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1.
林信伟  林浩然  张庆 《水产学报》1993,17(4):281-288
采用离体灌流孵育和腹腔注射方法,研究鲑鱼促性腺激素释放激素(GnRH)类似物 sGnRH-A(Arg~6Trp~?Leu~3Pro~?NEt-LHRH)和哺乳类GnRH类似物LHRH-A(Ala~5Pro~?-NEt-LHRH)对鲤鱼脑垂体生长激素(GH)分泌的直接刺激作用以及对草鱼鱼种 GH 分流和生长的促进作用。2分钟脉冲式 sGnRH-A 和 LHRH-A 以剂量依存形式直接刺激离体灌流孵育的鲤鱼脑垂体 GH分泌,且 sGnRH-A 刺激GH 分泌活性显著高于 LHRH-A。腹腔注射两种剂量(0.01μg/g 体重/周和0.001μg/g 体重/周)的 sGnRH-A 或LHRH-A(每周一次,共 6周)都能显著提高草鱼鱼种相对体重和相对体长生长率,并促进草鱼鱼种血清 GH 水平提高。sGnRH-A 和 LHRH-A 促进生长的作用是剂量依存的,且sGnRH-A的促进生长作用显著高于 LHRH-A。  相似文献   

2.
为了探讨在古老的软骨硬鳞鱼中促性腺激素(GtH)的双重内分泌调节作用,本实验设计用离体灌流的方法研究促黄体素释放激素类似物(LHRH-A)和多巴胺(DA)对施氏鲟脑垂体碎片分泌GtH的影响。引入10、100和1 000 nmol/L 3个浓度的LHRH-A对施氏鲟脑垂体碎片3次脉冲式刺激实验;每次间隔1 h,持续5 min,研究不同剂量LHRH-A对鲟鱼脑垂体释放GtH的作用;用200 nmol/L DA对施氏鲟脑垂体碎片持续2 h灌流后引入5 min的1 000nmol/L LHRH-A刺激实验,研究DA如何抑制鲟鱼脑垂体释放GtH。每5 min收集一管灌流液,用放射免疫测定法(RIA)检测灌流液中GtH的含量。结果显示,低剂量LHRH-A随着刺激引入脑垂体释放GtH出现波浪式的增加,中、高剂量出现释放延后现象。LHRH-A在10nmol/L到1 000 nmol/L范围内对刺激脑垂体释放GtH没有剂量依存关系。DA对施氏鲟脑垂体碎片GtH的分泌没有显著影响,但是可以抑制LHRH-A引起的GtH分泌,即DA不能抑制施氏鲟GtH的基础分泌,而只能抑制LHRH-A诱导的GtH分泌。研究结果证明,在高等硬骨鱼类中存在的双重神经内分泌调节在古老的鲟鱼中也存在。  相似文献   

3.
《中国水产科学》2005,12(2):113-118
性类固醇激素对性腺发育期间的鱼类促性腺激素(GTH)分泌有负反馈作用,而对性未成熟的鱼类GTH分泌有正反馈作用.本实验选取性腺发育中期的长臀(鱼危)(Cranoglanis bouderius)进行研究,将实验用鱼分成4组(实验重复3次,每组共用6尾鱼,)①持续性17β-雌二醇(17β-Estradiol,E2)处理;②E2在注入促性腺激素释放激素类似物(Analogue of gonadotropin-releasing hormone,GnRH-A)脉冲刺激的处理;③持续性甲基睾酮(17α-methyltestosterone,MT)处理;④MT在注入GnRH-A脉冲刺激的处理;采用离体灌流孵育和GTH放射免疫测定的方法研究E2和MT对长臀(鱼危)脑垂体GTH分泌的影响.持续性的E2(1μmol/L)处理能显著性地抑制长臀(鱼危)脑垂体碎片基础GTH的分泌,而持续性的MT(1μmmol/L)处理能抑制长臀(鱼危)3脑垂体碎片基础GTH的分泌,同时E2和MT处理能抑制GnRH-A刺激的GTH分泌,而高浓度的E2和MT处理(10μmol/L)要比低浓度的E2和MT处理(0.1μmol/L)对长臀(鱼危)脑垂体碎片基础GTH释放抑制能力强.这些结果表明,在离体实验中,E2和MT对性腺发育中期的长臀(鱼危)脑垂体的GTH的分泌具有负反馈的作用,并且可能直接参与了长臀(鱼危)脑垂体的GTH调节.  相似文献   

4.
李林明 《河北渔业》2020,(1):1-3,53
应用组织切片和免疫组织化学的方法在中国鲎脑神经中定位了3种离子通道的分布。研究检测到Na~+通道和K~+通道免疫阳性细胞和阳性纤维,但没有检测到Ca~(2+)通道的免疫阳性。Na~+通道主要分布在中间体神经纤维网和背面中央细胞群,K~+通道分布于背面侧后方第二细胞群和背面中央细胞群。  相似文献   

5.
性类固醇激素对性腺发育期间的鱼类促性腺激素(GTH)分泌有负反馈作用,而对性未成熟的鱼类GTH分泌有正反馈作用.本实验选取性腺发育中期的长臀(鱼危)(Cranoglanis bouderius)进行研究,将实验用鱼分成4组(实验重复3次,每组共用6尾鱼,):①持续性17β-雌二醇(17β-Estradiol,E2)处理;②E2在注入促性腺激素释放激素类似物(Analogue of gonadotropin-releasing hormone,GnRH-A)脉冲刺激的处理;③持续性甲基睾酮(17α-methyltestosterone,MT)处理;④MT在注入GnRH-A脉冲刺激的处理;采用离体灌流孵育和GTH放射免疫测定的方法研究E2和MT对长臀(鱼危)脑垂体GTH分泌的影响.持续性的E2(1μmol/L)处理能显著性地抑制长臀(鱼危)脑垂体碎片基础GTH的分泌,而持续性的MT(1μmmol/L)处理能抑制长臀(鱼危)3脑垂体碎片基础GTH的分泌,同时E2和MT处理能抑制GnRH-A刺激的GTH分泌,而高浓度的E2和MT处理(10μmol/L)要比低浓度的E2和MT处理(0.1μmol/L)对长臀(鱼危)脑垂体碎片基础GTH释放抑制能力强.这些结果表明,在离体实验中,E2和MT对性腺发育中期的长臀(鱼危)脑垂体的GTH的分泌具有负反馈的作用,并且可能直接参与了长臀(鱼危)脑垂体的GTH调节.  相似文献   

6.
性类固醇激素对性腺发育期间的鱼类促性腺激素(GTH)分泌有负反馈作用，而对性未成熟的鱼类GTH分泌有正反馈作用。本实验选取性腺发育中期的长臀鮠(Cranoglanis bouderius)进行研究，将实验用鱼分成4组(实验重复3次，每组共用6尾鱼，)：①持续性17β-雌二醇(17β-Estradiol，E2)处理；②E2在注入促性腺激素释放激素类似物(Analogue of gonadotropin—releasing hormone，GnRH-A)脉冲刺激的处理；③持续性甲基睾酮(17α-methyltestosterone，MT)处理；④MT在注入GnRH-A脉冲刺激的处理；采用离体灌流孵育和GTH放射免疫测定的方法研究E2和MT对长臀鮠脑垂体GTH分泌的影响。持续性的E2(1μmol／L)处理能显著性地抑制长臀鮠脑垂体碎片基础GTH的分泌，而持续性的MT(1μmmol／L)处理能抑制长臀鮠脑垂体碎片基础GTH的分泌，同时E2和MT处理能抑制GnRH-A刺激的GTH分泌，而高浓度的E2和MT处理(10μmol／L)要比低浓度的E2和MT处理(0．1μmol／L)对长臀鮠脑垂体碎片基础GTH释放抑制能力强。这些结果表明，在离体实验中，E2和MT对性腺发育中期的长臀鮠脑垂体的GTH的分泌具有负反馈的作用，并且可能直接参与了长臀鮠脑垂体的GTH调节。  相似文献   

7.
将体质量(6.77±0.51) g凡纳滨对虾饲养在200 L玻璃纤维桶中,每桶50尾,设置2个温度(恒温30℃和1 h内由30℃急升至33℃),每个温度设置以氯化铵溶液调节的4个氨氮质量浓度(0、5、15、25 mg/L),共8个试验组,每组3个平行。胁迫72 h时测定鳃中Na~+/K~+-ATP酶与Ca~(2+)-ATP酶活性以及肌肉和鳃中游离氨基酸含量,分析高温与氨氮复合胁迫对凡纳滨对虾渗透压生理调节的影响。试验结果显示:(1)同一温度下,30℃时,25 mg/L氨氮组的Na~+/K~+-ATP酶活性和5 mg/L氨氮组的Ca~(2+)-ATP酶活性均显著升高,而33℃时,3个氨氮胁迫组Na~+/K~+-ATP酶和Ca~(2+)-ATP酶活性均显著升高(P0.05);(2)同一氨氮质量浓度下,30℃和33℃试验组的Na~+/K~+-ATP酶和Ca~(2+)-ATP酶活性均差异显著,且25 mg/L氨氮质量浓度下33℃试验组酶活性显著低于30℃试验组(P0.05);(3)氨氮质量浓度为15 mg/L和25 mg/L时,33℃试验组鳃和肌肉游离氨基酸总含量均显著高于30℃组(P0.05);(4)30℃和33℃试验组与氨氮胁迫下,肌肉中丙氨酸含量均随氨氮质量浓度升高而显著增加,且33℃试验组显著高于30℃组(P0.05)。试验结果表明,高温与氨氮复合胁迫对凡纳滨对虾Na~+/K~+-ATP酶和Ca~(2+)-ATP酶活性以及游离氨基酸含量影响显著,会造成凡纳滨对虾渗透压生理调节功能紊乱。  相似文献   

8.
为了探讨淡水贝类Ca2+吸收和转运信号传递机理,采用激光共聚焦技术研究了三角帆蚌不同组织细胞在静息状态下细胞内游离Ca2+浓度,以及水体Ca2+浓度对外套膜组织细胞内钙沉积的影响。试验选取10只健康的三角帆蚌,分别获得外套膜外膜、内膜、斧足、腮及内脏团上表皮组织细胞,短期培养后用Fluo-3/AM荧光探针孵育细胞1 h,观察细胞内Ca2+荧光强度。研究结果表明,蚌不同组织细胞内Ca2+荧光强度存在显著差异,外套膜外膜细胞内Ca2+荧光强度最高,内脏团上表皮细胞的最低(P<0.05);育珠三角帆蚌在相同Ca2+浓度的孵育水平下,外套膜细胞内Ca2+荧光强度比非育珠蚌都有增加的趋势,其中在1.25 mmol/L添加组中,两组外套膜内膜细胞内Ca2+荧光强度差异达到显著水平(P<0.05);不同Ca2+孵育水平对细胞内Ca2+荧光强度有显著影响(P<0.05),随着Ca2+在孵育液中浓度的升高,外套膜细胞内Ca2+荧光强度显著增强(P<0.05),表明外套膜是从外界吸收Ca2+的主要组织,蚌体珍珠的培育增强了其对Ca2+的沉积,并且水体Ca2+浓度在1.25～3.00 mmol/L有助于蚌体内Ca2+的贮藏,这对进...  相似文献   

9.
对圆口铜鱼(Coreius guichenoti)精浆离子和氨基酸成分及精液生理特性进行了检测分析。结果显示,圆口铜鱼精液pH值为7.3,呈弱碱性;精液浓度为39.7%,精子密度为5.3×10~9个/mL;精浆离子以Na~+含量88.7 mmol/L最高,其次是K~+,之后为Ca~(2+)、Mg~(2+)、Zn~(2+)、Cu~(2+);精浆水解氨基酸总量为2 872.69μmol/100mL,其中以脯氨酸含量最高,蛋氨酸、酪氨酸和组氨酸含量最低。该结果填补了圆口铜鱼繁殖生物学的相关数据,为圆口铜鱼规模化人工繁育提供了基础资料。  相似文献   

10.
作者采用膜片钳技术之内面向外记录模式观察了河蟹（Eriocheir sinensis）眼柄视神经节端髓X器官（MTXO）神经内分泌细胞对0~1mmol•L－1 ATP的反应,发现河蟹眼柄MTXO细胞表达ATP敏感钾通道（KATP）。电生理特征研究结果表明,在细胞膜内外两侧的Ｋ+浓度均为200mmol•L－1时,KATP呈弱的内向整流性,电导为68pS,有翻转电位。灌流ATP对KATP通道的开放产生浓度依赖性抑制作用,当细胞外液中ATP浓度超过0.1mmol•L－1后,去极化刺激不能诱发KATP电流,并且1mmol•L－1ATP可明显阻断KATP开放活动。胆固醇等甾醇类物质对河蟹眼柄MTXO细胞KATP无明显的影响,但0.1mmol•L－1优降糖可完全阻断KATP的单通道开放。ATP敏感钾通道（KATP）受内源性ATP的调控,在细胞代谢与兴奋性耦联中起重要作用,提示河蟹眼柄MTXO细胞的代谢活动对神经多肽激素的分泌产生了反馈调节作用,胆固醇等甾醇类物质未通过调节KATP的活动调控细胞的分泌活动。本文结果为阐明甲壳动物眼柄神经多肽激素分泌的调控机制奠定了基础。  相似文献   

11.
In this study, the direct actions of serotonin (5HT) on gonadotropin (GTH)-II and growth hormone (GH) release in the goldfish were tested at the pituitary cell level. 5HT (10 nM - 10 µM) stimulated GTH-II but inhibited GH release from perifused goldfish pituitary cells in a dose-dependent manner. The minimal effective dose of 5HT tested to suppress basal GH secretion (10 nM) was 10-fold lower than that to stimulate GTH-II release (100 nM). The GTH-II releasing effect of 5HT was abolished by repeated 5HT treatment (10 µM) whereas the corresponding inhibition on GH release was unaffected. These results suggest that 5HT receptors on goldfish gonadotrophs and somatotrophs exhibit intrinsic differences in terms of sensitivity to stimulation and resistance to desensitization. Salmon GTH-releasing hormone (sGnRH, 100 nM) stimulated GTH-II and GH release from goldfish pituitary cells. The GTH-II releasing action of sGnRH was unaffected by simultaneous treatment of 5HT (1 µM). However, the corresponding GH response to sGnRH (100 nM) was inhibited. In the goldfish, dopamine is known to stimulate GH release through activation of pituitary D1 receptors. In the present study, the GH-releasing action of dopamine (1 µM) and the D1 agonist SKF38393 (1 µM) was significantly reduced by 5HT (1 µM). To examine the receptor specificity of 5HT action, the effects of 5HT1 and 5HT2 analogs on GTH-II and GH release were tested in goldfish pituitary cells. The 5HT1 agonist 8OH DPAT (0.1 and 1µM) and 5HT2 agonist methyl 5HT (0.1 1µM) mimicked the GTH-II releasing effect of 5HT. The 5HT1 agonist 8OH DPAT (0.1 and 1µM) also stimulated GH release but the 5HT2 agonist methyl 5HT (0.1 and 1µM) was inhibitory to basal GH secretion. In addition, 5HT (1µM) -stimulated GTH-II release was abolished by the 5HT1 antagonist methiothepin (10µM) and 5HT2 antagonist mianserin (10µM). Similarly, the inhibitory action of 5HT (1µM) on basal GH release was blocked by the 5HT2 antagonist mianserin (10µM). The 5HT1 antagonist methiothepin (10µM) was not effective in this regard. These results, taken together, indicate that 5HT exerts its regulatory actions on GTH-II and GH release in the goldfish directly at the pituitary cell level, probably through interactions with other regulators including sGnRH and dopamine. The GTH-II releasing action of 5HT is mediated through 5HT2 and possibly 5HT1 receptors. The inhibition of 5HT on basal GH release is mediated through 5HT2 receptors only. Apparently, 5HT1 receptors are not involved in this inhibitory action. In this study, a paradoxical stimulatory component of 5HT on GH release by activating 5HT1 receptors is also implicated.  相似文献   

12.
Studies in mammals have shown that synthetic Met-enkephalin derivatives, called growth hormone-releasing peptides (GHRPs), stimulate growth hormone (GH) release. In the present study, GHRP-6 action on GH secretion was examined in vivo and in vitro in sexually immature grass carp. GHRP-6 injected intraperitoneally had no influences on serum GH levels in juvenile grass carp. Following intraperitonal injection of GHRP-6 and dopamine (DA) or cysteamine hydrochloride (CSH), alone and in combination into juvenile grass carp, DA and CSH were effective in elevating serum GH levels, but GHRP-6 was not effective in this respect; in addition, the synergistic action of GHRP-6 and DA or CSH on GH secretion was not seen. In this work, we had adapted and validated a perifusion system and a culture system for GH regulation studies. In a perifusion system, GHRP-6 (1000 to 0.1 nM), GHRP-6 (0.1 to 1000 nM), GHRP-6 (1 μM), and Hexarelin (an analog of GHRP, 1 μM) had no action on GH release from juvenile grass carp pituitary fragments or cells. Under static incubation conditions, GHRP-6 was inactive on GH release from juvenile grass carp pituitary fragments after 1 h and 6 h incubation, but human growth hormone-releasing hormone (hGHRH; 1 to 100 nM) as positive control could stimulate GH release in a dose-dependent manner. Furthermore, when GHRP-6 (100 nM) in combination static incubation with neuropeptides [e.g., hGHRH (100 nM), salmon gonadotropin-releasing hormone analogue (sGnRH-A) (100 nM), or D-Ala6,Pro9-NEt-luteinizing hormone-releasing hormone (D-Ala6,Pro9-NEt-LHRH, LHRH-A) (100nM)], GHRP-6 did not strengthen GH secretion actions of neuropeptides, and at the same time neuropeptides also did not modify the effects of GHRP-6 on GH secretion. The present results obtained using in vivo and in vitro techniques adapted for GH regulation studies show that GHRP-6 does not function as a GH-releasing factor in juvenile grass carp as it does in tilapia, amphibians, chickens, and mammals.  相似文献   

13.
Profiles of plasma growth hormone (GH) in male tilapia hybrid (Oreochromis niloticus x O. aureus) were measured and compared at different times of the year. The profiles did not appear to be repetitive, however, differences in their nature were observed at the different seasons; the most erratic profiles were seen in the height of the reproductive season (July), while the peaks were more subdued in the spring and disappeared in the autumn. Peaks in male fish were more prominent than in the females when measured in July. Perifused pituitary fragments from fish with a high GSI responded to salmon gonadotropin-releasing hormone (sGnRH) analog (10 nM-1 M), while those from fish with a low GSI barely responded to even the highest dose. Exposure of perifused pituitary fragments from sexually-regressed fish to carp growth hormone-releasing hormone (cGHRH; 0.1 M) or sGnRH (I M) stimulated GH release only after injection of the fish with methyl testosterone (MT; 3 injections of 0.4 mg kg 1). The same MT pretreatment did not alter the response to dopamine (DA; 1 or 10 M). GH pituitary content in MT-treated fish was lower than in control fish, which may be explained by the higher circulating GH levels in these fish, but does not account for the increased response to the releasing hormones. Castration abolished the response of cultured pituitary cells to sGnRH (I fM-100 nM) without altering either their basal rate of secretion or circulating GH levels. Addition of steroids to the culture medium (MT or estradiol at 10 nM for 2 days) enabled a GH response to sGnRH stimulation in cells from sexually regressed fish. Pituitary cells which had not been exposed to steroids failed to respond to sGnRH, although their response to forskolin or TPA was similar to that of steroid-exposed cells. It would appear, therefore, that at least one of the effects of the sex steroids on the response to GnRH is exerted proximally to the formation of cAMP, or PKC, presumably at the level of the receptor. An increase in the number of receptors to the GH-releasing hormones, following steroid exposure, would explain also the changing nature of the GH secretory profile in different stages of the reproductive season.  相似文献   

14.
The effects of thyrotropin-releasing hormone (TRH) on growth hormone (GH) and gonadotropin (GtH) release, and the influences of somatostatin (SRIF), the dopamine agonist apomorphine (APO) and extracellular calcium on basal and TRH-induced GH release were examined using an in vitro perifusion system for pituitary fragments of common carp (Cyprinus carpio). Five minute pulses of different dosages of TRH stimulated a rapid and dose-dependent increase in GH release from the perifused pituitary fragments with an ED50 of 9.7 ± 2.3 nM. TRH was ineffective on GtH release. SRIF significantly inhibited basal and TRH-induced GH release from the perifused pituitary fragments, and the effects of SRIF were dose-dependent. APO induced a dose-dependent increase in basal and TRH-stimulated GH release from the perifused pituitary fragments. Increasing the concentrations of extracellular calcium from 0 mM to 1.25 mM resulted in an increase in basal and TRH-induced GH release. The high dose of calcium (6.25 mM) caused a slight decrease in basal and TRH-induced GH release compared with those at a concentration of 1.25 mM.
Résumé Les effets de la thyrotropine (TRH) sur la sécrétion d'hormone de croissance (GH) et de gonadotropine (GTH), et de la somatostatine (SRIF), de l'apomorphine (APO), antagoniste dopaminergique, et du calcium extracellulaire sur les sécrétions basale et stimulée de GH ont été étudiées in vitro par périfusion, de fragments d'hypophyses de carpe (Cyprinus carpio). Des applications de 5 minutes de TRH à différentes concentrations induisent une stimulation rapide et dose dépendante de la sécrétion de GH (ED50 = 9.7 ± 2.3 nM). Le TRH est sans effet sur la sécrétion de GTH. Le SRIF inhibe la sécrétion basale de GH ainsi que la résponse hypophysaire à l'action du TRH. Son action est dose dépendante. L'apomorphine induit une augmentation dose dépendante de la sécrétion basale de GH et potentialise l'action du TRH sur la stimulation de la sécrétion de GH. Des effets équivalents sont induits par des concentrations croissantes de calcium extra cellulaire de 0 à 1.2 mM, alors qu'à une concentration de 6.25 mM des effets opposés sont obtenus.
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15.
In vivo andin vitro techniques were used to examine the influence of various vertebrate peptides on growth hormone (GH) secretion in the goldfish. Tetradecapeptide somatostatin (SRIF-14) was found to inhibit GH secretionin vitro from perifused pituitary fragments, whereas similar concentrations of a salmonid SRIF peptide (sSRIF-25) did not affect GH secretion from the goldfish pituitary fragments. This indicates that SRIF receptors on the goldfish pituitary are very specific for SRIF-14-like peptides. Salmon gonadotropin (GTH)-releasing hormone (sGnRH) was found to elevate serum GH levels in male goldfish. The dopamine antagonist pimozide alone or injected in combination with sGnRH did not influence serum GH levels, although injection of pimozide alone significantly elevated serum GTH levels, in addition to potentiating the effects of sGnRH on GTH secretion. sGnRH stimulated GH secretion from goldfish pituitary fragmentsin vitro, indicating that sGnRH acts directly at the level of the pituitary to stimulate GH secretion in the goldfish. These results suggest that GnRH may also function as a GH-releasing factor in the goldfish, although the release-inhibitory factors for GH and GTH secretion do appear to be separate and distinct. Two human GH-releasing hormone (hGHRH) peptides were found to be ineffective in altering GH secretionin vitro from the perifused pituitary fragments. Consequently, a role for a mammalian GHRH-like peptide in the hypothalamic regulation of GH secretion in the goldfish remains questionable.  相似文献   

16.
The objective of the present study was to confirm previous results on the mediation of GnRH signal in tilapia by providing evidence from experiments in cultured pituitary cells and from perifusion experiments using a GnRH-antagonist. After 4 days in culture under identical conditions, cells taken from pituitaries of fish maintained at 26°C were more sensitive to GnRHa ([D-Ala6, Pro9-NEt]-LHRH) than those taken from fish maintained at 19°C. Cells from female pituitaries were more responsive than those from males. taGTH release in culture was augmented by Ca2+ ionophore (A23187; 1–100 μM) or ionomycin (0.02–10 μM). The response of perifused pituitary to GnRH was reduced by nimodipine (1–10 μM) indicating that Ca2+ influx via voltage-sensitive Ca2+ channels is involved in the stimulation of GTH release. Activation of protein kinase C by OAG (1-oleyl-2-acetyl glycerol; 0.16–160 μM) or TPA (1-O-tetra-decanoyl phorbol-13-acetate; 1.25–125 nM) resulted in a dose-dependent stimulation of taGTH release from cultured cells. Arachidonic acid (0.33–330 μM) also augmented the release of taGTH from the culture. Four sequential pulses of sGnRH (100 nM) at 2h intervals resulted in surges of taGTH release from perifused pituitary fragments; the surges were similar in magnitude with no signs of desensitization. Sequential stimulation with graded doses of sGnRH (0.1 nM to 1 μM) in the presence of GnRH-antagonist ([Pro2,6, Trp3]-GnRH) resulted in an attenuation of taGTH release. However, the GnRH-antagonist did not alter the pattern of forskolin-stimulated GTH release, indicating that forskolin stimulation is exerted at the level of the adenohypophyseal cells. It is concluded that, as in other vertebrates, the transduction of GnRH stimulation of GTH release involves Ca2+ influx through voltage-sensitive Ca2+ channels, mobilization of the ion from intracellular sources, arachidonic acid and activation of PKC. Adenylate cyclase-cAMP system us also involved in the mediation but its relationship with other transduction cascades requires further investigations.  相似文献   

17.
The roles of salmon GnRH (sGnRH) and gonadal steroid hormones in regulation of LH synthesis and release were examined in primary pituitary cell cultures of masu salmon (Oncorhynchus masou). Pituitaries were taken from fish at four reproductive stages: in March (initiation of sexual maturation); May (early maturation); July (pre-spawning); and September (spawning period). Amounts of LHβ subunit mRNA in the pituitary cells were determined by real-time PCR, and LH levels in the medium were determined by RIA. sGnRH and gonadal steroids including estradiol-17β (E2), testosterone (T) and 11-ketotestosterone (11-KT) were added to the cultures to examine their direct effects on LH response. sGnRH had no significant effect on LHβ mRNA levels at any stages, although a stimulatory trend was noted in March. In contrast, E2 and T considerably increased LHβ subunit mRNA levels in March and May during initial stages of maturation, and the effects were less pronounced in July and September. On the other hand, sGnRH stimulated LH release at all stages in the males and the effects were most prominent in July and September. E2 and T also stimulated LH release in July and September, but their effects were weaker than that of sGnRH. The present results indicate that sGnRH and gonadal steroids directly regulate LH synthesis and release in masu salmon pituitary cells: sGnRH mainly stimulates LH release in the late stage of sexual maturation; whereas, E2 and T are effective in stimulating LH synthesis at earlier stages of maturation.  相似文献   

18.
Growth hormone (GH) secretion from organ-cultured pituitaries of the eel (Anguilla japonica) was studied during incubation in a defined medium for 2 weeks, using a homologous radioimmunoassay which does not distinguish between the two molecular forms of eel GH. The total amount of GH secreted increased gradually during the incubation period; so that the amount of GH released on day 14 was about 30 times greater than that on day 1. On day 14, the proportion of GH released relative to the total amount of GH present (the sum of GH released into the medium and residual content in the pituitary) was 96% and the amount produced on day 14 was 4 times greater than the content in the unincubated pituitary. Somatostatin (SRIF, 1.8 × 10-7 M) inhibited the increase in GH release. On day 7, the proportion of GH released by pituitaries treated with SRIF (28%) was less than that released by the control pituitary (91%). There was no significant difference in GH release between the pituitaries incubated in isotonic medium (300 mOsm) and those in hypotonic medium (240 mOsm) for 2 weeks except for the first 3 days, when the pituitaries in hypotonic medium secreted significantly greater amounts of GH than those incubated under isotonic condition. Hypertonic medium (350 mOsm) had no effect on GH release except for significant inhibition on days 6 and 14. When secretion of the two forms of GH (GH I and II) was examined after separation by polyacrylamide gel electrophoresis followed by densitometry, slightly more GH I tended to be secreted than GH II during the culture period, although the effects of SRIF and osmolality of the media on GH I release were similar to those on GH II. It is concluded that GH secretion and production in the eel is mainly under the inhibitory control of hypothalamus, and that osmolality has a minimum influence on the GH release.  相似文献   

19.
The mechanisms of pituitary adenylate cyclase activating polypeptide (PACAP) action on goldfish growth hormone (GH) release were investigated by examining GH release responses from dispersed goldfish pituitary cells to a synthetic mammalian (m)PACAP38 peptide. It was established that GH release stimulated by 2-h exposure to mPACAP38 was concentration-dependent, attenuated by the PACAP receptor antagonist mPACAP6–38, and subject to neuroendocrine modulation by somatostatin. Maximal mPACAP38-stimulated GH release was not additive to the responses elicited by either the adenylate cyclase activator forskolin or the cyclic (c)AMP analog 8-bromo-cAMP. The GH responses to mPACAP38, forskolin and 8-bromo-cAMP, either alone or in combination, were abolished by H89, a protein kinase A (PKA) inhibitor. SQ22536, an adenylate cyclase inhibitor, attenuated forskolin- and mPACAP38-stimulated GH release. In contrast, mPACAP38-stimulated GH release were additive to the responses to two protein kinase C (PKC) activators and unaffected by two PKC inhibitors. These results suggest that the stimulatory action of PACAP on GH secretion is mediated through a cAMP- / PKA-dependent mechanism, whereas the involvement of PKC appears unlikely. The ability of mPACAP38 to further enhance maximal GnRH (PKC)-dependent GH release, but not dopamine D1 agonist (PKA)-dependent GH secretion, is consistent with this hypothesis. A possible involvement of Ca2+ in PACAP action is also suggested. Two inhibitors of voltage-sensitive Ca2+ channel reduced the GH responses to mPACAP38 in static incubation; conversely, mPACAP38 increased intracellular [Ca2+] in identified, single goldfish somatotropes.  相似文献   

20.
It has been established that secretion of gonadotropin (GtH) and growth hormone (GH) release in goldfish are both stimulated by GtH-releasing hormone (GnRH); in addition GtH secretion is inhibited by dopamine D2 mechanisms. In the present study, depletion of protein kinase C (PKC) in goldfish pituitary cells reduced the GtH and GH responses to GnRH and an activator of PKC in static culture. In perifusion studies, GtH released in response to sGnRH analog was greatly attenuated in PKC-depleted cells, however, hormone responses to forskolin were enhanced. Stimulation of dopamine D2 receptors reduced the GtH, but not the GH, responses elicited by PKC activators. These results indicate that PKC participates in the GtH and GH responses to natural neuroendocrine regulators in the goldfish.
Résumé Il a été établi que chez le poisson rouge, les sécrétions de gonadotropine (GtH) et d'hormone de croissance (GH) sont toutes les deux stimulées par la gonadolibérine (GnRH); de plus, la sécrétion de GtH est inhibée par des mécanismes dopaminergiques de type D2. Dans le présent travail, la déplétion de la teneur en protéine kinase C (PKC) dans des cellules hypophysaires de poisson rouge réduit les résponses en GtH et GH au GnRH et à un activateur de la PKC de cellules maintenues en incubation statique. Dans des cellules maintenues en périfusion et soumises à une déplétion en PKC, la GtH libérée en réponse à un analogue du sGnRH est fortement diminuée, cependent les réponses hormonales à la forskoline sont augmentées. La stimulation des récepteurs dopaminergiques D2 réduit, dans le cas d'action d'activateur de la PKC, la réponse en GtH mais pas en GH. Ces résultats indiquent que la PKC est impliquée dans les mécanismes de régulation de GtH et GH par des facteurs neuroendocriniens naturels.
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