A collection of neurons in the upper lumbar spinal cord (lumbar segments 3 and 4) of male rats project to the lower lumbar spinal cord (lumbar segments 5 and 6) and release a gastrin-releasing peptide (GRP) to the somatic and autonomic regions, which are known to regulate male sexual reflexes. The GRP plays some special functions when bound to the specific GRP receptor (GRPR). The spinal GRP system is regulated by androgens. Accumulating evidence shows that GRP plays an important role in rat penile erection and ejaculation, and pharmacological stimulation of GRPRs with a specific agonist can restore penile reflexes and ejaculation in castrated male rats. Therefore, the GRP system appears to be a potential therapeutic target for the treatment of erectile dysfunction or ejaculatory dysfunction. The present paper briefly reviews the recent studies on the role of the spinal GRP system in regulating the sexual function of males.
Androgens ; metabolism ; Animals ; Ejaculation ; physiology ; Gastrin-Releasing Peptide ; metabolism ; physiology ; Male ; Penile Erection ; physiology ; Rats ; Spinal Cord ; metabolism

OBJECTIVETo study the expression of gastrin(GAS) and gastrin releasing peptide(GRP) in patients with gastric cancer and investigate the clinical significance.

METHODSThe expression of GAS and GRP in sixty patients with gastric cancer was detected by using tissue chip technique and immunohistochemical methods.

RESULTSThe positive rates of GAS and GRP were 30.0% and 11.7% respectively in 60 cases with gastric cancer. The positive rates of GAS and GRP were higher in moderately and poorly differentiated cancers than those in well differentiated cancer (P< 0.05). The positive rates of GAS and GRP were significantly higher in mucinous adenocarcinoma and signet-ring cell carcinoma than those in other types of gastric cancer (P< 0.05). The positive expression of GAS and GRP in gastric cancer was correlated with lymph node metastasis (P< 0.05).

CONCLUSIONTissue chip technique is a feasible,rapid,economic and accurate approach for screening clinical tissue specimens on a large scale.

Adult ; Aged ; Female ; Gastrin-Releasing Peptide ; metabolism ; Gastrins ; metabolism ; Humans ; Immunohistochemistry ; methods ; Male ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Staging ; Protein Array Analysis ; Stomach Neoplasms ; metabolism ; pathology

Since GABA and its related enzymes had been determined in beta-cells of pancreas islets, effects of GABA on pancreatic exocrine secretion were investigated in the isolated perfused rat pancreas. GABA, given intra-arterially at concentrations of 3, 10, 30 and 100 microM, did not exert any influence on spontaneous or secretin (12 pM)-induced pancreatic exocrine secretion. However, GABA further elevated cholecystokinin (10 pM)-, gastrin-releasing peptide (100 pM)- or electrical field stimulation-induced pancreatic secretions of fluid and amylase, dose-dependently. The GABA-enhanced CCK-induced pancreatic secretions were completely blocked by bicuculline (10 microM), a GABAA receptor antagonist but not affected by saclofen (10 microM), a GABA(B) receptor antagonist. The enhancing effects of GABA (30 microM) on CCK-induced pancreatic secretions were not changed by tetrodotoxin (1 microM) but partially reduced by cyclo-(7-aminoheptanonyl-Phe-D-Trp-Lys-Thr[BZL]) (10 microM), a somatostatin antagonist. In conclusion, GABA enhances pancreatic exocrine secretion induced by secretagogues, which stimulate enzyme secretion predominantly, via GABA(A) receptors in the rat pancreas. The enhancing effect of GABA is partially mediated by inhibition of islet somatostatin release. GABA does not modify the activity of intrapancreatic neurons.
Amylases/metabolism ; Animal ; Baclofen/pharmacology ; Baclofen/analogs & derivatives* ; Bicuculline/pharmacology ; Cholecystokinin/metabolism ; Dose-Response Relationship, Drug ; Electric Stimulation ; GABA/pharmacology* ; GABA Antagonists/pharmacology ; Gastrin-Releasing Peptide/metabolism ; Hormones/pharmacology ; In Vitro ; Pancreas/secretion* ; Pancreas/enzymology ; Pancreas/drug effects* ; Rats ; Receptors, GABA-A/metabolism ; Secretin/metabolism ; Somatostatin/pharmacology ; Tetrodotoxin/pharmacology