Biomedical subjects

L F Tseng

Publications and source records attributed to L F Tseng.

At least 91 records · Page 5Linked to original sources

PubMed1993

Increase of nitric oxide by L-arginine potentiates beta-endorphin- but not mu-, delta- or kappa-opioid agonist-induced antinociception in the mouse.

L-Arginine pretreated i.c.v. produced a time- and dose-dependent potentiation of beta-endorphin-induced inhibition of the tail-flick response in ICR mice. However, the inhibition of the tail-flick response induced by morphine, DAMGO ([D-Ala2,NMePhe4,Gly5-ol]enkephalin), DPDPE ([D-Pen2,D-Pen5]enkephalin or U50,488H given i.c.v. was not potentiated by i.c.v. pretreated L-arginine. The results indicate that L-arginine selectively potentiates antinociception induced by epsilon-opioid receptor agonist, but not mu-, delta- or kappa-opioid receptor agonist. L-Arginine pretreated i.t. did not potentiate i.c.v. administered beta-endorphin-induced inhibition of the tail-flick response, indicating that the potentiating effect of L-arginine on beta-endorphin-induced antinociception is located at the supraspinal sites but not at the spinal sites.

Analgesics↗

PubMed1993

Spinal delta 2 but not delta 1 opioid receptors are involved in intracerebroventricular beta-endorphin-induced antinociception in the mouse.

The antinociception induced by beta-endorphin given intracerebroventricularly (i.c.v.) has been previously demonstrated to be mediated by the release of Met-enkephalin and subsequent stimulation of delta receptors in the spinal cord for antinociception. The present study was designed to determine what type of opioid receptor, delta 1 or delta 2, in the spinal cord is involved in i.c.v. beta-endorphin-induced antinociception. Antinociception was assessed by the tail-flick test in male ICR mice. NTB (0.2-20 nmol) and NTI (0.22-2.2 nmol), selective delta 2 receptor antagonists, given intrathecally (i.t.) dose-dependently attenuated i.c.v. beta-endorphin-induced inhibition of the tail-flick response. On the other hand, BNTX (0.02-2.2 nmol), a selective delta 1 receptor antagonist, given i.t., did not block i.c.v. beta-endorphin-induced antinociception. The tail-flick inhibition induced by DAMGO, a mu receptor agonist, or U50,488H, a kappa receptor agonist, was not blocked by i.t. BNTX, NTB or NTI. It is concluded that delta 2 but not delta 1 receptors in the spinal cord are involved in i.c.v. beta-endorphin-induced antinociception.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1993

Nitric oxide synthase immunoreactivity in the rat, mouse, cat and squirrel monkey spinal cord.

The distribution of nitric oxide synthase-immunoreactive neurons was examined in the spinal cord of rats, mice, cats and squirrel monkeys at the light microscopic level. Some sections were processed for choline acetyltransferase immunoreactivity. Double-labeling techniques were used to assess possible co-localization of nitric oxide synthase and choline acetyltransferase immunoreactivity in the same spinal neurons. Nitric oxide synthase-immunoreactive neurons were concentrated in three fairly well-defined regions of the spinal cord of all species studied: (i) the intermediolateral cell column of the thoracic and sacral segments, (ii) lamina X of all segments, and (iii) the superficial layers of the dorsal horn of all segments. A few nitric oxide synthase-immunoreactive neurons were scattered in the deeper laminae and the ventral horn. There were fewer nitric oxide synthase-positive neurons in monkey spinal lamina X and dorsal horn than in similar locations of rodents and felines. Double-staining showed that not all choline acetyltransferase-positive neurons in the intermediate cell column and lamina X were nitric oxide synthase-immunoreactive. In the ventral horn, choline acetyltransferase-positive neurons (presumed motoneurons) were nitric oxide synthase-negative. In addition to cell bodies, nitric oxide synthase-positive fibers were scattered in the dorsal, lateral and ventral horns of all species. Finally, punctate nitric oxide synthase-immunoreactive fibers were seen traversing the dorsal, lateral and ventral white matter, and reaching the respective gray matter. The present study shows that, in spite of quantitative differences, the pattern of distribution of nitric oxide synthase-positive neurons in the spinal cord was similar across the four species. The concentration of nitric oxide synthase-positive neurons in the autonomic nuclei and laminae I, II and X of all four species underscores a prominent role of these neurons in visceral and sensory functions.

Amino Acid Oxidoreductases↗

PubMed1993

Use of the cytomegalovirus antigenemia (CMV-Ag) assay for the detection of CMV in the blood of AIDS patients.

Direct specimen testing was performed on 186 peripheral blood specimens to identify the presence of antigen to cytomegalovirus (viz., the cytomegalovirus antigenemia (CMV-Ag) assay). Confirmatory testing was performed using the shell vial indirect immunofluorescence assay (SVA-IFA), the indirect immunoperoxidase assay (TC-IPA), and conventional tube culture isolation (TC-CPE). The primary reagent for the CMV-Ag assay consisted of anti-CMV monoclonal antibody directed against the internal matrix structural phosphoprotein (1C3; Clonatec-Biosoft, France). The 72-kDa early nuclear antigen (Dupont) was utilized in the SVA-IFA and the TC-IPA. All test systems received an equal number of polymorphonuclear leukocytes in the inoculum. CMV was detected and isolated from 30% (55/186) of the specimens evaluated by either one or a combination of the tests. Detection and (or) isolation of CMV from blood by the CMV-Ag assay, SV-IFA, TC-IPA, and TC-CPE occurred at a rate of 17 (31/186), 12 (22/186), 16 (29/186), and 26% (49/186). Three of 55 positive specimens were identified only by the CMV-Ag assay; each patient in question, however, had at least one previous CMV isolate. No significant differences in sensitivity occurred between the CMV-Ag assay, the SVA-IFA, or the TC-IPA. However, TC-CPE including the blind passage of all negative tube cultures yielded a significantly larger number of positive blood specimens than either of the rapid detection methodologies. The CMV-Ag assay encompasses the benefits of a nonculture system, is simple to perform and easy to read, permits a same-day diagnosis, and requires less reagents than the routinely used SVA-IFA or TC-IPA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

PubMed1993

Spinal involvement of both dynorphin A and Met-enkephalin in the antinociception induced by intracerebroventricularly administered bremazocine but not morphine in the mouse.

Previous reports show the tail-flick inhibition induced by bremazocine given i.c.v. is mediated by supraspinal stimulation of both epsilon and kappa opioid receptors and the spinal activation of descending serotonergic and opioid systems. The present studies questioned what endogenous opioid peptides in the spinal cord were involved in i.c.v. bremazocine-induced antinociception in male ICR mice. beta-Endorphin, trans(+-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]- benzene-acetamide methane sulfonate (U50,488H) and morphine were used as reference compounds for epsilon, kappa and mu opioid receptor activity, respectively. Intrathecal pretreatment with antibody to Met-enkephalin dose-dependently attenuated the antinociception induced by i.c.v. bremazocine or beta-endorphin but not morphine or U50,488H; whereas intrathecal (i.t.) pretreatment with antibody to dynorphin A (1-13) dose-dependently blocked the antinociception induced by i.c.v. bremazocine or U50,488H but not beta-endorphin or morphine. Intrathecal Leu-enkephalin and beta-endorphin antibodies did not block i.c.v. bremazocine, beta-endorphin or morphine antinociception. Intrathecal Met-enkephalin or dynorphin A (1-17) increased the tail-flick latency at 1 to 2 min. Met-enkephalin given i.t. blocked the antinociception induced by i.c.v. DPDPE, bremazocine and beta-endorphin but not morphine or U50,488H whereas i.t. dynorphin A (1-17) pretreatment blocked the inhibition induced by i.c.v. U50,488H and bremazocine but not DPDPE, beta-endorphin or morphine. Bremazocine given i.c.v. did not exhibit antianalgesic activity in our studies. The dynorphin released by i.c.v. bremazocine for antinociception appears to be different from the dynorphin released by morphine for antianalgesia.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1992

Nitric oxide synthase immunoreactivity in rat spinal cord.

Immunoreactivity to nitric oxide synthase (NOS-IR) and choline acetyltransferase (ChAT-IR) was detected in the adult rat spinal cord using the avidin-biotin-peroxidase technique. Intensely stained NOS-positive neurons with cell processes were observed in the intermediolateral cell column of the thoracic and sacral segments and around the central canal of all segments. These areas also contained ChAT-IR neurons. A number of small- to medium-sized NOS-IR cells were noted in the superficial and deeper laminae throughout the entire cord. NOS-IR was not detected in the ventral horn motoneurons, which were, however, ChAT-IR. The results indicate that NOS-IR is present in autonomic preganglionic neurons and in selected neurons in the dorsal horn and lamina X, but appears to be absent in motoneurons.

Amino Acid Oxidoreductases↗

PubMed1992

Release of immunoreactive [Met5]enkephalin and cholecystokinin from the spinal cord by beta-endorphin administered intraventricularly in the pentobarbital-anesthetized rat.

Beta-endorphin (4 micrograms) injected i.v.t. induced the release of immunoreactive [Met5]enkephalin and sulfated cholecystokinin octapeptide (CCK-8s) from the spinal cord in the pentobarbital-anesthetized rat. The inhibition of the tail-flick response induced by beta-endorphin given i.v.t. was antagonized by i.t. injection of CCK-8s and potentiated by i.t. administration of the antibody to CCK-8s. The findings give support to the hypothesis that endogenous CCK-8s in the spinal cord may play a negative feedback role in modulating beta-endorphin-induced antinociception.

Anesthesia↗

PubMed1992

Pentobarbital attenuates antinociception induced by i.c.v. morphine but not beta-endorphin in the mouse.

The effects of pentobarbital anesthesia (45 mg/kg i.p.) on the inhibition of the tail-flick response induced by beta-endorphin and morphine injected intracerebroventricularly (i.c.v.) and intrathecally (i.t.) were studied in male ICR mice. Pentobarbital anesthesia attenuated the inhibition of the tail-flick response induced by morphine but not beta-endorphin given i.c.v. However, the tail-flick inhibition induced by morphine given i.t. was not attenuated by pentobarbital. beta-Endorphin-(1-27) (3 micrograms) given i.c.v. or naloxone (2 micrograms) given i.t. blocked inhibition of the tail-flick response induced by morphine given i.c.v. only in pentobarbital-anesthetized mice but not in conscious mice. beta-Funaltrexamine (beta-FNA, 2.5 micrograms) given i.c.v. or yohimbine (2 micrograms) and methysergide (2 micrograms) injected i.t. blocked the morphine (i.c.v.)-induced inhibition of the tail-flick response in conscious mice but not in pentobarbital-anesthetized mice. The results indicate that pentobarbital attenuates the morphine-induced inhibition of the tail-flick response by inhibiting descending noradrenergic and serotonergic pathways and uncovers a descending opioid system. The tail-flick inhibition induced by supraspinal morphine is mediated by stimulation of mu-opioid receptors in conscious mice and epsilon-opioid receptors in pentobarbital-anesthetized mice. The epsilon-opioid receptor-mediated descending system activated by supraspinally injected beta-endorphin is not attenuated by pentobarbital anesthesia.

Animals↗

PubMed1992

The tail-flick inhibition induced by beta-endorphin administered intrathecally is mediated by activation of kappa- and mu-opioid receptors in the mouse.

The inhibition of the tail-flick response induced by beta-endorphin given i.c.v. has been demonstrated to be mediated by the stimulation of epsilon- but not mu-, delta- or kappa-opioid receptors. beta-Endorphin given i.t. also inhibited the tail-flick response. The present studies were designed to determine what types of opioid receptors in the spinal cord were involved in i.t. beta-endorphin-induced tail-flick inhibition. Blockade of kappa-opioid receptors by coadministration of nor-binaltorphimine or Win 44,441-3 with beta-endorphin given i.t. dose dependently inhibited i.t. beta-endorphin-induced inhibition of the tail-flick response. Blockade of mu-opioid receptors by i.t. coadministration of D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 with beta-endorphin blocked i.t. beta-endorphin-induced inhibition of the tail-flick response. I.t. injection of delta-opioid receptors antagonists, ICI 174,864 and naltrindole, or epsilon-opioid receptor antagonist, beta-endorphin-(1-27), did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. Blockade of alpha 2-adrenoceptors and 5-HT receptors by i.t. injection of yohimbine and methysergide, respectively, also did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. The results indicate that the inhibition of the tail-flick response induced by beta-endorphin given i.t. is mediated by the stimulation of kappa- and mu-opioid receptors but not delta- and epsilon-opioid receptors, alpha 2-adrenoceptors or 5-HT receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1992

Different radiant heat intensities differentiate intracerebroventricular morphine- from beta-endorphin-induced inhibition of the tail-flick response in the mouse.

The antinociceptive effects of morphine and beta-endorphin given intracerebroventricularly (i.c.v.) or intrathecally (i.t.) were evaluated by inhibition of the tail-flick and hot-plate paw-licking responses evoked by three different intensities of heat stimulation (low, intermediate and high) in male ICR mice. Morphine given i.c.v. was more potent in inhibiting the tail-flick response evoked by low than high intensity of heat stimulus. beta-Endorphin given i.c.v., on the other hand, was equally potent in inhibiting the tail-flick response evoked by different intensities of heat. This differential effect of morphine and beta-endorphin was not shown when morphine and beta-endorphin were given i.t. Morphine and beta-endorphin given i.c.v. or i.t. were equally potent in inhibiting the paw-licking response at different intensities of hot-plate temperature. Our results suggest that morphine given i.c.v. may inhibit high intensity heat-evoked tail-flick response spinally and inhibits low intensity heat-evoked tail-flick response supraspinally. Our results also provide additional evidence for different neural mechanisms of antinociceptive action of morphine and beta-endorphin.

Analgesia↗

PubMed1992

Increase of nitric oxide production by L-arginine potentiates i.c.v. administered beta-endorphin-induced antinociception in the mouse.

Pretreatment (i.c.v.) of mice with L-arginine but not D-arginine potentiated beta-endorphin-induced (i.c.v. administered) inhibition of the tail-flick response. The potentiation was attenuated by N omega-nitro-L-arginine methyl ester, a selective inhibitor of nitric oxide synthase. This observation suggests that increased production of nitric oxide from L-arginine mediates the potentiation of beta-endorphin-induced antinociception.

Amino Acid Oxidoreductases↗

PubMed1992

Improved detection of cytomegalovirus viremia in AIDS patients using shell vial and indirect immunoperoxidase methodologies.

One hundred twelve peripheral blood specimens were tested for the presence of cytomegalovirus (CMV) by the tube culture indirect immunoperoxidase (TC-IPA) procedure, the shell vial assay [shell vials were pre- and postinoculation treated with medium containing 2 of 10% fetal bovine serum (FBS) or 100 micrograms% cortisol] (SV-IFA), and conventional (MRC-5) tube cultures (TC-CPE). CMV was detected in 25 (22%) of the 112 specimens tested by at least one of these methods. The detection/isolation of CMV among the 25 positive specimens in shell vials maintained with 2% FBS, 100 micrograms% cortisol + 2% FBS, and 10% FBS was 36, 44, and 52%, respectively. Detection/isolation of the virus from blood by TC-IPA and TC-CPE was 52% and 76%, respectively. A significantly greater CMV detection rate occurred using TC-CPE compared to SV-IFA treated with medium supplemented with an FBS concentration of 2% (P = .0132), but not medium containing the higher serum supplement or the glucocorticoid (P greater than .05). Differences in the identification of a CMV viremia were observed by IPA, SV-IFA, and TC-CPE methodologies on a patient-to-patient basis, denoting the necessity of incorporating each methodology into the CMV screening panel. Demographic analysis of 82 AIDS patients showed a CMV viremia prevalence of 9% (2/28) in intravenous drug users, 57% (27/47) in homosexual patients, and 22% (2/9) in heterosexual and transfusion patients. Overnight (24 hr) storage of whole blood at 4 or 24 degrees C, respectively, reduced CMV recovery by 40% and 65%, when tested by TC-CPE.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Opportunistic Infections↗

PubMed1992

Intrathecal cholecystokinin octapeptide attenuates the antinociception and release of immunoreactive Met-enkephalin induced by intraventricular beta-endorphin in the rat.

The effects of cholecystokinin octapeptide (CCK8s) given intrathecally (i.t.) on antinociception and the release of immunoreactive Met-enkephalin in the spinal perfusate induced by intraventricular (i.vt.) injection of beta-endorphin were studied in anesthetized rats. beta-Endorphin (5 micrograms) given i.vt. inhibited the tail-flick response. The inhibition of the tail-flick response induced by beta-endorphin was blocked dose-dependently by CCK8s (0.1-7 micrograms) given i.t. The antagonistic effect of CCK8s on beta-endorphin-induced inhibition was blocked dose dependently by co-intrathecal injection of proglumide (3 and 10 micrograms), a CCK8s receptor antagonist. beta-Endorphin (5 micrograms) given i.vt. elicited a release of immunoreactive Met-enkephalin in the spinal perfusate. Repeated injections of the same dose of beta-endorphin released about the same amount of the immunoreactive Met-enkephalin in the spinal perfusate. CCK8s at concentrations from 1 x 10(-9) to 1 x 10(-6) M added into the spinal perfusate decreased the release of Met-enkephalin induced by beta-endorphin given i.vt. in a dose-dependent manner. The results suggest that CCK8s may attenuate beta-endorphin-induced inhibition of the tail-flick response by inhibiting the release of Met-enkephalin from the spinal cord.

Animals↗

PubMed1992

Forebrain sites differentially sensitive to beta-endorphin and morphine for analgesia and release of Met-enkephalin in the pentobarbital-anesthesized rat.

The mapping of the forebrain regions sensitive to beta-endorphin and morphine for antinociception was performed in pentobarbital-anesthetized rats. The antinociception was assessed by the tail-flick test. The sites most sensitive to beta-endorphin (2 micrograms) for inhibition of the tail-flick response were located in the ventromedial regions of the forebrain such as medial posterior nucleus accumbens, medial preoptic area and arcuate hypothalamic nucleus. Other areas such as anterior nucleus accumbens, dorsomedial hypothalamic nucleus, posterior hypothalamus, lateral hypothalamus, caudate nuclei, thalami and cerebral cortex were not sensitive to beta-endorphin for the tail-flick inhibition. The sites sensitive to morphine sulfate (4 micrograms) for inhibition of the tail-flick response were located in regions of medial preoptic nucleus and arcuate hypothalamic nucleus. Posterior nucleus accumbens, which is sensitive to beta-endorphin, was not sensitive to morphine for antinociception. Morphine injected into this site did not produce tail-flick inhibition in both conscious and pentobarbital-anesthetized rats. The inhibition of the tail-flick response induced by beta-endorphin (2 micrograms) from posterior nucleus accumbens, medial preoptic area and arcuate hypothalamic nucleus was blocked by the administration of beta-endorphin-(1-27), an epsilon opioid receptor blocker, but not by D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2, a mu opioid receptor blocker. On the other hand, the inhibition induced by morphine (4 micrograms) from medial preoptic area and arcuate hypothalamic nucleus was blocked by D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2, but not by beta-endorphin-(1-27).(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMed1992

Involvement of supraspinal epsilon and mu opioid receptors in inhibition of the tail-flick response induced by etorphine in the mouse.

Etorphine, a potent opioid agonist, has been reported to bind to both mu and epsilon opioid receptors. The present studies were designed to determine what types of opioid receptors and neurotransmitters for descending pain control systems were involved in antinociception induced by etorphine in mice. Morphine, a typical mu opioid receptor agonist, and beta-endorphin, an epsilon opioid receptor agonist, were used for comparison. Antinociceptive response induced by etorphine (20 ng) given i.c.v was blocked by i.c.v administration of D-Phe-Cys-Tyr-D-Tyr-Orn-Thr-Pen-Thr-NH2 (CTOP, 25 ng) and beta-endorphin-(1-27) [beta-EP-(1-27)] (6 micrograms), but not ICI 174,864 (ICI, 5 micrograms) or norbinaltorphimine (N-BNI, 5 micrograms). The antinociception induced by i.c.v. etorphine was also antagonized by the i.c.v. pretreatment of beta-funaltrexamine (beta-FNA, 50 ng, 24 hr). Intracerebroventricular administration of beta-EP-(1-27) (3 micrograms) caused a further attenuation of the i.c.v. etorphine-induced antinociception in mice pretreated with beta-FNA. The antinociceptive response induced by morphine (2 micrograms) given i.c.v. was blocked by i.c.v. administration of CTOP (25 ng) or beta-FNA (50 ng), but not beta-EP-(1-27) (6 micrograms), ICI (5 micrograms) or N-BNI (5 micrograms). These results indicate that the antinociception induced by etorphine given i.c.v. is mediated by the stimulation of both mu and epsilon opioid receptors whereas the antinociception induced by morphine given i.c.v. is mediated by the stimulation of mu, but not epsilon opioid receptors at supraspinal sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗

PubMed1992

Involvement of dynorphin A and not substance P in the spinal antianalgesic action of capsaicin against morphine-induced antinociception in mice.

In previous publications we proposed that dynorphin A (1-17) (Dyn) functions as an antianalgesic agent in the spinal cord of mice. Whether endogenously released or administered directly to the spinal cord, this antianalgesic action attenuates the antinociceptive effect of morphine (Mor) in the mouse tail-flick test. Because this action of Dyn in the spinal cord appeared to be congruous with the function of substance P (SP), experiments were designed to compare the actions of the two on Mor-induced antinociception. Inhibition of the tail-flick response induced by i.c.v. administration of Mor was attenuated by intrathecal (i.t.) administration of SP or Dyn. This antianalgesic effect of Dyn (5 fmol) but not SP (74 pmol) was antagonized by naloxone and nor-binaltorphimine administered i.t. Capsaicin (Cap) i.t. at a 0.1-microgram dose, like SP and Dyn, antagonized the antinociceptive effect of Mor given i.c.v. Excellent evidence exists to indicate that, in rats, Cap (30-70 micrograms i.t.) releases SP in the spinal cord and that Mor inhibits this release. Present experiments indicated, however, that i.t. administration of low doses of Cap (0.05-0.5 microgram) in mice preferentially released Dyn and not SP as based on the following results. 1) The antianalgesic action of Cap i.t. against Mor i.c.v. was antagonized by naloxone and nor-binaltorphimine i.t. as was Dyn i.t. (but not SP i.t.). 2) A SP antagonist, (D-Pro2, D-Phe7, D-Trp9)-SP, did not reverse the effect of Cap or Dyn given i.t., even though it antagonized the effect of SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMed1992

Cholecystokinin administered intrathecally selectively antagonizes intracerebroventricular beta-endorphin-induced tail-flick inhibition in the mouse.

The effects of sulfated cholecystokinin octapeptide (CCK8s) given intrathecally (i.t.) or intracerebroventricularly (i.c.v.) on inhibition of the tail-flick and paw-licking hot-plate responses induced by beta-endorphin, morphine, D-Ala2-N-Me-Phe4-Gly-ol-Enkephalin (DAMGO) and D-Pen2-D-Pen5-Enkephalin (DPDPE), given i.t. or i.c.v., were studied in male ICR mice. CCK8s (1 ng) given i.t. effectively antagonized inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin (2 micrograms) and DPDPE (10 micrograms) but not morphine (4 micrograms) or DAMGO (0.02 microgram). However, CCK8s given i.t. did not affect inhibition of the hot-plate response induced by any of the opioid agonists. CCK8s (0.2-40 ng) in combination with beta-endorphin (2 micrograms) or morphine (4 micrograms) given i.c.v. did not affect beta-endorphin- or morphine-induced inhibition of the tail-flick and hot-plate responses. CCK8s and its fragments given i.t. attenuated i.c.v. beta-endorphin-induced tail-flick inhibition with different potencies and efficacies. CCK8s was the most potent compound in antagonizing i.c.v. beta-endorphin-induced tail-flick inhibition. The rank order of potencies was CCK8s greater than CCK(27-33) much greater than caerulein. All three compounds were efficacious, whereas CCK(30-33) was not, in antagonizing beta-endorphin-induced tail-flick inhibition. Intrathecal administration of CCK8s (1 ng) significantly attenuated the tail-flick inhibition induced by i.t. beta-endorphin (0.5-1 microgram) and DPDPE (5 micrograms) but not morphine (0.5-1 microgram), DAMGO (5 ng), norepinephrine (5 ng) or serotonin (16 micrograms).(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMed1991

Involvement of epsilon and kappa opioid receptors in inhibition of the tail-flick response induced by bremazocine in the mouse.

Bremazocine, a benzomorphan, has been reported to have kappa, mu and epsilon opioid receptor binding activities. The present studies were then designed to determine what types of opioid receptors and neurotransmitters were involved in inhibiting the tail-flick response induced by bremazocine in male ICR mice. U50, 488H, a prototypic kappa agonist, was used for comparison. Bremazocine, at doses from 0.1 to 1 microgram given i.c.v., dose-dependently inhibited the tail-flick response. The paw-licking hot plate response, even at high doses of bremazocine, was not completely inhibited. The inhibition of the tail-flick response induced by bremazocine (1 microgram) given i.c.v. was blocked by i.c.v. coadministration of beta-endorphin-(1-27) (3 and 6 micrograms), an epsilon opioid receptor antagonist and norbinaltorphimine (4 micrograms), a kappa opioid receptor antagonist. On the other hand, the inhibition induced by i.c.v. U50,488H (40 micrograms) was blocked by i.c.v. norbinaltorphimine, but not beta-endorphin-(1-27). D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 (CTOP; 0.5 microgram) and beta-funaltrexamine (beta-FNA; 2.5 micrograms), selective mu opioid receptor antagonists, and ICI 174,864 (10 micrograms), a delta-opioid receptor antagonist, which blocked the effects induced by DAMGO (16 ng) and DPDPE (20 micrograms), respectively, did not block inhibition of the tail-flick response induced by bremazocine (1 microgram) given i.c.v. The inhibition of the tail-flick response induced by i.t. administration of bremazocine (1 microgram) was blocked by i.t. coadministration of norbinaltorphimine but not CTOP, ICI 174,864, or beta-endorphin-(1-27).(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗