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Biomedical subjects

Z S Herman

Publications and source records attributed to Z S Herman.

At least 73 records · Page 4Linked to original sources
PubMed1983

The effect of a single temazepam administration on enkephalin content in the striatum and hypothalamus of the rat.

Temazepam, a benzodiazepine ataractic, given in a dose of 10 mg/kg ip to rats depressed the striatal contents of met-enkephalin and leu-enkephalin by 60 and 35% resp. The changes were most pronounced 30 min after the treatment. In the hypothalamus temazepam produced a short-lasting elevation of met-enkephalin content (225% of the control value). The pattern of changes produced by temazepam resembles that described for diazepam. This suggests that enkephalins participate in the pharmacological effects of benzodiazepine ataractics on the central nervous system.

Animals↗
PubMed1983

Effect of prostaglandins on chloropromazine induced catalepsy in mice.

The effect of prostaglandins (PGs) F1 alpha, F2 alpha, E2, D2, A1, B1 and I2 administered intracerebroventricularly (i.c.v.) in mice in a dose of 1 microgram on catalepsy induced by chloropromazine (2.5 mg/kg i.p.) was examined. It was demonstrated that only PGF2 alpha reduced significantly the chloropromazine induced catalepsy, while PGI2 intensified it. The other examined PGs were without any effect on chlorpromazine catalepsy. The results show the modifying role of some PGs on chloropromazine effects on central dopaminergic receptors in mice.

Animals↗
PubMed1982

Reliability of the pair-defect-sum approximation for the strength of valence-bond orbitals.

The pair-defect-sum approximation to the bond strength of a hybrid orbital (angular wave functions only) is compared to the rigorous value as a function of bond angle for seven types of bonding situations, with between three and eight bond directions equivalent by geometrical symmetry operations and with only one independent bond angle. The approximation is seen to be an excellent one in all cases, and the results provide a rationale for the application of this approximation to a variety of problems.

Journal Article↗
PubMed1981

To the problem of biologically active conformation of enkephalin.

A semi-rigid structural analog of [Leu5] enkephalin, possessing the azo-bridge between Tyr1 and Phe4 residues, was synthesized, along with two other linear enkephalin analogs: [4'-amino Phe4] enkephalin and [4'/hydroxyphenyl/-azo Phe4] enkephalin. The results of the determination of the analgesic activity of the synthesized compounds suggest that the biologically active conformation of the enkephalin molecule should be such that both aromatic rings, Tyr1 and Phe4, are situated in close proximity.

Analgesics↗
PubMed1981

Tuftsin and D-Arg3-tuftsin possess analgesic action.

Tuftsin has marked analgesic activity but is less potent than D-Arg3-tuftsin. The absence of an antagonistic effect of naloxone on tuftsin and its analogue suggests that these substances do not act on opiate receptors. Tuftsin and its analogues may represent a new class of substances of interest in the search for new analgesics.

Analgesics↗
PubMed1981

Studies on the behavioral and hypotensive effects of intraventricular prostacyclin (PGI2) in rats.

Intraventricular injection of prostacyclin (PGI2) slightly depressed the general behavior and produced a weak hypothermia in rats. It shortened the response to a thermal nociceptive stimulus and intensified catalepsy caused by chloropromazine and haloperidol. PGI2 did not change concentration of noradrenaline, 4-hydroxytryptamine, 5-hydroxyindoleacetic acid and dopamine in different brain areas. It markedly lowered blood pressure and increased respiration. The duration of central hypotensive effect of PGI2 was shortened after 6-hydroxydopamine on 5,6-dihydroxytryptamine pretreatment. The possible involvement of a central mechanism in the hypotensive action of PGI2 requires further clarification.

Animals↗
PubMed1981

Enhanced responses to muscarine in rats treated chronically with atropine.

Rats were treated for 14 or 30 days with 10 mg/kg sc atropine (AT) daily. 24 h after the last dose of At, 50 micrograms of muscarine (MU) was injected intracerebroventricularly (ivtr.). Long-term atropinization enhanced the behavior induced by MU. These data support our previous suggestion that chronic blockade of central muscarinic receptors induces their hypersensitivity.

Animals↗
PubMed1981

Effects of cholinomimetics, cholinolytics and atypical antidepressants in the behavioral despair test in the rat.

The effect of some cholinolytics, cholinomimetics and atypical antidepressants on behavior of rats forced to swim (in the "behavioral despair test") was investigated. In addition, the relation between the test performance and the inborn level of exploratory and locomotor activities was studied. Cholinomimetics prolonged, while cholinolytics and antidepressants shortened the immobility phase ("despair reaction"). The "despair reaction" was less pronounced in rats with high motor exploratory activity level.

Animals↗
PubMed1979

Mediation of central prostaglandin effects by serotoninergic neurons.

Ten days after administration of 5,6-dihydroxytryptamine, which causes degeneration of central serotoninergic neurons, the depressive behavioral effects of PGF2 alpha and PGE2 were evidently inhibited. Central chemical serotoninectomy abolished the hyperthermic and hypertensive effects of PGF2 alpha, but only slightly affected those of PGE2. It is concluded that serotoninergic neurons mediate the depressive behavioral action of both PGF2 alpha and PGE2. They also mediate the hyperthermic and hypertensive action of PGF2 alpha but not of PGE2. This suggests that these prostaglandins have different central modes of action.

5,6-Dihydroxytryptamine↗
PubMed1979

Central cholinergic receptor supersensitivity after long-term atropine administration.

Rats were treated with a single dose of atropine (AT) at 5 mg/kg, or every day for 14 or 31 days with the same dose of AT, 3 h after the single dose and 24 h after the last dose of chronically administered AT, 10 micrograms of ACh was injected intracerebroventricularly, and two tests were used to examine the behavior of the animals. The tremorigenic effect of oxotremorine was also measured in mice treated with 10 mg/kg of AT for 1 month. It was shown that a single dose of AT antagonized ACh-induced behavior. The long-term treatment with AT enhanced the depressive-behavior of ACh in rats and the tremorigenic effect of oxotremorine in mice. The results suggest that long-term blockade of central cholinergic receptors induces their hypersensitivity.

Acetylcholine↗