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Biomedical subjects

Satoshi Ogawa

Publications and source records attributed to Satoshi Ogawa.

At least 37 records · Page 2Linked to original sources
PubMed2006

Japanese randomized trial for investigation of a combined therapy of amiodarone and implantable cardioverter defibrillator in patients with ventricular tachycardia and fibrillation: the Nippon ICD Plus Pharmachologic Option Necessity study design.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) are the most effective therapy in reducing the mortality of patients with life-threatening ventricular tachyarrhythmias. However, the ICD cannot prevent the recurrence of tachycarida attacks and that limits the clinical usefulness of them. The Nippon ICD Plus Pharmachologic Option Necessity (NIPPON) trial was designed as the first prospective randomized study to test the hypothesis whether amiodarone could improve the patient's clinical outcome by reducing the amount of ICD therapy in the Japanese patient population. METHODS AND RESULTS: Approximately 400 patients with organic heart disease and spontaneous episode(s) of sustained ventricular tachycardia/fibrillation (VT/VF) will be randomly assigned to one of 2 groups; the amiodarone group and non-amiodarone group. Both groups of patients will be followed at least for 24 months. The end-point committee will adjudicate events in a blinded fashion. The primary end-points of this study are determination of the appropriate therapy from the ICD and alteration of the assigned treatment because of its harmful effects and/or frequent ICD therapies. CONCLUSION: The NIPPON study is expected to confirm our understanding of the prognostic and therapeutic usefulness of adjuvant amiodarone therapy for patients with an ICD and with a history of sustained VT/VF.

Amiodarone↗
PubMed2006

Expression analysis of alternative oxidase gene (aox1) with enhanced green fluorescent protein as marker in citric acid-producing Aspergillus niger.

In a citric acid-producing filamentous fungus Aspergillus niger WU-2223L, a cyanide- and antimycin A-insensitive and salicylhydroxamic acid-sensitive respiratory pathway functions in the mitochondria besides the cytochrome pathway and is catalyzed by alternative oxidase (AOX). We constructed an A. niger transformant strain AOXEGFP-1 expressing a fusion gene, aox1-egfp, encoding AOX and enhanced green fluorescent protein (EGFP) to visually analyze the expression levels of aox1 without disruption of mycelia. In strain AOXEGFP-1, the localization of the fusion protein AOX-EGFP in the mitochondria was clearly confirmed because the sites of the green fluorescence by AOX-EGFP were in agreement with those of the red fluorescence of the mitochondria stained with MitoTracker Red CMXRos. When strain AOXEGFP-1 was cultivated with antimycin A, which inhibits the cytochrome pathway at the level of cytochrome bc(1) to cytochrome c and increases the expression level of aox1, EGFP fluorescence intensity increased with an increase in AOX activity measured as duroquinol oxidase activity. Moreover, EGFP fluorescence was detected in strain AOXEGFP-1 regardless of the glucose concentration in the cultivation media: for example, when cultivations were performed with 10, 30, 60 and 120 g/l glucose, EGFP fluorescence was usually detected in the mitochondria. These results indicate that aox1 was constitutively expressed regardless of the glucose concentration in A. niger.

Aspergillus niger↗
PubMed2006

Production of low-estrogen goldfish diet for in vivo endocrine disrupter test.

A low-estrogenic diet for goldfish Carassius auatus was produced for an in vivo estrogen activity test, because commercial fish feed has estrogenic activity and may affect the results of estrogen assays. The newly produced diet (FD5) was formulated with defatted rice bran and casein, and did not contain any soybean meal or fish meal. Phytoestrogen contents (genistein, daidzein, equol, and coumestrol) of FD5 were measured by liquid chromatography-mass spectroscopy/mass spectroscopy (LC-MS/MS) and compared with those of the commercial trout diet (TD) and carp diet (CD). The genistein, daidzein, and coumestrol contents of TD and CD were much higher (5-2000 times) than those of FD5, but equol was detected only in FD5. Estrogenic activity of the fish diets was estimated in vitro by the yeast estrogen-screen assay (YES assay). The estrogenic activity was detected in TD and CD, but not in FD5. The in vivo estrogenic activity of the diets was examined by determining the production of vitellogenin in male goldfish. When male goldfish were fed TD or CD, plasma vitellogenin levels increased, but fish that were fed FD5 maintained low vitellogenin levels. These results indicate that FD5 produced in the present study has a low estrogenic activity, and FD5 would be suitable for the in vivo estrogen activity test using goldfish.

Animals↗
PubMed2005

Low-dose aspirin for prevention of stroke in low-risk patients with atrial fibrillation: Japan Atrial Fibrillation Stroke Trial.

BACKGROUND AND PURPOSE: Although the efficacy of anticoagulant therapy for primary prevention of stroke in patients with nonvalvular atrial fibrillation (NVAF) has been established, efficacy of antiplatelet therapy for low-risk patients is disputable in Japanese patients because of the frequent hemorrhagic complications. We examined the efficacy and safety of aspirin therapy in Japanese patients with NVAF in a prospective randomized multicenter trial. METHODS: Patients with NVAF were randomized to an aspirin group (aspirin at 150 to 200 mg per day) or a control group without antiplatelet or anticoagulant therapy. Primary end points included cardiovascular death, symptomatic brain infarction, or transient ischemic attack. RESULTS: A total of 426 patients were randomized to aspirin group and 445 to no treatment. The trial was stopped earlier because there were 27 primary end point events (3.1% per year; 95% CI, 2.1% to 4.6% per year) in the aspirin group versus 23 (2.4% per year; 95% CI, 1.5% to 3.5% per year) in the control group, suggesting a low possibility of superiority of the aspirin treatment for prevention of the primary end point. In addition, treatment with aspirin caused a marginally increased risk of major bleeding (7 patients; 1.6%) compared with the control group (2 patients; 0.4%; Fisher exact test P=0.101). CONCLUSIONS: For prevention of stroke in patients with NVAF, aspirin at 150 to 200 mg per day does not seem to be either effective or safe. Further prospective studies are needed to determine the best preventive therapy for cerebrovascular events in Japanese patients with NVAF.

Aged↗
PubMed2005

Aging adversely affects postinfarction inflammatory response and early left ventricular remodeling after reperfused acute anterior myocardial infarction.

BACKGROUND AND AIMS: We have demonstrated that an increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of left ventricular (LV) remodeling. We sought to clarify the effect of aging on the postinfarction inflammatory response and LV remodeling. METHODS: We studied 102 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Serum CRP levels, plasma neurohormones and interleukin-6 (IL-6) levels, and LV volume by left ventriculography were serially measured. Patients were divided into two groups according to their age (>or=70 years, n=33; <70 years, n=69). RESULTS: There was no difference in use of cardiovascular drugs and coronary angiographic findings. Older patients had a greater increase in LV end-diastolic volume during 2 weeks after AMI (p=0.0007) and a higher peak CRP level (12.4+/-7.3 vs. 5.5+/-4.2 mg/dl, p<0.0001), although peak CK level was comparable between the two groups. Plasma atrial natriuretic peptide, brain natriuretic peptide and IL-6 levels were higher in older patients at 2 weeks and 6 months after AMI. CONCLUSIONS: Augmented and prolonged activation of the inflammatory system after AMI was observed in older patients, in association with exaggerated LV remodeling. Aging may adversely affect LV remodeling through modification of the inflammatory response after AMI.

Aged↗
PubMed2005

A long-acting prostacyclin agonist with thromboxane inhibitory activity for pulmonary hypertension.

RATIONALE: The balance between prostacyclin and thromboxane plays an important role in the regulation of pulmonary vascular tone. Recently, we developed ONO-1301, a novel, long-acting prostacyclin agonist with thromboxane synthase inhibitory activity. OBJECTIVES: We investigated whether modulation of prostacyclin/thromboxane balance by ONO-1301 ameliorates monocrotaline-induced pulmonary hypertension in rats. METHODS: After subcutaneous injection of monocrotaline or vehicle, rats were randomized to receive repeated subcutaneous administration of ONO-1301 or vehicle twice per day for 3 wk. MEASUREMENTS AND MAIN RESULTS: There was significant development of pulmonary hypertension 3 wk after monocrotaline injection. Treatment with ONO-1301 significantly attenuated the increases in right ventricular systolic pressure and ratio of right ventricular weight to body weight in monocrotaline rats. Furthermore, ONO-1301 significantly attenuated the increase in medial wall thickness of peripheral pulmonary arteries in monocrotaline rats. The half-life of plasma ONO-1301 concentration after a single subcutaneous administration was approximately 5.6 h. A single administration of ONO-1301 increased plasma cyclic adenosine 3', 5'-monophosphate level, which lasted at least up to 8 h. Treatment with ONO-1301 significantly decreased plasma 11-dehydro-thromboxane B2, a metabolite of thromboxane, in monocrotaline rats. Finally, Kaplan-Meier survival curves demonstrated that repeated administration of ONO-1301 improved survival rate in monocrotaline rats compared with vehicle administration (80 vs. 30% in 6-wk survival). CONCLUSIONS: Subcutaneous administration of a novel prostacyclin agonist (ONO-1301) markedly attenuated monocrotaline-induced pulmonary hypertension and improved survival in rats. The beneficial effects of ONO-1301 may occur through its long-lasting stimulation of cyclic adenosine 3', 5'-monophosphate and inhibition of thromboxane synthase.

Animals↗
PubMed2005

Cardiac neural crest cells contribute to the dormant multipotent stem cell in the mammalian heart.

Arodent cardiac side population cell fraction formed clonal spheroids in serum-free medium, which expressed nestin, Musashi-1, and multi-drug resistance transporter gene 1, markers of undifferentiated neural precursor cells. These markers were lost following differentiation, and were replaced by the expression of neuron-, glial-, smooth muscle cell-, or cardiomyocyte-specific proteins. Cardiosphere-derived cells transplanted into chick embryos migrated to the truncus arteriosus and cardiac outflow tract and contributed to dorsal root ganglia, spinal nerves, and aortic smooth muscle cells. Lineage studies using double transgenic mice encoding protein 0-Cre/Floxed-EGFP revealed undifferentiated and differentiated neural crest-derived cells in the fetal myocardium. Undifferentiated cells expressed GATA-binding protein 4 and nestin, but not actinin, whereas the differentiated cells were identified as cardiomyocytes. These results suggest that cardiac neural crest-derived cells migrate into the heart, remain there as dormant multipotent stem cells-and under the right conditions-differentiate into cardiomyocytes and typical neural crest-derived cells, including neurons, glia, and smooth muscle.

Animals↗
PubMed2005

Analysis of the electrophysiological properties and arrhythmias in directly contacted skeletal and cardiac muscle cell sheets.

OBJECTIVE: Autologous skeletal muscle cell (SM) transplantation into the in vivo heart sometimes induces serious arrhythmias. The purpose of this study was to investigate the electrophysiology of cardiomyocyte (CM) and SM in direct contact and to study the mechanism underlying the cause of arrhythmia using the recently developed cell sheet engineering technique. METHODS: Primary cultured rat neonatal SM and CM were prepared, and cell sheets were fabricated using temperature-responsive culture dishes. The action potential was recorded by a conventional microelectrode. Intracellular calcium concentration and optical mapping image of the action potential were recorded using Fluo-3 and di-4-ANEPPS, respectively. A video motion-detecting system was used for the detection of arrhythmias. RESULTS: SM myotubes occasionally displayed automaticity. SM sheets did not display synchronized contraction, but instead groups of myotubes contracted independently. The action potential of SM, induced by artificial pacing, did not expand to the entire sheet but was limited within a restricted, small area around the electrode, and it was unfeasible to generate an electrical connection or propagate an action potential between CM and SM sheets. SM sheets, in which some of the myotubes displayed automaticity, caused fibrillation-like contraction in the co-cultured CM sheets, and this arrhythmia was specifically blocked by the stretch-activated channel blocker GsMTx-4. CONCLUSIONS: These findings show that SM sheets do not contract synchronously or generate functional syncytia with the surrounding CM sheets and that stretch-induced arrhythmias due to spontaneous contraction of SM may occur in the CM sheet.

Action Potentials↗
PubMed2005

Syntheses and properties of emissive iridium(III) complexes with tridentate benzimidazole derivatives.

A series of novel emissive Ir(III) complexes having the coordination environments of [Ir(N--N--N)2]3+, [Ir(N--N--N)(N--N)Cl]2+, and [Ir(N--N--N)(N--C--N)]2+ with 2,6-bis(1-methyl-benzimidazol-2-yl)pyridine (L1, N--N--N), 1,3-bis(1-methyl-benzimidazol-2-yl)benzene (L2H, N--C--N), 4'-(4-methylphenyl)-2,2':6',2' '-terpyridine (ttpy, N--N--N), and 2,2'-bipyridine (bpy, N--N) have been synthesized and their photophysical and electrochemical properties studied. The Ir(III) complexes exhibited phosphorescent emissions in the 500-600 nm region, with lifetimes ranging from approximately 1-10 micros at 295 K. Analysis of the 0-0 energies and the redox potentials indicated that the lowest excited state of [Ir(L1)(L2)]2+ possessed the highest contribution of 3MLCT (MLCT = metal-to-ligand charge transfer) among the Ir(III) complexes, reflecting the sigma-donating ability of the tridentate ligand, ttpy < L1 < L2. The emission quantum yields (phi) of the Ir(III) complexes ranged from 0.037 to 0.19, and the highest phi value (0.19) was obtained for [Ir(L1)(bpy)Cl]2+. Radiative rate constants (k(r)) were 1.2 x 10(4) s(-1) for [Ir(ttpy)2]3+, 3.7 x 10(4) s(-1) for [Ir(L1)(bpy)Cl]2+, 3.8 x 10(4) s(-1) for [Ir(ttpy)(bpy)Cl]2+, 3.9 x 10(4) s(-1) for [Ir(L1)2]3+, and 6.6 x 10(4) s(-1) for [Ir(L1)(L2)]2+. The highest radiative rate for [Ir(L1)(L2)]2+ with the highest contribution of 3MLCT could be explained in terms of the singlet-triplet mixing induced by spin-orbit coupling of 5d electrons in the MLCT electronic configurations.

Journal Article↗
PubMed2005

Serum C-reactive protein elevation predicts poor clinical outcome in patients with distal type acute aortic dissection: association with the occurrence of oxygenation impairment.

BACKGROUND: Acute aortic dissection (AAD) is sometimes complicated by respiratory failure due to severe lung oxygenation impairment. Systemic activation of inflammatory system after aortic injury may play some roles in the development of this complication. The aim of this study was to determine the significance of serum C-reactive protein (CRP) elevation in the development of oxygenation impairment and clinical outcome with distal type AAD. METHODS AND RESULTS: A total of 61 patients, who were admitted with distal type AAD within 24 h from the onset, were examined. Serum CRP levels, white blood cell (WBC) counts and body temperature were measured serially for at least 4 days. Oxygenation impairment, defined as the lowest PaO2/FIO2 ratio < or = 200 mmHg, was noted in 31 patients (51%). In patients with oxygenation impairment, peak CRP levels (20.7+/-7.9 vs. 12.7+/-3.8 mg/dl, P < 0.001), peak WBC counts (14,600+/-3600 vs. 11,800+/-4300/mm3, P = 0.008) and body temperature (38.4+/-0.5 vs. 38.0+/-0.6 degrees C, P = 0.004) were significantly higher than those without. Peak CRP level was inversely correlated with the lowest PaO2/FIO2 (P < 0.001). Patients who underwent urgent surgical treatment and/or died in the hospital had higher peak CRP levels (25.1+/-12.3 vs. 16.1+/-7.4 mg/dl, P = 0.010) than those who did not. Multivariate analysis revealed that a peak CRP level > or = 15 mg/dl (relative risk = 12.6, P < 0.001) was an independent determinant of the development of oxygenation impairment. CONCLUSION: The greater serum CRP elevation after distal type AAD was associated with a higher incidence of oxygenation impairment and poor clinical outcome. Systemic activation of the inflammatory system after aortic injury may play an important role in the development of oxygenation impairment.

Acute Disease↗
PubMed2005

Localization of the three GnRH types and GnRH receptors in the brain of a cichlid fish: Insights into their neuroendocrine and neuromodulator functions.

The cognate receptor for any of the known gonadotropin-releasing hormones (GnRHs) has not been directly demonstrated. In order to establish this and shed light on the functions of GnRH types, we analyzed the neuroanatomical location and time of initial expression of three distinct GnRH receptors (GnRH-Rs) and the three endogenous GnRHs in the brain of developing and sexually mature tilapia Oreochromis niloticus using immunocytochemistry. In all age groups, including males and females, GnRH-RIA was seen specifically in gonadotropes (Parhar et al. [2002] J Neuroendocrinol 14:657-665) but was undetectable in the brain. On day 8 after fertilization, GnRH-RIB was first seen in the periventricular hypothalamus (lateral recess nucleus, posterior recess nucleus, posterior tuberal nucleus) and GnRH-RIII in the olfactory epithelium, olfactory bulb, telencephalon, preoptic region, mediobasal hypothalamus, thalamus, mesencephalon, and in the hindbrain. Double-label immunocytochemistry showed GnRH1 (Ser(8) GnRH)-immunoreactive neuronal processes projecting mainly to the proximal pars distalis of the pituitary, while GnRH2 (His(5), Trp(7), Tyr(8) GnRH) and GnRH3 (Trp(7), Leu(8) GnRH) fibers were observed in close association with cells containing GnRH-RIB and GnRH-RIII in the brain. These results suggest that GnRH-RIA might be hypophysiotropic in nature, whereas GnRH-RIB and GnRH-RIII could have additional neuromodulatory functions. Further, evidence of close proximity of GnRH-R-containing cells and neuronal processes of multiple GnRH types suggests complex cross-talk between several GnRH ligands and GnRH-Rs.

Animals↗
PubMed2005

Transient inhibition of BMP signaling by Noggin induces cardiomyocyte differentiation of mouse embryonic stem cells.

Embryonic stem (ES) cells are a promising source of cardiomyocytes, but clinical application of ES cells has been hindered by the lack of reliable selective differentiation methods. Differentiation into any lineage is partly dependent on the regulatory mechanisms of normal early development. Although several signals, including bone morphogenetic protein (BMP), Wnt and FGF, are involved in heart development, scarce evidence is available about the exact signals that mediate cardiomyocyte differentiation. While investigating the involvement of BMP signaling in early heart formation in the mouse, we found that the BMP antagonist Noggin is transiently but strongly expressed in the heart-forming region during gastrulation and acts at the level of induction of mesendoderm to establish conditions conducive to cardiogenesis. We applied this finding to develop an effective protocol for obtaining cardiomyocytes from mouse ES cells by inhibition of BMP signaling.

Animals↗
PubMed2005

Persistent cardiac aldosterone synthesis in angiotensin II type 1A receptor-knockout mice after myocardial infarction.

BACKGROUND: The renin-angiotensin-aldosterone system is implicated in the pathogenesis of heart failure. Pharmacological blockade of angiotensin II (Ang II)-dependent signaling is clinically effective in reducing cardiovascular events after myocardial infarction (MI) but still fails to completely prevent remodeling. The molecular basis underlying this Ang II-independent remodeling is unclear. METHODS AND RESULTS: Acute MI was induced by coronary ligation in wild-type (WT) and angiotensin II type IA receptor-knockout (AT1A-KO) mice. Left ventricular (LV) geometry, hemodynamics, and cardiac gene expression were evaluated on day 28. Severe LV remodeling and resultant cardiac dysfunction were observed in WT mice, whereas less marked, but still significant, LV remodeling and cardiac dysfunction were induced in AT1A-KO mice. Gene expression levels of aldosterone synthase and the cardiac aldosterone content were both elevated in the MI hearts, even in AT1A-KO mice. In AT1A-KO mice treated with spironolactone (20 mg/kg per day), LV remodeling, cardiac dysfunction, and cardiac gene expression of collagens and natriuretic peptides were almost normalized. CONCLUSIONS: Our results indicate that genetic blockade of AT1A signaling fails to arrest aldosterone production in cardiac tissues and that cardiac aldosterone plays a critical role in post-MI LV remodeling. The results suggest that spironolactone could be potentially effective in patients with MI, when used in combination with renin-angiotensin system blockade, by blocking the actions of aldosterone produced by Ang II-independent mechanisms.

Aldosterone↗
PubMed2005

Nonmammalian gonadotropin-releasing hormone molecules in the brain of promoter transgenic rats.

Mammalian gonadotropin-releasing hormone (GnRH1) and nonmammalian immunoreactive GnRH subtypes were examined in transgenic rats carrying an enhanced GFP (EGFP) reporter gene driven by a rat GnRH1 promoter. Double-label immunocytochemistry was performed on EGFP(+)/GnRH1 brain sections by using antisera against GnRH1, GnRH2 (chicken II), GnRH3 (salmon), or seabream GnRH. EGFP(+)/GnRH1 neurons were in the septal-preoptic hypothalamus but not in the midbrain, consistent with GnRH1-immunopositive neurons in WT rats. Apparent coexpression of EGFP(+)/GnRH1 with other GnRH subtypes was observed. All EGFP(+) neurons in the septal-preoptic hypothalamus were GnRH1-immunopositive. However, only approximately 80% of GnRH1-immunopositive neurons were EGFP(+), which awaits further elucidation. GnRH subtypes-immunopositive fibers and EGFP(+)/GnRH1 fibers were conspicuous in the organum vasculosum of the lamina terminalis, median eminence, and surrounding the ependymal walls of the third ventricle and the aqueduct in the midbrain. These results demonstrate that the expression of the EGFP-GnRH1 transgene is restricted to the bona fide GnRH1 population and provide clear morphological evidence supporting the existence of GnRH1 neuronal subpopulations in the septal-preoptic hypothalamus, which might be driven by different segments of the GnRH promoter. This genetic construct permits analyses of promoter usage in GnRH neurons, and our histochemical approaches open questions about functional relations among isoforms of this peptide, which regulates reproductive physiology in its behavioral and endocrine aspects.

Animals↗
PubMed2005

Granulocyte colony-stimulating factor attenuates early ventricular expansion after experimental myocardial infarction.

OBJECTIVE: In the early phase after transmural myocardial infarction (MI), the infarcted myocardium undergoes replacement by scar tissue, which is essential for preserving the structural integrity of the infarcted tissue. Transforming growth factor (TGF)-beta1, which is known as a fibrotic cytokine, plays a pivotal role in the reparative fibrosis after MI. It is reported that granulocyte colony-stimulating factor (G-CSF) can accelerate wound healing. The aim of our study was to investigate the effect of G-CSF on early ventricular expansion after MI. METHODS: MI was induced by ligation of the left coronary artery in male Wistar rats. G-CSF (20 microg/kg/day, MI-GCSF) or saline (MI-saline) was injected subcutaneously 3 h after MI and every 24 h thereafter for 7 days. Hemodynamic and echocardiographic studies were performed at 14 days. Expression of TGF-beta1 and procollagen type I and type III mRNA in both the infarcted and noninfarcted areas was studied by quantitative RT-PCR at 1, 3, 7, and 14 days after MI. Histological studies were performed at 7 days. RESULTS: MI-GCSF had higher LV max dP/dt, lower LV end-diastolic pressure, and smaller LV end-diastolic and end-systolic dimensions compared to MI-saline. Infarct size was not different between MI-GCSF and MI-saline. Expression of TGF-beta1 mRNA in the infarcted area at 3 days was significantly higher in MI-GCSF than in MI-saline. Expression of procollagen type I and type III mRNA in the infarcted area at 3 days was higher in MI-GCSF compared to MI-saline, and the peak mRNA levels were earlier in MI-GCSF. In the noninfarcted area, there was no difference in TGF-beta1 mRNA expression between MI-GCSF and MI-saline. Histologically, collagen accumulation in the infarcted area at 7 days was more prominent in MI-GCSF than in MI-saline. CONCLUSION: G-CSF treatment improves early post-infarct ventricular expansion through promotion of reparative collagen synthesis in the infarcted area, suggesting some beneficial effect of G-CSF on the infarct healing process.

Animals↗
PubMed2005

Three GnRH receptor types in laser-captured single cells of the cichlid pituitary display cellular and functional heterogeneity.

The role of multiple gonadotropin-releasing hormone receptor (GnRH-R) types in the regulation of gonadotropic and nongonadotropic cells remains speculative. To address this issue, we developed a technology integrating laser-captured microdissection of single digoxigenin-labeled pituitary cells coupled with real-time quantitative PCR to examine the expression profiles of three endogenous GnRH-R types (R1, R2, and R3) in immature and mature males of tilapia Oreochromis niloticus. Here, in addition to gonadotropes (luteinizing and folicle-stimulating hormone, FSH), we show GnRH-Rs are also present in lactotropes, somatotropes, thyrotropes, melanotropes (melanocyte-stimulating hormone, MSH), corticotropes and somatolactin cells. Subpopulations of pituitary cells express single (42.9%), multiple (32.4%) or lack (24.7%) GnRH-Rs. In immature males, the percentage of FSH cells containing combinations of GnRH-Rs was significantly higher (R1+R2: 24%, P <0.05; R1+R2+R3: 25%, P <0.01) than in mature males, whereas the percentage showing only R1 and R1 and R3 transcripts (P <0.05) was higher in mature males. Significantly greater copies of R1 and R3 transcripts were found in MSH cells of immature and mature males, respectively (P <0.05). GnRH-R transcripts in other pituitary cells (lactotropes, R1 and R2; somatolactin cells/thyrotropes/corticotropes, R1, R2, and R3) were significantly higher in mature males (P <0.05) but were unaltered in somatotropes and luteinizing hormone cells. Thus, FSH and MSH cells are required for both reproductive states, whereas other pituitary cells are recruited only during testicular maturation. The differential expression of GnRH-Rs in gonadotropic and nongonadotropic cells demonstrates cellular and functional heterogeneity of mechanisms controlling normal sexual development.

Animals↗
PubMed2005

The olfactory organ modulates gonadotropin-releasing hormone types and nest-building behavior in the tilapia Oreochromis niloticus.

Direct olfactory inputs to any of the known gonadotropin-releasing hormone (GnRH) containing neurons have not been demonstrated. Therefore, the rationale of this study was to examine whether olfactory inputs might in some way interact with the GnRH system(s) to synchronize reproductive behaviors. In order to establish this, we used anosmic mature male tilapia to investigate changes in reproductive behaviors, gonadal morphology, and GnRH1, GnRH2, and GnRH3 cellular morphology and change in GnRH mRNA levels by real-time polymerase chain reaction. Bilateral removal of the olfactory rosettes followed by occlusion of the nasal cavity (ORX) inhibited nest-building behavior, but had no effect on aggressive and sexual behaviors or gonadal morphology. ORX failed to alter the morphological features of GnRH1, GnRH2, and GnRH3 (cell number, size, GnRH optical density), but significantly decreased copies of GnRH1 and GnRH2 mRNAs. GnRH immunoreactive fibers were not evident in the olfactory nerve and rosettes. DiI application to the olfactory nerve labeled inputs primarily to the glomerular layer of the olfactory bulbs and extrabulbar inputs to the forebrain but not to GnRH neurons. These results provide evidence that the olfactory rosette is crucial for modulating nest-building behavior through second-order olfactory pathways interacting with GnRH1 and GnRH2 neuronal systems.

Aggression↗