儿茶酚胺激动剂和阻断剂对大鼠胃粘膜适应性细胞保护作用的影响

本文观察了儿茶酚胺激动剂和阻断剂对大鼠慢性应激诱发的胃粘膜适应性细胞保护作用的影响,并分析内源性生长抑素与保护作用的关系。结果表明,慢性应激诱导的大鼠胃粘膜适应性保护作用在交感神经切除后完全消失,多巴胺或异丙肾上腺素使保护作用部分恢复,去甲肾上腺素无作用;在交感神经完整大鼠,心得安或氟哌啶醇可抑制慢性应激诱发的保护作用,酚妥拉明无作用。血浆生长抑素在应激及交感神经切除后均无显著变化。提示慢性应激时交感肾上腺系统的激活参与了大鼠胃粘膜适应性保护作用,且可能通过多巴胺及肾上腺能β受体介导。     

Assignment of markers by using polymerase chain reaction on pools of swine flow-sorted chromosomes

Gene chromosomal assignment can be realized not only by somatic hybrid panels but also by spot-blot hybridization or polymerase chain reaction (PCR) of flow-sorted chromosomes. We propose a swine chromosome assignment strategy by PCR amplification on pooled chromosomal DNA, which allows assignment despite possible chromosomal contamination during sorting. Each pool contains three different chromosomes, each chromosome being present in one or two pools. We present concordant results obtained for eight markers already mapped to different swine chromosomes and we assign the somatostatin gene to chromosome 13, a new marker in the pig genome.     

Effects of ketamine on the cholecystokinin,somatostatin, substance P,and thyrotropin releasing hormone in discrete regions of rat brain

Intraperitoneal injection of ketamine (100 mg/kg body weight) significantly reduces the levels of cholecystokinin (CCK) somatostatin (SRIF), and substance P (SP)-like immunoreactivity in various regions of rat brain. No significant change in thyrotropin releasing hormone (TRH)-like immunoreactivity was observed. Neuropeptide systems may be involved in the neuropharmacologic effects of ketamine.     

铃蟾肽(Bombesin)对离体灌流大鼠胃的胃泌素、生长抑素、胰升糖素及胃酸释放的影响

本研究用离体大鼠胃灌流技术来观察铃蟾肽对胃-肠激素及胃酸分泌的影响。2×10~(?)mol/L铃蟾肽以0.3ml/min速度作动脉内输注,可刺激胃酸的分泌,自2.50±0.05×10~(-1)增至5.50±1.50×10~(-1)mEq/min,但与外源性五肽胃泌素无协同作用。铃蟾肽引起两次性的门脉中胃泌索及生长抑素的释放,但抑制胰升糖素释放。这三种激素的基础释放率分别为:胃泌素62±8pg,生长抑素5.9±1.1ng,胰升糖素0.40±0.03ng/min;2×10~(-8)mol/L铃蟾肽以0.3ml/min作动脉内输注,胃泌素及生长抑素的峰值分别为1,000±20pg及12.2±2.0ng/min,胰升糖素的最低值为0.17±0.05ng/min,三种激素的反应均与铃蟾肽的浓度成正比。在胃腔流出液中也可测到上述三种激素,但量要少得多。     

半胱胺对猫脊髓背角神经元伤害性热反应的抑制

在戊巴比妥钠麻醉和脊髓腰-1段全横切的16只猫上,观察生长抑素(somatostatin,SOM)的耗竭剂半胱胺对伤害性热刺激脚跖皮肤和电刺激胫后神经所引起的脊髓背角Ⅳ-Ⅵ层神经元单位反应的影响。静脉注射半胱胺50mg/kg对电刺激神经引起的伤害性反应无影响,100mg/kg可使被测试的13个神经元单位中的8个单位反应明显抑制。而静脉注射半胱胺50mg/kg可明显抑制伤害性热刺激所引起的脊髓背角神经元单位反应。用微电极将半胱胺微压注入背角胶质层也使背角神经元的伤害性热反应明显抑制,但只使13个单位中的7个单位对电刺激神经引起的伤害性反应轻度抑制。半胱胺对背角神经元伤害性反应的抑制可能由于耗竭了背角中的生长抑素。本文讨论了半胱胺对背角神经元伤害性热反应的抑制明显强于电刺激神经所诱发的伤害性反应的抑制的可能机制。     

缺锌对大鼠学习记忆功能及其脑区生长抑素和加压素含量的影响

目的和方法：本实验用避暗法检测缺锌对大鼠学习记忆的影响,并用放免法测定不同脑区生长抑素和加压素含量的变化。结果：缺锌使大鼠学习记忆功能明显降低,同时下丘脑、海马和皮层等脑组织生长抑素和加压素含量明显降低。缺锌后补锌可使大鼠学习记忆功能及其海马中生长抑素和加压素含量恢复到正常状况。结论：缺锌降低大鼠学习记忆功能与锌对脑组织尤其是海马内源性生长抑素和加压素代谢的调节有关。     

Pituitary somatostatin receptors: dissociation at the pituitary level of receptor affinity and biological activity for selective somatostatin analogs

High affinity and saturable binding of [125I-Tyr11]somatostatin (SS) is described in membrane homogenates from a pituitary transplantable tumor (GH4C1) rich in somatotrophs (KD for SS = 0.67 nM; Bmax = 30 fmol/mg protein). Binding characteristics and pharmacology are similar to those measured on normal pituitary membranes. The potency of various SS analogs highly correlates with that measured in in vitro bioassay for growth hormone. This suggests that those GH4C1 membranes are a good model for SS receptors on somatotrophs. Interestingly however, analogs in which the Asn5 is deleted (Des-Asn5) or D-Ser replaces Ser13 show dissociated potencies between the various assays: [D-Ser13] analogs are more potent in pituitary than in GH4C1 membranes binding assay. Des-Asn5-modified analogs are much more potent in both pituitary binding assays than in the bioassay. This could reflect a multiplicity of SS receptor subtypes in pituitary.     

Distinct recruitment of feedforward and recurrent pathways across higher-order areas of mouse visual cortex

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A bioactive somatostatin analog without a type II' beta-turn: synthesis and conformational analysis in solution.

A cyclic somatostatin analog [structure: see text] (1) has been synthesized. Biological assays show that this compound has strong binding affinities to somatostatin hsst2 and hsst5 receptor subtypes (5.2 and 1.2 nM, respectively, and modest affinity to hsst4 (41.1 nM)). Our conformational analysis carried out in DMSO-d6 indicates that this compound exists as two structures arising from the trans and cis configurations of the peptide bond between Phe7 and N-alkylated Gly8. However, neither conformer exhibits a type II' beta-turn. This is the first report of a potent bioactive somatostatin analog that does not exhibit a type II' beta-turn in solution. Molecular dynamics simulations (500 ps) carried out at 300 K indicate that the backbone of compound 1 is more flexible than other cyclic somatostatin analogs formed by disulfide bonds.