Pub Date : 2003-12-20DOI: 10.2330/JORALBIOSCI1965.45.418
N. Wakana, S. Akutsu, A. Yamane
To determine whether clenbuterol, a β2-adrenergic agonist, affects the mass and fiber type of the mouse masseter muscle by altering the expressions of insulin-like growth factors (IGFs), their receptors (IGFRs), and their binding proteins (IGFBPs), we analyzed changes in the myofiber diameter, the expressions of myosin heavy chain (MHC) mRNAs, the markers for muscle fiber type, and the expressions of IGF, IGFR, and IGFBP mRNAs. In addition, to identify a possible contribution of muscle satellite cells in the change of the mouse masseter induced by clenbuterol, we analyzed the expressions of the myoD family (myf5, myoD, myogenin, and MRF4) and myocyte nuclear factor (MNF) mRNAs, and performed immunolocalization for proliferating cell nuclear antigen (PCNA), because they are all markers for activated and quiescent satellite cells. Clenbuterol (40 μg/ml) was orally administered to 6-month-old mice via their drinking water for 2 weeks. The relative amounts of mRNAs were analyzed by competitive polymerase chain r action in combination with reverse-transcription. The administration of clenbuterol increased the myofiber diameter by 26% (p<0.001), but it did not significantly change the amounts of MHC mRNAs, suggesting that clenbuterol induced hypertrophy but did not alter the fiber type. The administration of clenbuterol increased the amount of mRNA for IGF-I by 219% (p<0.05), but it decreased that for IGFBP3 by 21% (p<0.001). The amounts of mRNAs for all genes except for IGF-I and IGFBP3, and the immunolocalization for PCNA were not significantly changed by clenbuterol. These results suggest that clenbuterol induces hypertrophy in the mouse masseter muscle and that IGF-I and IGFBP3 are involved in the clenbuterol-induced hypertrophy, but the satellite cells might not be involved.
{"title":"Effects of Clenbuterol, a β2-adrenergic Agonist, on the Myofiber Diameter, Fiber Type, and Expressions of Insulin-like Growth Factors in the Adult Mouse Masseter Muscle","authors":"N. Wakana, S. Akutsu, A. Yamane","doi":"10.2330/JORALBIOSCI1965.45.418","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.418","url":null,"abstract":"To determine whether clenbuterol, a β2-adrenergic agonist, affects the mass and fiber type of the mouse masseter muscle by altering the expressions of insulin-like growth factors (IGFs), their receptors (IGFRs), and their binding proteins (IGFBPs), we analyzed changes in the myofiber diameter, the expressions of myosin heavy chain (MHC) mRNAs, the markers for muscle fiber type, and the expressions of IGF, IGFR, and IGFBP mRNAs. In addition, to identify a possible contribution of muscle satellite cells in the change of the mouse masseter induced by clenbuterol, we analyzed the expressions of the myoD family (myf5, myoD, myogenin, and MRF4) and myocyte nuclear factor (MNF) mRNAs, and performed immunolocalization for proliferating cell nuclear antigen (PCNA), because they are all markers for activated and quiescent satellite cells. Clenbuterol (40 μg/ml) was orally administered to 6-month-old mice via their drinking water for 2 weeks. The relative amounts of mRNAs were analyzed by competitive polymerase chain r action in combination with reverse-transcription. The administration of clenbuterol increased the myofiber diameter by 26% (p<0.001), but it did not significantly change the amounts of MHC mRNAs, suggesting that clenbuterol induced hypertrophy but did not alter the fiber type. The administration of clenbuterol increased the amount of mRNA for IGF-I by 219% (p<0.05), but it decreased that for IGFBP3 by 21% (p<0.001). The amounts of mRNAs for all genes except for IGF-I and IGFBP3, and the immunolocalization for PCNA were not significantly changed by clenbuterol. These results suggest that clenbuterol induces hypertrophy in the mouse masseter muscle and that IGF-I and IGFBP3 are involved in the clenbuterol-induced hypertrophy, but the satellite cells might not be involved.","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"79 1","pages":"418-427"},"PeriodicalIF":0.0,"publicationDate":"2003-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90863208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-12-20DOI: 10.2330/JORALBIOSCI1965.45.428
Y. Wada, R. Fujisawa, Y. Kuboki
Bisphosphonates are widely known as inhibitors of formation and resorption of mineralized tissues. However, it is uncertain how bisphosphonates affect calcium phosphate precipitation and matrix synthesis in mineralized tissues. Several histological approaches have been done to study hard tissues affected by bisphosphonates. In this study, we used a bisphosphonate for biochemical investigation to study the mechanisms of biological mineralization and considered the effects of the bisphosphonates.Hydroxyethylidene-1, 1-bisphosphonate (HEBP) was administered to rats by subcutaneous injection of 10mg P/kg for seven weeks. The incisors of the rats were removed and the dentin matrix proteins were analyzed biochemically. The amount of matrix proteins was relatively increased in the incisors of the experimental rats, though mineralization of the incisors of the those rats was reduced compared with that of the control rats. Dentin phosphophoryns, unique phosphoproteins of dentin, were also elevated in the experimental rats. Nevertheless, the composition of other non-collagenous proteins of dentin was essentially unchanged by the treatment.Inhibition of mineralization by bisphosphonate may not be mediated by inhibition Of synthesis of noncollagenous matrix proteins, but mainly by inhibition of calcium phosphate deposition. Moreover, it is possible that the synthesis of phosphophoryns was promoted by the treatment.
{"title":"Changes of the Rat Dentin Matrix Proteins Affected by Long-term Administration of Hydroxyethylidene-1,1-bisphosphonate (HEBP).","authors":"Y. Wada, R. Fujisawa, Y. Kuboki","doi":"10.2330/JORALBIOSCI1965.45.428","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.428","url":null,"abstract":"Bisphosphonates are widely known as inhibitors of formation and resorption of mineralized tissues. However, it is uncertain how bisphosphonates affect calcium phosphate precipitation and matrix synthesis in mineralized tissues. Several histological approaches have been done to study hard tissues affected by bisphosphonates. In this study, we used a bisphosphonate for biochemical investigation to study the mechanisms of biological mineralization and considered the effects of the bisphosphonates.Hydroxyethylidene-1, 1-bisphosphonate (HEBP) was administered to rats by subcutaneous injection of 10mg P/kg for seven weeks. The incisors of the rats were removed and the dentin matrix proteins were analyzed biochemically. The amount of matrix proteins was relatively increased in the incisors of the experimental rats, though mineralization of the incisors of the those rats was reduced compared with that of the control rats. Dentin phosphophoryns, unique phosphoproteins of dentin, were also elevated in the experimental rats. Nevertheless, the composition of other non-collagenous proteins of dentin was essentially unchanged by the treatment.Inhibition of mineralization by bisphosphonate may not be mediated by inhibition Of synthesis of noncollagenous matrix proteins, but mainly by inhibition of calcium phosphate deposition. Moreover, it is possible that the synthesis of phosphophoryns was promoted by the treatment.","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"14 1","pages":"428-436"},"PeriodicalIF":0.0,"publicationDate":"2003-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82015938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-12-20DOI: 10.2330/JORALBIOSCI1965.45.437
Kyoko Watanabe, Y. Azuma, S. Shirasu, M. Daito, K. Ohura
Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflammatory cytokines. Recently, it has been shown that A 2 a adenosine receptor (A 2 aR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory responses. It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the inflammation. However, very little, if anything, is known about the effect of bacterial LPS on the expression of A 2 aR during an infection of bacteria. The aim of this study is to evaluate the effects of adenosine, ATP and LPS on the expression of A 2 aR and toll-like receptor 4 (TLR 4), which is a receptor for LPS, in the mouse macrophage cell line RAW 264. Adenosine and ATP failed to affect proliferation in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly potentiated the expression of TLR 4, but not of A 2 aR. ATP and LPS markedly potentiated the expression of A 2 aR and TLR 4, respectively. Moreover, adenosine and ATP did not affect the expression of A 2 aR and TLR 4 in the presence of LPS, respectively. This study revealed that adenosine, ATP and LPS affect the expression of A 2 aR and TLR 4 in macrophages.
{"title":"Alteration of the Expression of A 2 a Adenosine Receptor and Toll-like Receptor 4 in Macrophage Cell Lines","authors":"Kyoko Watanabe, Y. Azuma, S. Shirasu, M. Daito, K. Ohura","doi":"10.2330/JORALBIOSCI1965.45.437","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.437","url":null,"abstract":"Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflammatory cytokines. Recently, it has been shown that A 2 a adenosine receptor (A 2 aR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory responses. It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the inflammation. However, very little, if anything, is known about the effect of bacterial LPS on the expression of A 2 aR during an infection of bacteria. The aim of this study is to evaluate the effects of adenosine, ATP and LPS on the expression of A 2 aR and toll-like receptor 4 (TLR 4), which is a receptor for LPS, in the mouse macrophage cell line RAW 264. Adenosine and ATP failed to affect proliferation in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly potentiated the expression of TLR 4, but not of A 2 aR. ATP and LPS markedly potentiated the expression of A 2 aR and TLR 4, respectively. Moreover, adenosine and ATP did not affect the expression of A 2 aR and TLR 4 in the presence of LPS, respectively. This study revealed that adenosine, ATP and LPS affect the expression of A 2 aR and TLR 4 in macrophages.","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"20 1","pages":"437-444"},"PeriodicalIF":0.0,"publicationDate":"2003-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87789602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-12-20DOI: 10.2330/JORALBIOSCI1965.45.397
M. Kageyama, I. Itoh
The morphology of the muscle bundle in the deep layer of the anterior temporal muscle was observed using cadavers for anatomical practice. With regard to the infratemporal crest, which is the origin of the muscle bundle, its cranial bone surface morphology was also observed, and the following results were obtained:1. This muscle bundle was thought to be part of the anterior muscle bundle of the temporal muscle, considering the innervation and fascial conditions.2. In elderly specimens, processes were noted on the bone surface of the infratemporal crest, which is the origin of this muscle bundle.3. The length of this muscle bundle was 36.85±2.78mm, and the width was 12.49±1.37mm, with an inclination angle of 80.83±2.46° to the auriculo-orbital plane (FH. plane).These findings suggested that although the deep muscle bundle is part of the anterior muscle bundle in the superficial layer, the muscle bundle developed as an independent muscle fascicle, causing changes in the bone surface in the adhesion area of the muscle, due to strong force applied during mandibular movement.
{"title":"Orientation of the Deep Part of the Human Temporal Muscle and Morphological Study of the Infratemporal Crest.","authors":"M. Kageyama, I. Itoh","doi":"10.2330/JORALBIOSCI1965.45.397","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.397","url":null,"abstract":"The morphology of the muscle bundle in the deep layer of the anterior temporal muscle was observed using cadavers for anatomical practice. With regard to the infratemporal crest, which is the origin of the muscle bundle, its cranial bone surface morphology was also observed, and the following results were obtained:1. This muscle bundle was thought to be part of the anterior muscle bundle of the temporal muscle, considering the innervation and fascial conditions.2. In elderly specimens, processes were noted on the bone surface of the infratemporal crest, which is the origin of this muscle bundle.3. The length of this muscle bundle was 36.85±2.78mm, and the width was 12.49±1.37mm, with an inclination angle of 80.83±2.46° to the auriculo-orbital plane (FH. plane).These findings suggested that although the deep muscle bundle is part of the anterior muscle bundle in the superficial layer, the muscle bundle developed as an independent muscle fascicle, causing changes in the bone surface in the adhesion area of the muscle, due to strong force applied during mandibular movement.","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"1 1","pages":"397-406"},"PeriodicalIF":0.0,"publicationDate":"2003-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89035824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-08-20DOI: 10.2330/JORALBIOSCI1965.45.180
Hitoshi Kawanabe, S. Kinoshita, H. Ishikawa, K. Taniguchi
This study examined the ultrastructural changes in the palatal bone surface induced by scar tissue formation on the palate. Male 20-day-old Wistar rats were divided into experimental and control groups. In the experimental group the bilateral mucoperiosteum was excised in the lateral one third of the palate. At the 6th week following the surgical procedure, changes in the lamina propria and bone surface of the denuded bone area were investigated by light and scanning electron microscopy . In the control group, fibrous connective tissue with horizontally oriented collagen fibers were found beneath the epithelium , and there was periosteum along the bony surface. Scanning electron microscopy of the control group showed regularly arranged blood vessel holes on the bone surface. The experimental group showed dense fibrous connective tissue with matted collagen fibers were present in the lateral operated area without periosteum . Scanning electron microscopy showed rough bone surface with vague appearance of collagen bundle structures. Fewer blood vessel holes were seen on the bone surface than in the control group . The results suggested that scar tissue formation by mucoperiosteal denudation of the palate deteriorates vascular supply to the bone, which results in the palatal bone growth inhibition. 抄録:口 蓋裂患者では,幼 少期にpush back法 による口蓋形成手術が広く行われているが,術 後の瘢痕組織が 上顎骨の成長を抑制すると報告されている。本研究では,実 験的に生後20日 齢ラットの口蓋粘膜を一部除去して 瘢痕形成を行い,術 後6週 。 対照群の口蓋粘膜は,角 化重層扁平上皮,上 皮下の線維性結合組織よりなり,口 。実 験群では,不 規則な角化重層扁平上皮とその直下に瘢痕性結合組織がみられ,骨 。走査電顕 〒814-0193 福 岡 県福 岡 市早 良区 田村2-15-1 川鍋 仁ほか:ラ ツト口蓋部瘢痕形成が骨表面の微細構造に与える影響 181 像では,対 ,ま た骨表面の粗〓化と骨基質の膠原線維束の不明瞭化が認 められた。以上より,術 後の瘢痕形成は骨への栄養供給の低下とともに ,口 蓋骨の成長に影響を与えることが示 唆された。
{"title":"Influence of Scar Tissue Formation on Ultrastructure of the Palatal Bone Surface in Rats","authors":"Hitoshi Kawanabe, S. Kinoshita, H. Ishikawa, K. Taniguchi","doi":"10.2330/JORALBIOSCI1965.45.180","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.180","url":null,"abstract":"This study examined the ultrastructural changes in the palatal bone surface induced by scar tissue formation on the palate. Male 20-day-old Wistar rats were divided into experimental and control groups. In the experimental group the bilateral mucoperiosteum was excised in the lateral one third of the palate. At the 6th week following the surgical procedure, changes in the lamina propria and bone surface of the denuded bone area were investigated by light and scanning electron microscopy . In the control group, fibrous connective tissue with horizontally oriented collagen fibers were found beneath the epithelium , and there was periosteum along the bony surface. Scanning electron microscopy of the control group showed regularly arranged blood vessel holes on the bone surface. The experimental group showed dense fibrous connective tissue with matted collagen fibers were present in the lateral operated area without periosteum . Scanning electron microscopy showed rough bone surface with vague appearance of collagen bundle structures. Fewer blood vessel holes were seen on the bone surface than in the control group . The results suggested that scar tissue formation by mucoperiosteal denudation of the palate deteriorates vascular supply to the bone, which results in the palatal bone growth inhibition. 抄録:口 蓋裂患者では,幼 少期にpush back法 による口蓋形成手術が広く行われているが,術 後の瘢痕組織が 上顎骨の成長を抑制すると報告されている。本研究では,実 験的に生後20日 齢ラットの口蓋粘膜を一部除去して 瘢痕形成を行い,術 後6週 。 対照群の口蓋粘膜は,角 化重層扁平上皮,上 皮下の線維性結合組織よりなり,口 。実 験群では,不 規則な角化重層扁平上皮とその直下に瘢痕性結合組織がみられ,骨 。走査電顕 〒814-0193 福 岡 県福 岡 市早 良区 田村2-15-1 川鍋 仁ほか:ラ ツト口蓋部瘢痕形成が骨表面の微細構造に与える影響 181 像では,対 ,ま た骨表面の粗〓化と骨基質の膠原線維束の不明瞭化が認 められた。以上より,術 後の瘢痕形成は骨への栄養供給の低下とともに ,口 蓋骨の成長に影響を与えることが示 唆された。","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"7 1","pages":"180-186"},"PeriodicalIF":0.0,"publicationDate":"2003-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79674521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-08-20DOI: 10.2330/JORALBIOSCI1965.45.169
Yukiko Iwabuchi, K. Okuda-Akabane, Kinya Narita
The taste of sodium salts is due to sodium ions . However, the role of anions in salt taste is less well understood. In the present study , we recorded the responses to sodium salts from the frog glossopharyn geal nerve (GL) and explored how anions are involved in salt taste . The frog GL responds to relatively high concentrations of sodium salts (>0 .1M). The order of effectiveness of sodium salts in producing a response was NaCl>Na2SO4>Na gluconate (NaGlu) . It has been reported that addition of 1mM NiCl2 to tastants greatly enhances the responses to NaCl and reduces threshold concentration for NaCl to 0 .02M. In the present study, we used stimulating solutions with 1mM NiCl2 . In the presence of NiCl2, the stimulating effects of NaCl differed markedly from those of Na2SO4 and NaGlu . The order of effectiveness of sodium salts with 1mM NiCl2 was NaCl>>Na2SO4>NaGlu . In the experiments of stimulation with a mixture of NaCl plus other salts in the presence of Ni2+, we found that gluconate-(Glu-) had an inhibitory effect on the responses to NaCl, whereas SO42had no effect . Since Glu-(a large anion) is unable to pass through tight junctions between taste cells and only interacts with apical membrane of taste cells , it is likely that Na+receptor sites (XNa) responsible for the responses to sodium may not reside in the basolateral membra ne, but in the apical receptor membrane. An explanation for these results is provided by the hypothesis that X Na i nteracts with anion-binding element (Y) that is affected by anions and with Ni2+binding element (T) that is affected by Ni2+. Cl--Y complexes are important for enhancement of the response to Na+ . Gluantagonizes the effect of Cl-. Ni2+ can induce increases in the affinity of Y for Cl, in the affinity of XNa for Na+ and enhancement of the response to Nat via T. 〒020-8505 岩 手 県盛 岡市 中央 通 1-3-27 170 歯 基 礎 誌45: 169-179, 2003. 抄録:Na塩 の味覚 はNa+に 起 因す る。しか し,Na+受 容 にお ける陰 イオ ンの役割 は不 明 であ る。本研 究 は カエ ル舌咽 神経 のNa塩 応 答 を記録 し,Na塩 応 答 にお ける陰 イオ ンの役 割 を調 べ た もの で あ る。 カ エル舌 咽 神 経 は 0.1M以 上 のNa塩 に応答 す る。Na塩 の興 奮効果 の順 序 はNaCl>Na2SO4>Na gluconate (NaGlu)で あっ た。 Na塩 応 答 は刺激 液へ の1mM NiCl2の 添 加 に よ り応 答 が増強 され るこ とが知 られて い る。1mM NiCl2の 存 在下 で はNaCl応 答 が顕著 に増 強 され,NaClの 閾値 は0 .02Mに まで減 少 す る。本 実験 で は1mM NiCl2を 含 む刺激 液 を用 い た。1mM NiCl2の 存在 で,NaClの 刺 激効果 はほか のNa2SO4お よびNaGluの それ とは顕 著 に異 な り, 興 奮効 果 の順序 はNaCl>>Na2SO4>NaGluと なった。1mM NiCl2存 在下 でNaClと ほか のNa塩 の混 合液 の 実験 か ら,次 の結果 を得 た。gluconate-(Glu-)はNaCl応 答 に対 し抑制効 果 が あ り,SO42-は 特別 な効 果 を もた なか った。大 きな陰 イオ ンのGlu-は 味細胞 間 の タイ トジャ ンク シ ョンを通 過 で きず味 細胞 の先 端受 容膜 に しか作 用 しない ので,Na塩 応 答 を引 き起 こすNa+受 容 サ イ ト(XNa)は 基底 外側膜 には存在 せ ず,先 端受 容膜 に存 在 す る もの と思 われ る。本実験 結果 の説 明 として次 の モデル を考 えた。XNaは 陰 イオ ンによ って影響 され る陰 イ オ ン結 合 要素(Y)お よびNi2+に よって影響 され るNi2+結 合 要素(T)と 相互 作 用 を もつ。Cl--Y複 合体 はNa塩 応答 の増 強 に重 要で あ る。Glu-はCl-の 効果 と拮抗 す る。Ni2+はTを 経 てYに 対 す るCl-の 親和 性 の増加 ,XNaに 対 す るNa+の 親 和性 の増 加 お よびNa+応 答 の増 強 を引 き起 こす。
{"title":"Salt Taste Responses in the Frog Glossopharyngeal Nerve: Anion Modulation of Nickel-enhanced Responses to Sodium Ions","authors":"Yukiko Iwabuchi, K. Okuda-Akabane, Kinya Narita","doi":"10.2330/JORALBIOSCI1965.45.169","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.169","url":null,"abstract":"The taste of sodium salts is due to sodium ions . However, the role of anions in salt taste is less well understood. In the present study , we recorded the responses to sodium salts from the frog glossopharyn geal nerve (GL) and explored how anions are involved in salt taste . The frog GL responds to relatively high concentrations of sodium salts (>0 .1M). The order of effectiveness of sodium salts in producing a response was NaCl>Na2SO4>Na gluconate (NaGlu) . It has been reported that addition of 1mM NiCl2 to tastants greatly enhances the responses to NaCl and reduces threshold concentration for NaCl to 0 .02M. In the present study, we used stimulating solutions with 1mM NiCl2 . In the presence of NiCl2, the stimulating effects of NaCl differed markedly from those of Na2SO4 and NaGlu . The order of effectiveness of sodium salts with 1mM NiCl2 was NaCl>>Na2SO4>NaGlu . In the experiments of stimulation with a mixture of NaCl plus other salts in the presence of Ni2+, we found that gluconate-(Glu-) had an inhibitory effect on the responses to NaCl, whereas SO42had no effect . Since Glu-(a large anion) is unable to pass through tight junctions between taste cells and only interacts with apical membrane of taste cells , it is likely that Na+receptor sites (XNa) responsible for the responses to sodium may not reside in the basolateral membra ne, but in the apical receptor membrane. An explanation for these results is provided by the hypothesis that X Na i nteracts with anion-binding element (Y) that is affected by anions and with Ni2+binding element (T) that is affected by Ni2+. Cl--Y complexes are important for enhancement of the response to Na+ . Gluantagonizes the effect of Cl-. Ni2+ can induce increases in the affinity of Y for Cl, in the affinity of XNa for Na+ and enhancement of the response to Nat via T. 〒020-8505 岩 手 県盛 岡市 中央 通 1-3-27 170 歯 基 礎 誌45: 169-179, 2003. 抄録:Na塩 の味覚 はNa+に 起 因す る。しか し,Na+受 容 にお ける陰 イオ ンの役割 は不 明 であ る。本研 究 は カエ ル舌咽 神経 のNa塩 応 答 を記録 し,Na塩 応 答 にお ける陰 イオ ンの役 割 を調 べ た もの で あ る。 カ エル舌 咽 神 経 は 0.1M以 上 のNa塩 に応答 す る。Na塩 の興 奮効果 の順 序 はNaCl>Na2SO4>Na gluconate (NaGlu)で あっ た。 Na塩 応 答 は刺激 液へ の1mM NiCl2の 添 加 に よ り応 答 が増強 され るこ とが知 られて い る。1mM NiCl2の 存 在下 で はNaCl応 答 が顕著 に増 強 され,NaClの 閾値 は0 .02Mに まで減 少 す る。本 実験 で は1mM NiCl2を 含 む刺激 液 を用 い た。1mM NiCl2の 存在 で,NaClの 刺 激効果 はほか のNa2SO4お よびNaGluの それ とは顕 著 に異 な り, 興 奮効 果 の順序 はNaCl>>Na2SO4>NaGluと なった。1mM NiCl2存 在下 でNaClと ほか のNa塩 の混 合液 の 実験 か ら,次 の結果 を得 た。gluconate-(Glu-)はNaCl応 答 に対 し抑制効 果 が あ り,SO42-は 特別 な効 果 を もた なか った。大 きな陰 イオ ンのGlu-は 味細胞 間 の タイ トジャ ンク シ ョンを通 過 で きず味 細胞 の先 端受 容膜 に しか作 用 しない ので,Na塩 応 答 を引 き起 こすNa+受 容 サ イ ト(XNa)は 基底 外側膜 には存在 せ ず,先 端受 容膜 に存 在 す る もの と思 われ る。本実験 結果 の説 明 として次 の モデル を考 えた。XNaは 陰 イオ ンによ って影響 され る陰 イ オ ン結 合 要素(Y)お よびNi2+に よって影響 され るNi2+結 合 要素(T)と 相互 作 用 を もつ。Cl--Y複 合体 はNa塩 応答 の増 強 に重 要で あ る。Glu-はCl-の 効果 と拮抗 す る。Ni2+はTを 経 てYに 対 す るCl-の 親和 性 の増加 ,XNaに 対 す るNa+の 親 和性 の増 加 お よびNa+応 答 の増 強 を引 き起 こす。","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"2 1","pages":"169-179"},"PeriodicalIF":0.0,"publicationDate":"2003-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74425220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-08-20DOI: 10.2330/JORALBIOSCI1965.45.151
Kaori Sato, H. Yagishita, Y. Kanri, Y. Taya, Y. Soeno, Rika Enari, T. Aoba
In the present study, we aimed to investigate changes in the mineral composition and solubility of rat bone under various regimens of fluoride administration in drinking water. Sprague-Dawley rats (male, 4-week-old at the beginning of fluoride administration) were used. We adopted two animal-housing protocols: (1) the age-matched animals were given 0ppm (control) or 50ppm fluoride as NaF in deionized water for various periods ranging from 2 to 16 weeks, and (2) the animals were housed for 10 weeks under fluoride regimens of 0 (control), 10, 30, 50, 70 or 90ppm. At the end of fluoride administration, the animals were sacrificed and then the diaphysial cortical bones of the femora and tibia were harvested. All bone samples were pulverized and deproteinated by low-temperature ashing prior to use in solubility measure-ments. The solubility of bone crystals was determined through a series of selid/solution equilibration at 25°C under 1.8% CO2/N2 gas environment. The results obtained showed that bone mineral composition was highly sensitive to the ingested fluoride, increasing the fluoridation degree of bone crystals up to a plateau around 1 wt%, i. e., one third of the theoretical content for fluorapatite. From the solubility data of bone samples collected according to both animal-housing protocols, it was proved that bone crystal solubility improved most substantially during the initial 6 weeks of fluoride administration and in the concentration range lower than 30-ppm fluoride in the drinking water. Further improvement of the solubility was only modest in magnitude (as indicated by changes in solubility product) even after fluoride ingestion over longer administration periods or at concentrations of 50-90ppm fluoride.
{"title":"Effects of Long-term Fluoride Administration on the Composition and Solubility of Rat Cortical Bone","authors":"Kaori Sato, H. Yagishita, Y. Kanri, Y. Taya, Y. Soeno, Rika Enari, T. Aoba","doi":"10.2330/JORALBIOSCI1965.45.151","DOIUrl":"https://doi.org/10.2330/JORALBIOSCI1965.45.151","url":null,"abstract":"In the present study, we aimed to investigate changes in the mineral composition and solubility of rat bone under various regimens of fluoride administration in drinking water. Sprague-Dawley rats (male, 4-week-old at the beginning of fluoride administration) were used. We adopted two animal-housing protocols: (1) the age-matched animals were given 0ppm (control) or 50ppm fluoride as NaF in deionized water for various periods ranging from 2 to 16 weeks, and (2) the animals were housed for 10 weeks under fluoride regimens of 0 (control), 10, 30, 50, 70 or 90ppm. At the end of fluoride administration, the animals were sacrificed and then the diaphysial cortical bones of the femora and tibia were harvested. All bone samples were pulverized and deproteinated by low-temperature ashing prior to use in solubility measure-ments. The solubility of bone crystals was determined through a series of selid/solution equilibration at 25°C under 1.8% CO2/N2 gas environment. The results obtained showed that bone mineral composition was highly sensitive to the ingested fluoride, increasing the fluoridation degree of bone crystals up to a plateau around 1 wt%, i. e., one third of the theoretical content for fluorapatite. From the solubility data of bone samples collected according to both animal-housing protocols, it was proved that bone crystal solubility improved most substantially during the initial 6 weeks of fluoride administration and in the concentration range lower than 30-ppm fluoride in the drinking water. Further improvement of the solubility was only modest in magnitude (as indicated by changes in solubility product) even after fluoride ingestion over longer administration periods or at concentrations of 50-90ppm fluoride.","PeriodicalId":14631,"journal":{"name":"Japanese Journal of Oral Biology","volume":"C-19 1","pages":"151-160"},"PeriodicalIF":0.0,"publicationDate":"2003-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85054317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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