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Biomedical subjects

L F Tseng

Publications and source records attributed to L F Tseng.

At least 19 recordsLinked to original sources
PubMed1979

Behavioral activities of opioid peptides and morphine sulfate in golden hamsters and rats.

The behavioral effects of beta-endorphin, [D-Ala2, D-Leu5]-enkephalin and morphine were investigated in golden hamsters and in rats. In golden hamsters, beta-endorphin and [D-Ala2, D-Leu5]-enkephalin induced loss of righting reflex, whereas morphine caused no such effect. Both opiate peptides and morphine caused the inhibition of tail-flick response and catalepsy in rats. beta-Endorphin was the most potent, followed by [D-Ala2, D-Leu5]-enkephalin and then by morphine. The catalepsy induced in rats by [D-Ala2, D-Leu5]-enkephalin was different from that of beta-endorphin and morphine in that it produced catalepsy without muscular rigidity. beta-Endorphin and [D-Ala2, D-Leu5]-enkephalin caused hypothermia in golden hamsters; morphine was less active in altering the body temperature. beta-Endorphin caused hypothermia at high doses and hyperthermia at low doses in rats. These heterogenous behavioral responses indicate that multiple types of receptors mediate the effects of opiates in the central nervous system.

Animals↗
PubMed1979

beta-Endorphin: synthesis of analogs modified at the carboxyl terminus with increased activites.

Three analogs of human beta-endorphin (beta h-EP) have been synthesized: [Gly31]beta h-EP, [Gly31]beta h-endorphinamide, and [Gly31]beta h-endorphinylglycine. All are more active than beta h-EP in both the guinea pig ileum bioassay and the opiate receptor binding assay. The last two analogs are about twice as active as beta h-EP in an assay for analgesia. Modification at position 31 and extension at the COOH terminus may afford a route toward analogs with even greater biological activity.

Analgesics↗
PubMed1979

Hydroxytryptamine uptake inhibitors block para- methoxyamphetamine-induced 5-HT release.

1 Activation of mycolonic twitch activity (MTA) of suprahyoideal muscle after p-methoxyamphetamine (PMA) administration in rats anaesthetized with urethane has previously been reported to be due to brain 5-hydroxytryptamine (5-HT) release. Increased MTA caused by PMA was blocked by chlorimipramine (0.1 to 1 mg/kg) and fluoxetine (0.3 to 3 mg/kg) but not by desipramine (3 mg/kg). 2 The 5-hydroxytryptophan-induced increase of MTA of suprahyoideal muscle in rats pretreated with pargyline was not blocked by chlorimipramine but was blocked by methysergide. 3 [3H]-5-HT was injected intraventricularly 30 min before the beginning of ventricular perfusion with artificial cerebrospinal fluid in urethane anaesthetized rats. PMA (mg/kg i.v.) increased the release of [3H]-5-HT in the perfusate after injection. Chlorimipramine (0.1 to 1 mg/kg) and fluoxetine (0.1 to 1 mg/kg), injected 10 min before the PMA injection, caused a dose-related blockade of the increased release of [3H]-5-HT induced by PMA. Desipramine at 3 mg/kg slightly inhibited the increased release of [3H]-5-HT caused by PMA but was inactive at 1 mg/kg. 4 It is proposed that these 5-HT uptake inhibitors block the increased MTA caused by PMA by preventing the PMA-induced release of 5-HT in the central nervous system.

Amphetamines↗
PubMed1978

Effects of para-methoxyamphetamine and 2,5-dimethoxyamphetamine on serotonergic mechanisms.

A comparison of serotonergic effects of (+/-)-para-methoxyamphetamine (PMA) and (+/-)-2,5-dimethoxyamphetamine (2,5-DMA) was studied in rats. The activation of myoclonic twitch activity (MTA) of suprahyoideal muscle in urethane-anesthetized rats has been reported previously to involve central serotonergic and dopaminergic mechanisms. PMA (0.1--3.2 mg/kg i.v.) and 2,5-DMA (2--16 mg/kg i.v.) increased the MTA. The increased MTA caused by both PMA and 2,5-DMA was blocked by a 5-HT receptor blocker, methysergide, indicating that a serotonergic mechanism was involved. The increased MTA induced by PMA was reduced by a 5-HT synthesis inhibitor, para-chlorphenylalanine, (pCPA), and by a 5-HT uptake inhibitor, chlorimipramine. On the other hand, the increased MTA induced by 2,5-DMA was not blocked by pCPA or chlorimipramine. Using a ventricular perfusion technique in urethane-anesthetized rats, PMA (1.6 mg/kg) effectively increased the release of 3H-radioactivity from brain preloaded with 3H-5-HT before the initiation of perfusion whereas 2,5-DMA (16 mg/kg) decreased the release of 3H-radioactivity. Analysis of the perfusate by thin layer chromatography for 3H-5-HT and 3H-5-HIAA revealed an increased release of unchanged 3H-5-HT in the perfusate after the injection of PMA. The ratio of 3H-5-HT to 3H-5-HIAA was markedly increased after PMA but no alteration of this ratio was observed after 2,5-DMA. It is concluded that PMA elicits its pharmacological action indirectly by releasing 5-HT while 2,5-DMA acts directly on 5-HT receptors.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1978

beta-endorphin: synthesis and biological activity of shortened peptide chains.

Three analogs of beta-endorphin have been synthesized by the solid-phase method: betac-endorphin-(1--5)-(28--31), betac-endorphin-(6--31) and betah-endorphin-(1--5)-(16--31). The analgesic activities of these synthetic peptides relative to that of the parent molecule are reported. All three peptides at high doses exhibit either no or much weaker analgesic activity than beta-endorphin. These data suggest that the entire beta-endorphin molecule is necessary for full in vivo analgesic activity.

Amino Acid Sequence↗
PubMed1978

beta-Endorphin: synthesis and analgesic activity of several analogs modified in positions 2 and 5.

The solid-phase syntheses of [Sar2]-, [Ala2]-, [D-Leu2]-, [D-Lys2]-beta-endorphins and [Pro5]-, [Leu5]-, [D-Leu5]-, [D-Ala2, D-Leu5]-beta-endorphins are described. The synthetic peptides were purified by chromatography on carboxymethylcellulose and partition chromatography on Sephadex G-50. They were characterized by partition chromatography on agarose, thin-layer chromatography, paper electrophoresis, and amino acid analyses of acid and enzymic hydrolysates. Bioassay of the synthetic analogs for analgesic activity by the tail-flick method showed the D-Leu2 analog to be 48% as potent as betah-endorphin while the Ala2, D-Lys2, Leu5, and [D-Ala2, D-Leu5] analogs were 8 to 17% as active. The Sar2, D-Leu5, and Pro5 analogs were less than 1% as potent.

Amino Acid Sequence↗
PubMed1978

betah-endorphin: antidiuretic effects in rats.

Human beta-endorphin (betah-EP) inhibits urine flow in rats. This antidiuretic effect of the peptide occurs after intravenous and intraventricular injections. Intravenously, betah-EP is 24 times more potent than morphine. Intraventricularly, betah-EP is 24 times more potent than morphine. Intraventricularly, betah-EP is effective at doses (0.45 microgram) which have no antidiuretic activity when injected intravenously. This fact suggests that one site of the antidiuretic action of betah-endorphin may be in the central nervous system. Animals tolerant to morphine are also tolerant to the antidiuretic effects of betah-endorphin.

Animals↗
PubMed1977

Effects of withdrawal from chronic amphetamine intoxication on exploratory and stereotyped behaviors in the rat.

Rats were administered 3, 6, and 12 mg/kg of d-amphetamine s.c. twice daily on a weekly increasing staircase schedule. On days 1, 7, 14, and 28 after the last injection of amphetamine the animals were challenged with 1 and 3 mg/kg of d-amphetamine and their behavior was observed. The 7-, 14-, and 28-day withdrawn animals required less amphetamine than controls to induce stereotyped behaviors. However, it was found that withdrawn animals and control animals were equally sensitive to the effects of apomorphine. Reserpine pretreatment eliminated the differences between control and withdrawn animals. alpha-Methyl tyrosine pretreatment blocked the effects of 1 but not 3 mg/kg of d-amphetamine in the withdrawn animals. Possible chemical mechanisms underlying the change in amphetamine sensitivity in the withdrawn animals are discussed.

Animals↗