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Takeyasu Maeda

Publications and source records attributed to Takeyasu Maeda.

At least 19 recordsLinked to original sources
PubMed2006

Involvement of GDNF and its receptors in the maturation of the periodontal Ruffini endings.

Our recent study revealed an intense immunoreaction for GDNF and its receptors in the Ruffini endings, primary mechanoreceptors in the periodontal ligament, of young rats. However, no information is available for the expression of GDNF and its receptors during their development. The present study aimed to reveal postnatal changes in the immuno-expression of GDNF, GFRalpha1 and RET in the periodontal Ruffini endings of the rat incisors by double immunofluorescent staining. At postnatal day 3 (PO 3d), no structure with GDNF-, GFRalpha1-, or RET-immunoreaction existed in the periodontal ligament. The PGP 9.5-positive nerve fibers without GDNF- and RET-immunoreaction displayed a dendritic fashion at PO 1w, with a GFRalpha1-reaction found around these nerves. At PO 2w, GDNF-positive terminal Schwann cells occurred near the thick and dendritic axons, a part of which showed a RET-reaction, with no reactive cells near the thin nerves. The terminal Schwann cells became positive for GFRalpha1, but lacked RET-immunoreaction. At PO 3w, when the formation of the periodontal Ruffini endings had proceeded, GDNF-positive terminal Schwann cells began to increase in number. This stage-specific immuno-expression pattern suggests that GDNF is a key molecule for the maturation and maintenance of the periodontal Ruffini endings.

Age Factors↗
PubMed2006

Expression of GDNF and its receptors in the periodontal mechanoreceptor.

Our previous studies have revealed the involvement of signaling pathways of BDNF and NT-4/5 via TrkB in the development, regeneration, survival and maintenance of the Ruffini endings, primary mechanoreceptors in the periodontal ligament. However, the involvement of other neurotrophins remains unclear. The present study examined the expression of GDNF, GFRalpha1, and RET in the incisor periodontal ligament and trigeminal ganglion of young rats by RT-PCR and immunocytochemistry. All these mRNAs were detected in both tissues by RT-PCR. These immunoreactions were found in the terminal Schwann cells associated with the periodontal Ruffini endings, as confirmed by histochemistry for non-specific cholinesterase activity. Their axonal branches showed GFRalpha1- and RET-immunoreactions but lacked GDNF-immunoreactivity. In the trigeminal ganglion, about 30% of the neurons were immunoreactive to GFRalpha1 and RET. Averages of cross-sectional areas of their positive neurons demonstrated that they could mainly be categorized as medium-sized neurons. GDNF-immunoreaction was restricted to the satellite cells and not in trigeminal ganglion neurons. These findings indicate that GDNF mediates trophic effects on the survival and target innervation of the periodontal Ruffini endings via GFRalpha1 and RET.

Animals↗
PubMed2006

Expression of caveolin-1 in the rat temporomandibular joint.

This immunocytochemical study revealed the expression of caveolin-1, a major protein of caveolae, in the rat temporomandibular joint. In the synovial lining layer, immunoreactive products for caveolin-1 were detected on the cell membrane of the fibroblast-like type B cells, as confirmed by immunocytochemistry for heat shock protein 25. The cells in the articular disk, the articular layer, and zone of proliferation of the mandibular condyle also showed intense immunoreactions for caveolin-1.

Animals↗
PubMed2006

Localization of CD44 and hyaluronan in the synovial membrane of the rat temporomandibular joint.

Previous studies have pointed out a lack of adhesion structures in the synovial lining layer of the rat temporomandibular joint (TMJ) despite showing an epithelial arrangement. CD44, a major cell adhesion molecule, plays crucial roles as an anchor between cells and extracellular matrices by binding hyaluronan (HA) for the development of organs or the metastasis of tumors. The present study examined the localization of CD44 in the synovial membrane of the rat TMJ by immunocytochemistry for OX50, ED1, and Hsp25, which are markers for the rat CD44, macrophage-like type A, and fibroblast-like type B synoviocytes, respectively. Histochemistry for HA-binding protein (HABP) was also employed for the detection of HA. OX50 immunoreactions were found along the cell surface and, in particular, accumulated along the surface of the articular cavity. Observations by a double immunostaining and immunoelectron microscopy revealed that all the OX50-immunopositive cells were categorized as fibroblastic type B cells, which had many caveolae and a few vesicles reactive to intense OX50. However, the macrophage-like type A cells did not have any OX50 immunoreaction in the synovial lining layer. A strong HABP reaction was discernable in the extracellular matrix surrounding both OX50-positive and -negative cells in the synovial lining layers, exhibiting a meshwork distribution, but weak in its sublining layer. This localization pattern of CD44 and HABP might be involved in the formation of the epithelial arrangement of the synovial lining layer. Furthermore, OX50 immunonegativity in the type A cells suggests their low phagocytotic activity in the rat TMJ under normal conditions.

Animals↗
PubMed2006

Histochemical evidence of osteoclastic degradation of extracellular matrix in osteolytic metastasis originating from human lung small carcinoma (SBC-5) cells.

The aim of this study was to assess the dynamics of osteoclast migration and the degradation of unmineralized extracellular matrix in an osteolytic metastasis by examining a well-standardized lung cancer metastasis model of nude mice. SBC-5 human lung small carcinoma cells were injected into the left cardiac ventricle of 6-week-old BALB/c nu/nu mice under anesthesia. At 25-30 days after injection, the animals were sacrificed and their femora and/or tibiae were removed for histochemical analyses. Metastatic lesions were shown to occupy a considerable area extending from the metaphyses to the bone marrow region. Tartrate resistant acid phosphatase (TRAPase)-positive osteoclasts were found in association with an alkaline phosphatase (ALPase)-positive osteoblastic layer lining the bone surface, but could also be localized in the ALPase-negative stromal tissues that border the tumor nodules. These stromal tissues were markedly positive for osteopontin, and contained a significant number of TRAPase-positive osteoclasts expressing immunoreactivity for CD44. We thus speculated that, mediating its affinity for CD44, osteopontin may serve to facilitate osteoclastic migration after their formation associated with ALPase-positive osteoblasts. We next examined the localization of cathepsin K and matrix metallo-proteinase-9 (MMP-9) in osteoclasts. Osteoclasts adjacent to the bone surfaces were positive for both proteins, whereas those in the stromal tissues in the tumor nests showed only MMP-9 immunoreactivity. Immunoelectron microscopy disclosed the presence of MMP-9 in the Golgi apparatus and in vesicular structures at the baso-lateral cytoplasmic region of the osteoclasts found in the stromal tissue. MMP-9-positive vesicular structures also contained fragmented extracellular materials. Thus, osteoclasts appear to either select an optimized function, namely secreting proteolytic enzymes from ruffled borders during bone resorption, or recognize the surrounding extracellular matrix by mediating osteopontin/CD44 interaction, and internalize the extracellular matrices. Microsc.

Acid Phosphatase↗
PubMed2006

Histological and immunohistochemical changes in the submandibular gland in klotho-deficient mice.

The submandibular gland (SMG) has been regarded as an age-stable organ in spite of reports on its structural changes with aging. Although the klotho gene is involved in aging, little information is available regarding its effects on morphological changes of SMGs. The present study examined the histological and immunohistochemical features of SMGs in klotho-deficient mice--which are well-established aging models--by immunohistochemical and histochemical techniques. Five kinds of cellular markers--against NGF, EGF, Mnand Cu/Zn-SOD, and RITC-conjugated phalloidin--were used for the identification of cell types. In klotho-deficient mice, the SMGs lost their granular ducts and each lobe diminished. The granular duct showed strong immunoreactivities for NGF and EGF in the wild-type mice, but the NGF- and EGF-immunopositive ducts decreased in number remarkably in klotho-deficient mice. Interestingly, instead of a loss of the granular duct, the striated duct located on the distal portion in the homozygous mice came to show NGF- and EGF-immunoreactions. Neither Mn- and Cu/Zn-SOD immunoreactivities in the duct system nor the phalloidin- reaction in the myoepithelial cells differed between the wild-type and klotho-deficient mice. Our findings suggest that the klotho gene inhibited the differentiation of the granular duct from the striated duct due to the repression and/or down-regulation of sexual and growth hormones.

Animals↗
PubMed2005

Reduced osteoblastic population and defective mineralization in osteopetrotic (op/op) mice.

Osteopetrotic (op/op) mice fail to exhibit bone remodeling because of a defective osteoclast formation due to a lack of macrophage colony-stimulating factor. In this study, we investigated the femora of op/op mice to clarify whether the osteoblastic population and bone mineralization are involved in osteoclasts or their bone resorption. The op/op mice extended the meshwork of trabecular bones from the chondro-osseous junction to the diaphyseal region. In the femoral metaphyses of op/op mice, intense alkaline phosphatase (ALPase)-positive osteoblasts were observed on the metaphyseal bone in close proximity to the erosion zone of the growth plates. Von Kossa's staining revealed scattered mineralized nodules and a fine meshwork of mineralized bone matrices while the wild-type littermates developed well-mineralized trabeculae parallel to the longitudinal axis. In contrast to the metaphysis, some op/op diaphyses showed flattened osteoblasts with weak ALPase-positivity, and the other diaphyses displayed bone surfaces without a covering by osteoblasts. It is likely, therefore, that the osteoblastic population and activity were lessened in the op/op diaphyses. Despite the osteopetrotic model, von Kossa's staining demonstrated patchy unmineralized areas in the op/op diaphyses, indicating that a lower population and/or the activity of osteoblasts resulted in defective mineralization in the bone. Transmission electron microscopy disclosed few osteoblasts on the diaphyseal bones, and instead, bone marrow cells and vascular endothelial cells were often attached to the unmineralized bone. Osteocytes were embedded in the unmineralized bone matrix. Thus, osteoclasts appear to be involved in the osteoblastic population and activity as well as subsequent bone mineralization.

Alkaline Phosphatase↗
PubMed2005

Histochemical evidences on the chronological alterations of the hypertrophic zone of mandibular condylar cartilage.

The hypertrophic chondrocytes lack the ability to proliferate, thus permitting matrix mineralization as well as vascular invasion from the bone in both the mandibular condyle and the epiphyseal cartilage. This study attempted to verify whether the histological appearance of the hypertrophic chondrocytes is in a steady state during postnatal development of the mouse mandibular condyle. Type X collagen immunohistochemistry apparently distinguished the fibrous layer described previously as the "articular zone," "articular layer," and "resting zone" from the hypertrophic zone. Interestingly, the ratio of the type X collagen-positive hypertrophic zone in the entire condyle seemed higher in the early stages but decreased in the later stages. Some apparently compacted cells in the hypertrophic zone showed proliferating cell nuclear antigen (PCNA) immunoreaction, indicating the potential for cell proliferation at the early stages. As the mice matured, in contrast, they further enlarged and assumed typical features of hypertrophic chondrocytes. Apoptotic cells were also discernible in the hypertrophic zone at the early but not later stages. Consistent with morphological configurations of hypertrophic chondrocytes, immunoreactions for alkaline phosphatase, osteopontin, and type I collagen were prominent at the later stage, but not the early stage. Cartilaginous matrices demonstrated scattered patches of mineralization at the early stage, but increased in their volume and connectivity at the later stage. Thus, the spatial and temporal occurrence of these immunoreactions as well as apoptosis likely reflect the prematurity of hypertrophying cells at the early stage, and imply a physiological relevance during the early development of the mandibular condyles.

Alkaline Phosphatase↗
PubMed2005

Postnatal development of excitation propagation in the trigeminal subnucleus caudalis evoked by afferent stimulation in mice.

The postnatal development of nociceptive afferent activity expansion and its modulation features were examined in mice using an optical imaging technique. Developing mice (1-2 weeks old (N1-2 w), 3-4 weeks old (N3-4 w), 5-6 weeks old (N5-6 w) and 7-8 weeks old (N7-8 w)) and neonatally capsaicin-treated mice were used. The propagation of neuronal excitation was measured by changes in fluorescent intensity in horizontal brain stem slices evoked by electrical stimulation to the trigeminal spinal tract. A single-pulse stimulation evoked excitation propagation in the trigeminal caudalis (Vc). The propagation area was larger in N1-2 w than in N7-8 w, and no differences were observed between capsaicin-treated and naive mice in the same age groups. Repetitive stimulation (100 Hz, 30 pulses) elicited long-lasting and widespread excitation propagation. The excitation propagation area was significantly larger in N7-8 w than in N1-2 w, N3-4 w and N5-6 w. This propagation was suppressed by 5 microM L-703.606, an NK1-receptor antagonist, suggesting that the repetitive stimulation-elicited excitation may require substance-P releases. Morphological observations demonstrated that the neural network in the Vc had grown by postnatal week 5. These results suggest that nociceptive afferent activity co-operatively matures with development of the network structure in the Vc, and that a mechanism for prolonged increase in central excitability is established during a later postnatal period.

Afferent Pathways↗
PubMed2005

Postnatal changes in the spatial distributions of substance P and neurokinin-1 receptor in the trigeminal subnucleus caudalis of mice.

Nociceptive afferent signals from the orofacial area are transmitted to the trigeminal subnucleus caudalis (Vc) through the release of glutamate and/or substance P (SP). Although nociceptive transmission and/or modulating mechanisms are known to develop during the postnatal period, the specific developmental changes in nociception and/or modulation remain unclear. The present study examined postnatal changes in the spatial relationship between SP and its receptor, the NK1 receptor (NK1R), in the mouse Vc by immunohistochemistry and quantitative analysis. The medulla was removed from C57BL/6N mice (1, 2, 4, and 8 weeks of age) after perfusion and fixation, and cut horizontally at a thickness of 40 mum. The relative densities of SP- and NK1R-immunoreactive areas and their changes with age were assessed statistically. One- and 2-week-old mice showed relatively high densities of SP-positive structures in the marginal layer (Mar) and the deep part of the magnocellular layer (Mag). The SP distribution in the superficial Vc remained unchanged, but the density in the deep Mag gradually decreased with age, resulting in a complete loss after postnatal week 4. The NK1R-immunoreactivity exhibited a similar distribution pattern to that of SP, but the pattern remained unchanged during the postnatal period. Double-immunofluorescence staining for SP and NK1R demonstrated only moderate direct contact of SP-positive structures with NK1R in the superficial area. These separate distributions and the postnatal changes in SP and NK1R suggest the possibility of another nociceptive afferent transmission mechanism, that is, volume transmission, in the Vc other than synapse-mediated transmission.

Aging↗
PubMed2005

LEF1 is a critical epithelial survival factor during tooth morphogenesis.

LEF1 is a cell-type-specific transcription factor and mediates Wnt signaling pathway by association with its co-activator beta-catenin. Wnt signaling is known to be critical for the specification of cranial neural crest (CNC) cells and may regulate the fate diversity of the CNC during craniofacial morphogenesis. Loss of Lef1 results in arrested tooth development at the late bud stage and LEF1 is required for a relay of a Wnt signaling to a cascade of FGF signaling activities to mediate the epithelial-mesenchymal interaction during tooth morphogenesis. It remains unclear, however, what is the cellular mechanism of LEF1 signaling in regulating tooth morphogenesis. To test the hypothesis that LEF1 signaling regulates the fate of the dental epithelial and the CNC-derived mesenchymal cells during tooth morphogenesis, we investigated and compared the cellular migration, proliferation, and apoptotic activity within the tooth germ between the wild-type and Lef1 null mutant mice. Using the Wnt1-Cre/R26R transgenic system for indelibly marking the progenies of CNC cells, we show that there is no CNC migration defect in the Lef1 null mutant mice, indicating that the arrest in tooth development is not the result of shortage of the CNC contribution into the first branchial arch in the Lef1 mutant. Furthermore, there is no alteration in cell proliferation or condensation of the CNC-derived dental mesenchyme in the Lef1 null mutant, suggesting that LEF1 may not affect the cell cycle progression of the multipotential CNC cells during tooth morphogenesis. Importantly, apoptotic activity is significantly increased within the dental epithelium in the Lef1 null mutant mice. As the result of this increased cell death, the bud stage tooth germ fails to advance to the cap stage in the absence of Lef1. Inhibition of apoptotic activity by FGF4 rescues the tooth development in the Lef1 null mutant. Our studies suggest that LEF1 is a critical survival factor for the dental epithelial cells during tooth morphogenesis.

Animals↗
PubMed2005

Characteristic distribution of immunoreaction for estrogen receptor alpha in rat ameloblasts.

Estrogen has a diverse function, including cell proliferation and differentiation via estrogen receptors (ER), which have been reported to be the case in various tissues in addition to female reproductive organs. A recent immunocytochemical study has reported the expression of ERalpha, a subtype of ER, in rat odontoblasts, suggesting an involvement of estrogen in the differentiation of tooth-forming cells. However, there is no information on the ERalpha immunoexpression in ameloblasts. The present study was therefore undertaken to examine the localization of ERalpha immunoreaction in rat ameloblasts during amelogenesis. A computer-assisted quantitative analysis under a confocal laser scanning microscope was employed to demonstrate the stage-specific localization pattern of ERalpha immunoreaction. Immunohistochemistry of the rat enamel organ revealed ERalpha expression as nuclear localization in ameloblasts, stratum intermedium, stellate reticulum, and papillary layer, in addition to mature and immature odontoblasts. The ratio of immunopositive nuclei to total nuclei (immunopositive ratio) in ameloblasts was high at the apical loop region and gradually declined at the presecretory stage to zero at the secretory stage with statistically significant difference. The ERalpha immunolabeling pattern exhibited a periodic change at the maturation stage proper with constant higher labeling in ruffle-ended ameloblasts than in smooth-ended ameloblasts. The positive ratio was then followed by a statistically significant increase in immunolabeling thereafter. This stage-specific immunolabeling pattern during amelogenesis suggests a possible role of ERalpha in ameloblast proliferation and differentiation.

Ameloblasts↗
PubMed2005

Immunocytochemical localization of MAPKAPK-2 and Hsp25 in the rat temporomandibular joint.

One series of our research has shown an intense expression of immunoreaction for heat shock protein 25 (Hsp25) in various cellular elements in the rat temporomandibular joint (TMJ). This protein is the major substrate of mitogen-activated protein kinase-activated protein kinase-2 (MAPKAPK-2), which mediates an intracellular stress-activated signaling pathway to stimulate cytosolic actin reorganization under various stresses. The present study was undertaken to examine the localization of MAPKAPK-2 in the rat TMJ by immunocytochemical techniques. Furthermore, confocal microscopy with double staining was employed to demonstrate the colocalization of MAPKAPK-2 and Hsp25. Immunocytochemistry for MAPKAPK-2 showed an intense immunoreaction in the cytoplasm of the synovial lining cells, the endothelial cells, and the fibroblasts in the synovial membrane of the rat TMJ. Double immunostaining under a confocal microscope succeeded in demonstrating the colocalization of MAPKAPK-2 and Hsp25 immunoreactions in the cytoplasm of fibroblastic type B synoviocytes in the TMJ. On the other hand, the macrophage-like type A-cells expressed MAPKAPK-2 immunoreactions but lacked Hsp25 immunoreactivity. The cells in the articular disk and the chondrocytes in the maturative and hypertrophic layer of the mandibular cartilage also showed intense immunoreactions for MAPKAPK-2 and Hsp25. In addition to cytoplasmic localization, MAPKAPK-2 immunoreactions were found in the nucleus of some synovial lining cells, cells in the articular disk, and chondrocytes. Current observations imply the presence of the phosphorylation of Hsp25 via activated MAPKAPK-2 in the cytoplasm. MAPKAPK-2 and Hsp25 possibly participate in the induction of cytoskeletal changes to the various cellular elements in rat TMJ under normal conditions.

Animals↗
PubMed2005

Development of the articular cavity in the rat temporomandibular joint with special reference to the behavior of endothelial cells and macrophages.

Previous developmental studies on the temporomandibular joint (TMJ) have proposed several hypotheses on the formation of its articular cavity. However, detailed information is meager. The present study examined the formation process of the articular cavity in the rat TMJ by immunocytochemistry for CD31, RECA-1, and ED1, which are useful cellular markers for endothelial cells and monocyte/macrophage lineages, respectively. The upper articular cavity formation had begun by embryonic day 21 (E21) and was completed at postnatal day 1 (P1) in advance of the lower cavitation; the latter took place from P1 to P3. The occurrence and distribution pattern of the CD31-, RECA-1-, and ED1-positive cells differed between the upper and lower articular cavity-forming areas: the ED1-positive cells exclusively occurred in the area of the prospective upper articular cavity prior to its formation, while no ED1-positive cell appeared in the lower cavity-forming area. In contrast, the CD31- and RECA-1-positive endothelial cells were restricted to the lower cavity-forming area (never the prospective upper cavity) at E19 and diminished thereafter. Throughout the cavity formation, we failed to find any apoptotic cells in the cavity formation area, indicating no involvement of apoptosis in the cavity formation in TMJ. The present findings on the behaviors of endothelial cells and ED1-positive cells show a possibility of different mechanism in the cavity formation between the upper and lower articular cavities in the rat TMJ. The appearance of ED1-reactive cells and temporal vascularization may play crucial roles in the upper and lower articular cavity formation, respectively.

Animals↗
PubMed2005

A histological evaluation for guided bone regeneration induced by a collagenous membrane.

This study was designed to evaluate the histological changes during ossification and cellular events including osteogenic differentiation responding to collagenous bioresorbable membranes utilized for GBR. Standardized artificial bony defects were prepared at rat maxillae, and covered with a collagenous bioresorbable membrane. These animals were sacrificed at 1, 2, 3 and 4 weeks after the GBR-operation. The paraffin sections were subject to tartrate resistant acid phosphatase (TRAP) enzyme histochemistry and immunohistochemistry for alkaline phosphatase (ALP), osteopontin (OP) and osteocalcin (OC). In the first week of the experimental group, woven bone with ALP-positive osteoblasts occupied the lower half of the cavity. The collagenous membrane included numerous ALP-negative cells and OP-immunoreactive extracellular matrices. At 2 weeks, the ALP-, OP- and OC-immunoreactivity came to be recognizable in the region of collagenous membrane. Since ALP-negative soft tissue separated the collagenous membrane and the new bone originating from the cavity bottom, the collagenous membrane appeared to induce osteogenesis in situ. At 3 weeks, numerous collagen fibers of the membrane were embedded in the adjacent bone matrix. At 4 weeks, the membrane-associated and the cavity-derived bones had completely integrated, showing the same height of the periosteal ridge as the surrounding alveolar bones. The collagen fibers of a GBR-membrane appear to participate in osteogenic differentiation.

Animals↗
PubMed2005

Neurotrophin-4/5-depletion induces a delay in maturation of the periodontal Ruffini endings in mice.

Neurotrophin-4/5 (NT-4/5) - a member of the neurotrophic factors - is a ligand for TrkB, which has been reported to be expressed in the mechanoreceptive Ruffini endings of the periodontal ligament. The present study examined developmental changes in the terminal morphology and neural density in homozygous mice with a targeted disruption of the nt-4/5 gene and wild-type mice by immunohistochemistry for protein gene product 9.5 (PGP 9.5), a general neuronal marker, and by quantitative analysis using an image analyzer. Postnatal development of terminal Schwann cells was also investigated by enzymatic histochemistry for non-specific cholinesterase activity (ChE). Furthermore, the immuno-expression of TrkB and low affinity nerve growth factor receptor (p75-NGFR) was surveyed in the periodontal Ruffini endings as well as trigeminal ganglion. At postnatal 1 week, the lingual periodontal ligament of both types of mice contained PGP 9.5-positive nerve fibers showing a tree-like ramification with axonal swellings in their course. In both types of mice at 2 weeks of age, comparatively thick nerve fibers with a smooth outline increased in number, and frequently ramified to form nerve terminals with dendritic profiles. However, no typical Ruffini endings with irregular outlines observed in the adult wild-type mice were found in the periodontal ligament at this stage. At postnatal 3 weeks, typical Ruffini endings with irregular outlines were discernable in the periodontal ligament of the wild-type mice while the dendritic endings showing smooth outlines were restricted to the homozygous mice. After postnatal 8 weeks, both types of mice showed an increase in the number of Ruffini endings, but the morphology differed between the wild-type and NT-4/5 homozygous mice. In the wild-type mice, a major population of the Ruffini endings expanded their axonal branches and developed many microprojections, resulting in a reduction of endings with smooth outlines. In contrast, we failed to find such typical Ruffini endings in the periodontal ligament of the homozygous mice: A majority of the periodontal Ruffini endings continued to show smooth outlines at postnatal 12 weeks. Quantitative analysis on neural density demonstrated a reduction in the homozygous mice with a significant difference by postnatal 8 weeks. Enzymatic histochemistry for non-specific ChE did not exhibit a distinct difference in the distribution and density of terminal Schwann cells between wild-type and homozygous mice. Furthermore, TrkB and p75-NGFR mRNA and proteins did not differ in the trigeminal ganglion between the two types. The periodontal Ruffini endings also displayed immunoreactivities for TrkB and p75- NGFR in both phenotypes. These findings suggest that the nt-4/5 gene depletion caused a delay in the formation and maturation of the periodontal Ruffini endings in the mice by inhibiting the growth of the periodontal nerves at an early stage, and indicate that multiple neurotrophins such as NT- 4/5 and BDNF might play roles in the development and/or maturation of the periodontal Ruffini endings.

Animals↗
PubMed2005

Postnatal development of substance P-immunoreaction in the trigeminal caudalis of neonatally capsaicin-treated mice.

The trigeminal subnucleus caudalis (Vc) is a critical relay site for processing nociceptive afferent input from the orofacial area in addition to its modulation by neuroplastic change. Although an administration of capsaicin in neonates induces a selective destruction of substance P (SP)-immunoreactive nerve fibers, little information is available regarding its detailed effects on the Vc, particularly during postnatal development. The present study examined postnatal changes in the distribution of SP in the Vc and trigeminal ganglion (TG) by immunohistochemical techniques in naïve (NV) and neonatally capsaicin-treated (CP) mice, combined with a quantitative analysis. The neonatal mice received a single subcutaneous injection of capsaicin (50 mg/kg) at 48 hours after birth. The neural density of the SP-immunoreaction decreased to approximately a quarter of that in 1-week-old NV mice but increased to three-quarters of that in the NV in the superficial area after postnatal week 2. A double staining with SP and myelin basic protein confirmed the absence of any SP-immunoreaction in the myelinated nerve fibers in both NV and CP mice. The SP-immunoreaction never overlapped with non-peptidergic IB4-labeled neurons in the Vc and TG of either group. Neither the size distribution of SP-positive neurons nor their relative ratio in the TG differed between NV and CP mice at the ages of postnatal weeks 1 and 8. These findings indicate two putative origins for the emergent SP-immunoreaction in the superficial layer of the Vc of the CP mice: the surviving trigeminal neurons with SP against capsaicin treatment and/or intrinsic neurons/interneurons in the Vc without SP under normal conditions.

Animals↗