TBs act as a chemical receptor.

Animals↗
PubMed2005

Histopathological changes in the eyes in systemic lupus erythematosus: an electron microscope and immunohistochemical study.

This paper reports the histopathological findings in the eyes of a 26-year-old female patient diagnosed with systemic lupus erythematosus (SLE) with peripheral neuropathy. The patient had no significant ocular problems. She died of pneumonia after two years of suffering. The eyeballs were procured at autopsy and the retina, choroid and optic nerve processed for light and electron microscopy, and immunohistochemistry for immunoglobulin G (IgG), glial fibrillary acidic protein (GFAP), calbindin and parvalbumin. Histologically, there was haemorrhaging in the retinal nerve fibre layer. Ultrastructurally, the axons of this layer were swollen, and contained an unusual accumulation of microtubules and smooth endoplasmic reticulum. There were degenerative changes in the pericytes and smooth muscle cells of blood vessels. The capillary lumen was partially obliterated, and contained IgG, which was also detected throughout the choroid and wall of choroidal arterioles. The latter and Bruch's membrane showed fibrin deposits. The optic nerve showed infiltrated mononuclear cells near the degenerated axons, these axons lacked immunoreactivity to calbindin and parvalbumin. Compared to the control, the connective tissue sheaths of the central retinal vessels possessed a vast number of proliferated fibroblast cells, and trichrome staining showed transmural vessel scarring. Dense GFAP immunoreactivity was observed surrounding the vessel wall. These pathological changes are due to impaired blood circulation caused by haemorrhaging and vasculitis, and vessel occlusion by fibrin. The nature of the changes observed tends to indicate that a regular, thorough ophthalmic examination should be conducted even in the absence of significant ocular symptoms in SLE.

Adult↗
PubMed2005

Identification of dopaminergic neurons of nigral and ventral tegmental area subtypes in grafts of fetal ventral mesencephalon based on cell morphology, protein expression, and efferent projections.

Transplants of fetal ventral mesencephalic tissue are known to contain a mixture of two major dopamine (DA) neuron types: the A9 neurons of the substantia nigra pars compacta (SNpc) and the A10 neurons of the ventral tegmental area (VTA). Previous studies have suggested that these two DA neuron types may differ in their growth characteristics, but, because of technical limitations, it has so far been difficult to identify the two subtypes in fetal ventral mesencephalon (VM) grafts and trace their axonal projections. Here, we have made use of a transgenic mouse expressing green fluorescent protein (GFP) under the tyrosine hydroxylase promoter. The expression of the GFP reporter allowed for visualization of the grafted DA neurons and their axonal projections within the host brain. We show that the SNpc and VTA neuron subtypes in VM grafts can be identified on the basis of their morphology and location within the graft, and their expression of a G-protein-gated inwardly rectifying K+ channel subunit (Girk2) and calbindin, respectively, and also that the axonal projections of the two DA neuron types are markedly different. By retrograde axonal tracing, we show that dopaminergic innervation of the striatum is derived almost exclusively from the Girk2-positive SNpc cells, whereas the calbindin-positive VTA neurons project to the frontal cortex and probably also other forebrain areas. The results suggest the presence of axon guidance and target recognition mechanisms in the DA-denervated forebrain that can guide the growing axons to their appropriate targets and indicate that cell preparations used for cell replacement in Parkinson's disease will be therapeutically useful only if they contain cells capable of generating the correct nigral DA neuron phenotype.

Age Factors↗