PubMed Health⌕ Search

Biomedical subjects

L F Tseng

Publications and source records attributed to L F Tseng.

At least 127 records · Page 7Linked to original sources
PubMed1985

Release of immunoreactive Met-enkephalin from the spinal cord by intraventricular beta-endorphin but not morphine in anesthetized rats.

Effect of beta-endorphin and morphine injected intraventricularly on the release of immunoreactive Met-enkephalin, Leu-enkephalin and dynorphin1-13 from the spinal cord was studied in anesthetized rats. Intraventricular beta-endorphin, 16 micrograms, caused a marked spinal release of immunoreactive Met-enkephalin and to a much lesser extent, of immunoreactive Leu-enkephalin while intraventricular morphine, 40 micrograms, did not cause any significant release of immunoreactive enkephalins. The release of immunoreactive Met-enkephalin was not blocked by the pretreatment with 5 mg/kg naloxone, i.p. Immunoreactive dynorphin1-13 was not released by either beta-endorphin or morphine. High performance liquid chromatographic analysis indicated that immunoreactive Met-enkephalin released by beta-endorphin had a retention time identical to [3H]Met-enkephalin. These findings in conjunction with previous pharmacological studies suggest different modes of pharmacological action for beta-endorphin and morphine.

Animals↗
PubMed1985

Does nitrous oxide induce release of brain opioid peptides?

Increased concentrations of immunoreactive methionine-enkephalin but not leucine-enkephalin were measured in fractions of cerebrospinal fluid perfusate collected from ventricular-cisternally perfused, urethane-anesthetized rats exposed to a mixture of 75% nitrous oxide/25% oxygen for 60 min. These findings suggest that nitrous oxide might be capable of inducing the release of methionine-enkephalin in the central nervous system.

Animals↗
PubMed1985

Differential actions of intrathecal naloxone on blocking the tail-flick inhibition induced by intraventricular beta-endorphin and morphine in rats.

In the present study, it is proposed that the opioids applied to supraspinal brain sites produced their analgesic effects by the activation of different descending pain inhibitory systems. The blockade of the spinal endorphinergic system by intrathecal naloxone on the production of tail-flick inhibition induced by intraventricular beta-endorphin and morphine was then studied. Intraventricular injection of beta-endorphin and morphine produced an inhibition of the tail-flick response to the heat stimulus in rats. Intrathecal injection of naloxone at doses of 0.4 to 40 micrograms caused a dose-related blockade of the inhibition of the tail-flick response induced by intraventricular injection of beta-endorphin, and a high dose of naloxone (40 micrograms) completely blocked the tail-flick inhibition induced by intraventricular beta-endorphin (16 micrograms). On the other hand, intrathecal naloxone (12-120 micrograms) had only a very weak effect on the tail-flick inhibition induced by intraventricular morphine (40 micrograms). Intraventricular injection of naloxone at doses of 1.2 to 12 micrograms equally antagonized in a dose-dependent manner the tail-flick inhibition induced by intraventricular beta-endorphin and morphine. The results indicate that a spinal naloxone-sensitive endorphinergic system is involved in the production of beta-endorphin but not morphine-induced tail-flick inhibition, and suggest that intraventricular beta-endorphin and morphine elicit their pharmacological actions via the activation of different descending pain inhibitory systems; descending epsilon and mu systems for beta-endorphin and morphine, respectively, are proposed.

Analgesia↗
PubMed1984

Evidence that spinal endorphin mediates intraventricular beta-endorphin-induced tail flick inhibition and catalepsy.

Naloxone injected intrathecally had a different effect on the inhibition of the inhibition of the tail flick response produced by beta-endorphin and morphine injected intraventricularly. The intrathecal naloxone completely antagonized the effect of beta-endorphin but had only a very weak effect on morphine. In the same rats the cataleptic response to beta-endorphin was antagonized as well; however no definitive conclusion could be made regarding the antagonism of the morphine-induced catalepsy. The results indicate that spinal endorphin is involved in the production of intraventricular beta-endorphin-induced spinal tail flick inhibition and suggest that intraventricular beta-endorphin and morphine elicit their pharmacological action via the activation of different descending inhibitory systems.

Animals↗
PubMed1984

Dynorphin-(1-13)-like immunoreactivity in central nervous system and pituitary gland of spontaneously hypertensive rats.

We determined by radioimmunoassay concentration of dynorphin-(1-13)-like immunoreactivity in the central nervous system and pituitary gland of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs). Compared to WKYs, SHRs had significantly lower levels of dynorphin-(1-13)-like immunoreactivity in the hypothalamus and pituitary gland. However, such immunoreactivity in the cerebral cortex, caudate nucleus, diencephalon, brainstem and spinal cord of SHRs and WKYs were similar.

Animals↗
PubMed1983

Partial cross tolerance to D-Ala2-D-Leu5-enkephalin after chronic spinal morphine infusion.

The development of tolerance to morphine and cross tolerance to D-Ala2-D-Leu5-enkephalin (DADL) at spinal cord level to the inhibition of tail flick response was studied in rats tolerant to morphine. The long term intrathecal infusion of morphine sulfate was accomplished by means of an osmotic minipump. Intrathecal infusion of morphine sulfate (2 micrograms/hr) markedly elevated the tail flick latency measured 24 hr after the start of infusion. The increased tail flick latencies gradually decreased during 6 days of intrathecal infusion of morphine sulfate. Tolerance to morphine and DADL was determined by inhibition to the tail flick response after intrathecal administration of cumulative doses of morphine sulfate and DADL. Chronic intrathecal infusion of morphine induced a marked tolerance to morphine but developed only a slight cross tolerance to DADL. The results indicate that there exists two separate types of opioid receptor, mu- and delta-opioid receptor in the spinal cord of rats.

Animals↗
PubMed1983

Synthesis and properties of beta h-endorphin analogs containing the dynorphin-(1-13) sequence.

Two analogs of beta h-endorphin containing dynorphin-(5-13) or dynorphin-(6-13) sequence have been synthesized by the solid-phase method. Biological activities of the analogs have also been investigated. It was found that the opiate activity is about three times more than beta h-endorphin in the guinea pig ileum assay. Both analgesic potency and opiate receptor-binding activity of the analogs are lower when compared with beta h-endorphin. However, the analogs have interesting behavioral effects in mice.

Analgesics↗
PubMed1983

Inhibition of tail-flick and shaking responses by intrathecal and intraventricular D-Ala2-D-Leu5-enkephalin and beta-endorphin in anesthetized rats.

The present study compares the potencies of D-Ala2-D-Leu5-enkephalin (DADL) and beta-endorphin (beta-EP) injection intrathecally and i.c.v. on the inhibition of tail-flick and ice water-induced shaking responses in pentobarbital-anesthetized rats. Peptides were injected stereotaxically into the third ventricle or into the spinal subarachnoid space. The tail-flick response was measured 10 or 20 min after the injection of DADL or beta-EP, respectively, after which the rats were immersed for 5 min in ice water and the number of shakes was counted. Intrathecal DADL and beta-EP were equipotent in inhibiting both the tail-flick and shaking responses. However, treatment with naloxone (2 mg/kg i.p.) shifted the dose-response curve for both responses to the right more for the beta-EP than for DADL. Unlike the equipotency intrathecally, DADL by i.c.v. injection was less potent than beta-EP in inhibiting both the tail-flick and shaking responses. Previous results in the unanesthetized rat had also shown that i.c.v. DADL was less potent than beta-EP in inhibiting the tail-flick response. Thus, the spinal cord is sensitive to both DADL and beta-EP, whereas the supraspinal area is more sensitive to beta-EP. Also, because the potency of i.c.v. beta-EP for inhibiting tail-flick but not shaking was substantially reduced in anesthetized compared to unanesthetized rats, the neuronal substrates involved in inhibition of shaking are different from those of inhibition of the tail-flick. The differential sensitivities to i.c.v. vs. intrathecal administration and the unequal responses to the antagonistic action of naloxone indicate that DADL and beta-EP produce their action through different opioid receptors.

Analgesics↗
PubMed1982

Tolerance and cross tolerance to morphine after chronic spinal D-Ala2-D-Leu5-enkephalin infusion.

The development of tolerance and cross tolerance to morphine at spinal cord levels on the tall flick inhibition was studied in rats tolerant to D-Ala2-D-Leu5-enkephalin (DADL). The long term intrathecal infusion of DADL was accomplished by means of osmotic minipumps. Chronic intrathecal infusion of DADL for 5 days caused a shift of dose response curves of both DADL and morphine sulfate injected intrathecally to the right indicating that tolerance and cross tolerance to morphine had developed after long term intrathecal infusion of DADL. The shift of the dose response curve of DADL was parallel, whereas that of morphine was non-parallel and flattening. Concomitant intrathecal infusion of naloxone which was more sensitive in blocking mu-opioid receptor than delta-opioid receptor blocked the development of cross tolerance to morphine while the development of tolerance to DADL was left unaffected. The studies present the evidence that two types of opioid receptors, delta- and mu-opioid in the spinal cord of rats are involved in the development of tolerance by chronic DADL exposure.

Animals↗
PubMed1982

Cross tolerance to etorphine in rats tolerant to morphine-induced antidiuresis.

Previously in the analgesic tail flick assay, mice and rats implanted with morphine pellets were shown to be highly tolerant to subcutaneously administered morphine but not to etorphine. The present purpose was to see whether the same differential response would be found to the antidiuretic response of morphine and etorphine in water-loaded rats because the presence of such a differential response would be value in studying mechanisms of tolerance. Etorphine injected subcutaneously was about 1000x more potent than morphine in producing an antidiuretic response. Following chronic administration of morphine by pellet implantation, where the pellets remained in place during the drug challenge, profound tolerance developed to the antidiuretic effect of both morphine and etorphine. The dose-response curves for both were shifted to the right in non-parallel fashion with decreased slopes and antidiuretic efficacies. The large degree of tolerance developed to the antidiuretic effect of etorphine in morphine pellet implanted rats in contrast to the lack of development of tolerance to etorphine in the tail flick assay indicated that different mechanisms of development of tolerance exist for the two responses.

Animals↗
PubMed1981

Effects of beta-endorphin on body temperature in mice at different ambient temperatures.

The effect of intracerebroventricular injection of beta-endorphin (beta-END) on body temperature of mice was studied at ambient temperatures (Ta) of 10 degrees, 20 degrees and 31 degrees C. Doses between 0.1 and 10.0 microgram/mouse were studied. The lower (less than 1 microgram) doses of beta-END produced a hyperthermia at all Ta's studied. The higher doses of beta-END produced hyper- or hypothermia depending on the Ta. The subcutaneous injection of naloxone (1 mg/kg) antagonized the high dose hypothermic effects, but not the hyperthermic effect of beta-END. These data suggest that there may be different receptors and/or sites of action for high and low doses of beta-END.

Animals↗
PubMed1981

Human beta-endorphin: synthesis and biological activity of analogs with substitutions in positions 2, 9, 18, 27 and 31.

Four analogs of the opioid peptide human beta-endorphin (Bh-EP) have been synthesized: [D-Lys9, Phe27, Gly31]-beta h-EP, [D-PHe18,Phe27,Gly31]-beta h-EP, [D-Thr2,D-Lys9,Phe27,Gly31]-beta h-EP, and [D-Thr2,D-Phe18,Phe27,Gly31]-beta h-EP. All are practically indistinguishable from beta h-EP in the guinea pig ileum assay. All show diminished analgesic potency in the mouse tail-flick assay.

Amino Acid Sequence↗
PubMed1981

beta-Endorphin: isolation, amino acid sequence and synthesis of the hormone from horse pituitary glands.

Beta-endorphin has been isolated from equine pituitaries. Its amino acid sequence is identical to that of ovine, bovine and camel beta-endorphins except for substitution of the threonine residue at position 6 by serine. The equine beta-endorphin has also been synthesized by the solid-phase method. In comparison with the human hormone, equine beta-endorphin was shown to possess 3 times the receptor-binding activity in rat membrane preparations and 1.6 times the analgesic potency in the mouse tail-flick assay.

Amino Acid Sequence↗
PubMed1981

Effect of intraventricular beta-endorphin and morphine on hypothalamic-pituitary-adrenal activity and the release of pituitary beta-endorphin.

The effects of intraventricular (i.v.t.) morphine sulfate (MS) and beta-endorphin (beta-EP) on pituitary-adrenal activity and the release of pituitary beta-EP were studied in rats. Pituitary-adrenal activity was monitored by measuring plasma corticosterone (CS) levels. 45 min after i.v.t. injection, both MS and beta-EP caused dose-related increases in plasma CS, with beta-EP being approximately ten times more potent on a molar basis. MS injected i.v.t. at 0.3, 1.0, 3.0 and 10.0 microgram did not cause a significant reduction in pituitary immunoreactive (i.r.) beta-EP, but did cause an increase in plasma i.r. beta-EP at 3 microgram of MS. beta-EP injected i.v.t. at 1.5 microgram caused a reduction of pituitary i.r. beta-EP. Since i.v.t.-injected beta-EP may have contributed to the measured plasma i.r. beta-EP, a nonimmunoreactive analog (Des-Asn20-beta c-EP) was used to assess the change in plasma i.r. beta-EP. 5 microgram of DES-Asn20-beta c-EP injected i.v.t. caused increases in plasma i.r. beta-EP and CS, as well as a 40% reduction in pituitary i.r. beta-EP. The concomitant intraperitoneal (i.p.) injection of naloxone HCl (10 mg/kg) significantly blocked the increase in plasma CS induced by 5 microgram of beta-EP. When naloxone HCl, 10 mg/kg was injected alone, a significant increase in plasma CS was found. The results indicate that i.v.t. beta-EP is more potent than MS in causing the release of pituitary ACTH and beta-EP. These findings are consistent with a role for brain endorphins in the regulation of CRF release.

Animals↗