No abstract available.
Animals ; Dynorphins* ; Enkephalins* ; Prosencephalon* ; Rats* ; RNA, Messenger*

Immunohistochemical study have been made to examine the autonomic innervation of the human vas dererens following vasectomy one to 7 years previously. Samples from sites on the proximal (testicular) and distal (urethral) sides of the original vasectomy have been compared with control specimens as to the arrangement and distribution of autonomic nerves containing vasoactive intestinal polypeptide (VIP), catecholamine, substance-P and enkephalin. In contrast with tissues from the urethral portion and from controls, the testicular specimens revealed a marked reduction in the catecholeminergic innervation of the muscular layer. In addition VIPergic nerves distributed at the subepithelial layer were nearly absent from the testicular side of the vas deferens. The degrees of denervation were independent of the obstructive interval between vasectomy and vasectomy reversal. Substance-P and enkephalin containing nerves were rarely found from both sides of the vas deferens. Therefore, these findings suggest that the consequences of denervation of vas deferens may play an important role in those patients in whom infertility persists despite evidence of satisfactory mechanical continuity achieved by vasectomy reversal.
Autonomic Pathways ; Denervation ; Enkephalins ; Humans* ; Infertility ; Vas Deferens* ; Vasectomy* ; Vasoactive Intestinal Peptide ; Vasovasostomy

BACKGROUND: Activation of G-protein coupled-somatostatin receptors induces the release of calcium from inositol 1, 4, 5-trisphosphate-sensitive intracelluar stores. G-protein-coupled receptor signaling decreases with prolonged exposure to an agonist. SEBJECTS and METHODS: Fura-2-based digital Ca2+ imaging was used to study the effects of prolonged exposure to an agonist on the somatostatin-induced intracellular Ca2+ concentration([Ca2+]i) increases in NG108-15 cells, which were differentiated with CO2-independent medium and 10micrometer forskolin. RESULTS: Exposure to somatostatin(1micrometer) for 30 min completely desensitized the NG108-15 cells to a second somatostatin-induced response. The cells recovered gradually over 20 min following washout of the somatostatin. The desensitization was not due to depletion of the intracellular Ca2+ stores, and pretreatment for 30 min with bradykinin(100nM), which activates phospholipase C, or DADLE(D-Ala2-D-Leu5 enkephalin, 1microM), which activates phospholipase C, failed to cross-desensitize the somatostatin-evoked [Ca2+]i increases. Treatment with 8-cpt-cAMP(0.1mM) for 30min did not influence the somatostatin-induced[Ca2+]i increases. Phorbol 12, 13-dibutyrate(PdBu, 1microM) blocked the response completely. Down-regulation of PKC due to 24 h exposure of PdBu (1microM) inhibited the somatostatin-induced desensitization. CONCLUSION: Prolonged exposure of somatostatin to NG108-15 cells desensitized the somatostatin-induced release of Ca2+ from the intracelluar store, with protein kinase C also involved in the desensitization.
Calcium* ; Colforsin ; Down-Regulation ; Enkephalins ; GTP-Binding Proteins ; Inositol ; Protein Kinase C* ; Protein Kinases* ; Somatostatin ; Type C Phospholipases

Septic shock is one of the leading cause of death in hospitalized patients and mortality rates of up to 50 % have been reported. Despite all efforts, no regimen today seems to be successful in the treatment of septic shock. The endogenous opioid system (EOS) includes three major families of peptides: dynorphins, endorphins and enkephalins. Several lines of evidence indicate that EOS is implicated in the pathophysiology of anaphylactic and endotoxic shock. An opioid receptor blocker naloxone has been used extensively in studies for the role of EOS or endogenous opiod peptides (EOP). However, there have been few, if any, detailed investigative studies regarding the effect of naloxone on TNF-a production and the lethality in response to endotoxin, and tumorigenesis. ...continue...
Carcinogenesis* ; Cause of Death ; Dynorphins ; Endorphins ; Enkephalins ; Humans ; Melanoma ; Mortality ; Naloxone* ; Nitric Oxide ; Peptides ; Receptors, Opioid* ; Shock, Septic*

In the rat hippocampal formation, the time-course and dose-response of the expression of enkephalin and dynorphin gene were examined after kainate (KA) treatment with in situ hybridization histochemistry. The KA induced enkephalin and dynorphin mRNA expression in hippocampus occurred mainly in the dentate gyrus. The enkephalin mRNA expression appeared at 3hour after KA injection, increased dramatically at 6hour, and then decreses. At 24hour after KA injection, the expression of enkephalin mRNA disappeared. The dynorphin mRNA expression appeared at once after injection and increased dramatically at 3hour. Unexpectedly at 6hour after injection, the expression was decreased, and then increased less than the 3hour expression. The increased pattern persisted to 24hour after injection. Unexpected result was also encounted in the experiment of KA dose-response of enkephalin mRNA and dynorphin mRNA. In the hippocampal formation, in contrast with other areas, low dosage (8mg/kg) of KA induced more significant expression of both genes than high dosage (16mg/kg) of KA.
Animals ; Dentate Gyrus ; Dynorphins ; Enkephalins ; Gene Expression* ; Hippocampus* ; In Situ Hybridization ; Kainic Acid ; Opioid Peptides* ; Rats* ; RNA, Messenger ; Seizures*

BACKGROUND: We studied the time course of gene expression of dynorphin, enkephalin, c-fos, and the changes of allodynia, and the effect of chemical sympathectomy on the gene expression and allodynia in neuropathic rat. METHODS: In two groups of rat (Sprague-Dawley), the left L5 and L6 spinal nerves were tight ligated. In gene expression group (N=25), behavioral tests for mechanical allodynia and cold allodynia were perfomed for the next two weeks. After the test of allodynia, the expression of dynorphin, enkephalin, c-fos were assessed by Northern blot hybridization. In chemical sympathectomy group (N=16), after chemical sympathectomy (guanethidine 70 mg/kg intraperitoneally, from postoperative 7 days to 9 days), the changes of allodynia and the gene expression of enkephalin, c-fos were tested. RESULTS: Mechanical allodynia and cold allodynia was developed on the postoperative 3, 5, 7, 14 days. Preprodynorphin mRNA expression was reached peak level at the postoperative 8 hrs, sustained increase by the postoperative 3 days, but preproenkephalin mRNA expression increased slightly after operation. c-Fos mRNA expression was increased immediately at the postoperative 30 min, 1 hr, returned to normal level thereafter, and increased again on the postoperative 3, 5, 7 days that neuropathic pain was developed. Mechanical allodynia and cold allodynia were decreased by chemical sympathectomy. The increased c-fos mRNA expression and pain at postoperative 7 days was reduced by chemical sympathectomy. CONCLUSION: These results suggest that the transient gene expression of dynorphin and c-fos after tight ligation of L5 and L6 spinal nerves induces the development neuropathic pain, and late c-fos expression is related to neuropathic pain.
Animals ; Blotting, Northern ; Dynorphins* ; Enkephalins* ; Gene Expression* ; Hyperalgesia ; Ligation ; Neuralgia ; Rats* ; RNA, Messenger ; Spinal Nerves ; Sympathectomy, Chemical

BACKGROUND: The selective D1 dopamine agonist has been known to play a stimulatory role in substance-P synthesis in the striatum, but its effect on the enkephalin mRNA expression has not been well known in the striatum of unilateral 6-hydroxydopamine(OHDA)-lesioned rat. So we investigated the effect of selective D1 dopaminergic agonist on substance-P, enkephalin mRNA expression in the striatum with different time interval. METHODS: The lesioned rats were divided into two groups (treated and non-treated). Each group was subdivided according to time course after lesioning (2nd, 4th and 8th week). Dopamine 1 receptor agonist, SKF-38393 (5 mg/kg/ip) and the same volume of saline was injected to treated and nontreated group respectively. The levels of enkephalin and substance-P mRNA were determined by in situ-hydridization and the expression of mRNA levels were compared between the groups. RESULTS: The expression of striatal enkephalin mRNA was increased on lesioned side in all groups. Especially, SKF-38393 enhanced the striatal expression of enkephalin mRNA after lesioning 2nd week. After lesioning 4th week and 8th week, the effect of SKF-38393 was not significant. The striatal expression of substance-P mRNAs was significantly decreased on the lesioned side, especially at the 2nd weeks. This decrement of substance-P mRNA was reversed by SKF-38393 at the 2nd week. CONCLUSIONS: These data show that the selective D1 agonist SKF-38393 have an agonistic effect on direct pathway but antagonistic effect on indirect pathway in early course of Parkinsonian rat model.
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine ; Animals ; Dopamine ; Dopamine Agonists ; Enkephalins* ; Models, Animal* ; Rats* ; RNA, Messenger*

BACKGROUND: The selective D1 dopamine agonist has been known to play a stimulatory role in substance-P synthesis in the striatum, but its effect on the enkephalin mRNA expression has not been well known in the striatum of unilateral 6-hydroxydopamine(OHDA)-lesioned rat. So we investigated the effect of selective D1 dopaminergic agonist on substance-P, enkephalin mRNA expression in the striatum with different time interval. METHODS: The lesioned rats were divided into two groups (treated and non-treated). Each group was subdivided according to time course after lesioning (2nd, 4th and 8th week). Dopamine 1 receptor agonist, SKF-38393 (5 mg/kg/ip) and the same volume of saline was injected to treated and nontreated group respectively. The levels of enkephalin and substance-P mRNA were determined by in situ-hydridization and the expression of mRNA levels were compared between the groups. RESULTS: The expression of striatal enkephalin mRNA was increased on lesioned side in all groups. Especially, SKF-38393 enhanced the striatal expression of enkephalin mRNA after lesioning 2nd week. After lesioning 4th week and 8th week, the effect of SKF-38393 was not significant. The striatal expression of substance-P mRNAs was significantly decreased on the lesioned side, especially at the 2nd weeks. This decrement of substance-P mRNA was reversed by SKF-38393 at the 2nd week. CONCLUSIONS: These data show that the selective D1 agonist SKF-38393 have an agonistic effect on direct pathway but antagonistic effect on indirect pathway in early course of Parkinsonian rat model.
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine ; Animals ; Dopamine ; Dopamine Agonists ; Enkephalins* ; Models, Animal* ; Rats* ; RNA, Messenger*

Bovine adrenal medulla 22 (BAM22), an endogenous opioid peptide, is one of the cleavage products of proenkephalin A. It potently activates opioid receptors and sensory neuron-specific receptor (SNSR). The present study was aimed at investigating the effect of BAM22 on morphine tolerance. Intrathecal (i.t.) administration of morphine for 7 d produced morphine tolerance in rats. Then the rats were divided into three groups in which morphine, saline or BAM22 were administered i.t., respectively, on day 8, and morphine was given to all of the animals on day 9. It was found that morphine administered on day 9 resumed antinociceptive effects in BAM22 group, but not in saline or morphine group. The potency of morphine in BAM22 group was 48.5% of the maximal possible effect (MPE) detected by paw withdrawal test and the antinociception persisted for approximately 1 h. Following the similar treatment, morphine administered on day 9 reduced nocifensive behaviors by 3.2 min and 24 min in BAM22 group in the first and second phases, in the formalin test, respectively. The decreases were 45% and 82% of the corresponding values observed in saline group. Furthermore, following the treatment with BAM22 (10 nmol) on day 8 in morphine-tolerance rats, morphine administered on day 9 decreased the expressions of the heat-evoked c-Fos-like immunoreactivity (FLI) protein by approximately 80% in laminae I-II, III-IV and V-VI in the spinal cord at L4-L5 compared with that in saline or morphine group. The present study provided evidence at behavioral and cellular levels showing that BAM22 resumed antinociception of morphine. The results that the reversal effect of BAM22 on morphine tolerance was more efficient in persistent pain model than in acute pain may indicate that BAM22 differentially modulates morphine tolerance. The present study suggests that SNSR is involved in the modulation of morphine tolerance.
Animals ; Drug Tolerance ; Enkephalins ; pharmacology ; Morphine ; pharmacology ; Pain ; drug therapy ; Peptide Fragments ; pharmacology ; Rats ; Receptors, G-Protein-Coupled ; metabolism

OBJECTIVES: Research into emotional or behavioral stress typically focuses upon the hypothalamic-pituitary-adrenal axis. It is well established that the hypothalamic-pituitary-adrenocortical axis is subject to inhibitory control by opioids in a variety of animal species including pigs. Exposure to acute stress induces the upregulation of opioid receptors and the release of endogenous peptides which mediate the stress-induced analgesia. There is some literature substantiating that repeated stress can lead to changes in opioidergic neurotransmission. However, the changes are highly variable. This study was designed to observe the modulatory effect of repeated immobilization stress on opioidergic neurotransmission. METHODS: Male Sprague-Dawley rats weighing 150-200g were forced to suffer immobilization stress for 2 hours on each of 14 successive days. Then we examined the maximum binding capacity and affinity of each opioid subtypes(mu, delta, kappa). RESULTS: Repeated immobilization stress increased the binding of [3H]DPDPE on the delta-subtype opioid receptor in the striatum and hypothalamus. Saturation experiments followed by scatchard analyses of the results showed an increase in the density of delta-subtype opioid receptors, but the affinity of the delta-subtype opioid receptor remained unchanged. Repeated immobilization stress reduced enkephalin activity of striatum and hypothalamus. CONCLUSIONS: From these results, it could be concluded that repeated immobilization stress up-regulated the delta-subtype opioid receptors and reduced the activity of enkephalin, an endogenous ligand for the delta-subtype opioid receptor.
Analgesia ; Analgesics, Opioid ; Animals ; Axis, Cervical Vertebra ; Enkephalins ; Humans ; Hypothalamus ; Immobilization ; Male ; Peptides ; Rats* ; Rats, Sprague-Dawley ; Receptors, Opioid ; Swine ; Synaptic Transmission* ; Up-Regulation