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Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 127 records · Page 7Linked to original sources
PubMed1988

Endogenous oxytocin inhibits morphine tolerance through limbic forebrain oxytocin receptors.

It has previously been shown that endogenous oxytocin (OXT) inhibits the development of acute morphine tolerance. The role of OXT receptors in the central nervous system (CNS) was therefore studied by using a specific OXT receptor antagonist, N-acetyl-(2-O-methyltyrosin)-OXT (ACME-OXT). ACME-OXT (1 pg) was injected into the posterior olfactory nucleus, central amygdaloid nucleus, ventral hippocampus, caudate nucleus or lateral cerebral ventricle. The antagonist facilitated the development of tolerance to morphine when injected into the posterior olfactory nucleus, central amygdaloid nucleus or ventral hippocampal areas, which are known to contain OXT binding sites. When administered into the caudate nucleus (with no OXT binding sites) or the lateral cerebral ventricle, it had no effect on morphine tolerance. Our results suggest that the limbic forebrain OXT receptors play an important inhibitory role in adaptive responses to morphine.

Animals↗
PubMed1988

Effects of somatostatin on self-stimulation behaviour in rats pretreated with a receptor blocker.

The effects of somatostatin on lateral hypothalamic self-stimulation were investigated in rats pretreated with haloperidol, bicuculline, phenoxybenzamine or propranolol. Somatostatin decreased the rate of self-stimulation. Halperidol, bicuculline and phenoxybenzamine potentiated the somatostatin-induced depression of self-stimulation behaviour. Propranolol had no effect. It is suggested that dopaminergic, GABAergic and noradrenergic systems are involved in the somatostatin-induced depression of self-stimulation.

Animals↗
PubMed1988

The effects of somatostatin on the arachidonate cascade of platelets.

Somatostatin (10(-9) M) significantly elevated the synthesis of thromboxane B2 in rat platelets. The transformation of arachidonic acid to active lipoxygenase metabolites was suppressed by somatostatin (10(-9) and 10(-8) M). The ratio of the lipoxygenase/cyclooxygenase products was significantly reduced by the polypeptide (10(-9) and 10(-8) M) in rat platelets. Higher concentrations (10(-7), 10(-6) and 10(-5) M) of somatostatin did not modify the lipoxygenase pathway of the platelets. The synthesis of the vasoconstrictor - proaggregatory cyclooxygenase products was stimulated by the polypeptide (10(-9) and 10(-8) M), while the formation of vasodilatator - antiaggregatory cyclooxygenase metabolites was induced by higher concentrations of somatostatin (10(-7) and 10(-6) M). Somatostatin might act on the deacylation process of phospholipids, reducing the free arachidonic acid substrate level, resulting in a lower lipoxygenation rate in the platelets, which could be responsible for the increased formation of thromboxane. The contradictory results reported by others concerning the action of somatostatin on the platelet function might be explained by our results that the effect of somatostatin depends on the applied dose.

Animals↗
PubMed1988

Effects of receptor blockers on ACTH-induced changes in extinction of active avoidance reflex in rat.

The actions of blockers of dopaminergic receptors (haloperidol), alpha-receptors (phenoxybenzamine), beta-receptors (propranolol) and muscarinic cholinergic receptor (atropine) on the ACTH-induced delay of the extinction of active avoidance behavior were studied in rats. In the doses used, none of the receptor blockers modified the extinction of active avoidance behavior. ACTH delayed the extinction. However, the dopamine receptor blocker (haloperidol) and the muscarinic cholinergic receptor blocker (atropine) did prevent the action of ACTH in delaying the extinction of active avoidance behavior, whereas the alpha-(phenoxybenzamine) and beta- (propranolol) receptor blockers were ineffective. The results suggest that mainly dopaminergic and cholinergic mediations are involved in the delaying action of ACTH on the extinction of active avoidance behavior.

Adrenocorticotropic Hormone↗
PubMed1988

Antiamnesic effects of D-pipecolic acid and analogues of Pro-Leu-Gly-NH2 in rats.

The antiamnesic effects of prolyl-leucyl-glycinamide (PLG) and analogues of this tripeptide were investigated in rats. Retrograde amnesia was induced by electroconvulsive shock treatment and the degree of amnesia was characterized by the attenuation of one-trial learning passive avoidance response. PLG resulted in dose-dependent attenuation of retrograde amnesia. Structural modifications included N-terminal protection, substitution of the C-terminal NH2 group, replacement of the N-terminal amino acid, and replacement of the second amino acid of the tripeptide. Some tripeptides, all of them containing D-pipecolic acid instead of the N-terminal proline, were more effective than PLG. Therefore, D-pipecolic acid, D-pipecolamide and their N-terminally protected analogues were also investigated, and were found to have powerful antiamnesic effects.

Amnesia↗
PubMed1988

Effects of cholecystokinin-related peptides on self-stimulation behaviour in rats.

The effects of cholecystokinin octapeptide sulfate ester (CCK-8-SE), its N-terminal tripeptide (CCK-2-4-SE) and its C-terminal tetrapeptide (CCK-5-8) were investigated on hypothalamic self-stimulation in rats. CCK-8-SE and CCK-5-8 in 400 pmole doses inhibited self-stimulation behaviour, while CCK-2-4-SE was ineffective. In 80 pmole doses the peptides showed no effect. It is suggested that CCK-5-8 itself influences self-stimulation behaviour.

Animals↗
PubMed1988

Hypothalamo-neurohypophyseal neuropeptides and experimental drug addiction.

Oxytocin, a hypothalamo-neurohypophyseal neuropeptide was found to attenuate the development of tolerance to the analgesic action of morphine, heroin, beta-endorphin or D-Pro2-Met5-enkephalinamide. The effect of oxytocin on morphine tolerance was prevented by N alpha-acetyl-(2-0-methyltyrosine)-oxytocin or penicillamine1-(2-0-methyltyrosine)-lysine8-vasopressin, which are antagonists of oxytocin receptors. Oxytocin dose-dependently attenuated various signs of precipitated morphine withdrawal (e.g., stereotyped jumpings, hypothermia, body weight loss). The neuropeptide diminished intravenous self-administration of heroin in heroin-tolerant rats. It is concluded that brain oxytocin interferes with adaptive components of experimental drug addiction.

Animals↗
PubMed1988

The effect of atrial natriuretic factor on arginine-8-vasopressin and oxytocin levels in various brain regions and plasma.

The effect of intracerebroventricular (i.c.v.) treatment of rat atrial natriuretic factor III (ANF III; 0.5 microgram) was measured on the arginine-8-vasopressin (AVP) and oxytocin (OXT) contents of rat hypothalamic and limbic brain areas as well as those in the plasma. The hormone concentrations were determined by radioimmunoassay (RIA). The administration of ANF III in conscious euhydrated rats resulted in a significant reduction of both AVP and OXT contents in the hippocampus. Ether anesthesia interfered with the effect of ANF III, since in anesthetized rats ANF III reduced the levels of AVP and OXT in the septal regions, too. ANF III had no effect on the basal plasma AVP and OXT concentrations, however, the peptide inhibited the plasma AVP and OXT elevation induced by hyperosmosis (intraperitoneal injection of 2.5% NaCl). The results suggest that ANF III may be important in the control of the activity of both the peripheral (hypothalamo-neurohypophyseal) and the central (brain) AVP-ergic and OXT-ergic systems.

Animals↗
PubMed1988

Effects of neurohypophyseal hormones on food-reinforced classical conditioning in the rat.

The effects of different doses of lysine vasopressin (LVP) and oxytocin (OXT) were studied on the six-day acquisition or extinction of a food-reinforced classical conditioning reflex (conditional stimulus: light) when intraperitoneal (ip.) injections were carried out 20 min prior to the behavioural sessions. The highest (600 mU/kg) dose of LVP inhibited acquisition, and all LVP doses tested (150, 300 and 600 mU/kg) facilitated the extinction of conditioned behaviour. These same mU doses of OXT did not significantly affect the food-reinforced conditioning, although a consequent tendency towards increased performance (the opposite action to vasopressin) was observed. When 2.5 or 25 micrograms/kg doses of desglycinamide-arginine-vasopressin (DGAVP), a 500 micrograms/kg dose of prolyl-leucyl-glycinamide (PLG) or a 1200 mU/kg dose of OXT was injected during the extinction sessions, 2.5 micrograms/kg DGAVP and 1200 mU/kg OXT significantly facilitated extinction; the other treatments were without effect. LVP in a dose of 300 or 600 mU/kg and OXT in a dose of 300, 600 or 1200 mU/kg did not influence the food intake of 22 h food-deprived rats in a nonconditional situation. The present results indicate that the effects of LVP and OXT on memory display reinforcement-dependent characteristics, and are thus indirect or non-specific in nature.

Animals↗
PubMed1988

The effects of different receptor blockers on the H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH induced inhibition of extinction of active avoidance behaviour.

H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH after intracerebroventricular (icv.) administration inhibited the extinction of active avoidance behaviour for a short period. The dopamine receptor blocker haloperidol completely blocked this effect of the heptapeptide, while the muscarinic anticholinergic agent atropine only partly inhibited it. The alpha 1-receptor blocker phenoxybenzamine and the beta-receptor blocker propranolol did not significantly influence the extinction inhibition induced by the peptide. These results suggest that the dopaminergic and, in part the cholinergic system, play important roles in this behavioural action of H-Phe-Ile-Tyr-Ser-Tyr-Lys-OH.

Adrenergic alpha-Antagonists↗
PubMed1988

Differential effect of vasopressin on open-field activity and passive avoidance behaviour following intracerebroventricular versus intracisternal administration in rats.

The effects of lysine8-vasopressin (LVP) on the open-field activity and passive avoidance behaviour in rats were studied following intracerebroventricular (i.c.v.) and intracisternal (c.m.) administration. Following i.c.v. administration, LVP caused a long-lasting facilitation of the passive avoidance behaviour and did not influence open-field activity. When injected into the cisterna magna, on the other hand, the same amount of LVP was without effect on the passive avoidance behaviour, while decreasing open-field activity. It is concluded that the site of injection in the cerebrospinal space might be of importance in determining the behavioural effects of neuropeptides.

Animals↗
PubMed1988

Brain monoamines are involved in mediating the action of neurohypophyseal peptide hormones on ethanol tolerance.

Two doses (0.3 and 3 ng peptide/animal) of oxytocin (OXT) and lysine-8-vasopressin (LVP) were earlier found to inhibit the development of tolerance to the hypothermic effect of ethanol in mice upon icv. administration. In the present paper the possible central monoaminergic correlates of the behavioral data were investigated. In tolerant animals the steady-state level of noradrenaline (NA) was increased in the hypothalamus, as was that of dopamine (DA) in the medulla oblongata; the serotonin (5-HT) and DA levels were decreased in the striatum as compared to those in the non-tolerant control. In the peptide-pretreated animals the NA level was increased in the hypothalamus, the DA level in the striatum, and the 5-HT level in the hippocampus and striatum. Opposite changes were observed in the steady-state levels of the monoamines in the hippocampus and striatum as compared to those in the tolerant controls. The data suggest that the central monoamines may be involved in mediating the actions of neurohypophyseal peptides on ethanol tolerance.

Animals↗
PubMed1987

Microinjection of oxytocin into limbic-mesolimbic brain structures disrupts heroin self-administration behavior: a receptor-mediated event?

The systemic injection of oxytocin (OXT) decreases the self-administration of heroin in heroin-tolerant rats. Since OXT-ergic binding sites are present in limbic and mesolimbic brain regions, the effects of intracerebral microinjections of OXT were investigated. In heroin-tolerant rats, the microinjection of OXT (2 ng) into the anterodorsal part of the nucleus accumbens or into the ventral hippocampus disrupted the self-administration of heroin. The effect of intrahippocampal microinjections lasted longer than that of intraaccumbens injections. The administration of N alpha-acetyl-(2-0-methyltyrosine)-oxytocin (ACME-OXT), an inhibitor of oxytocin receptors, prevented the disruptive effect of intrahippocampal OXT injections on heroin self-administration. It is concluded that limbic-mesolimbic brain structures have an essential role in the expression of the disruptive action of OXT on heroin self-administration. It appears that OXT-ergic binding sites mediate the effects of OXT.

Animals↗
PubMed1987

Effects of beta-endorphin2-9 on arginine-8-vasopressin and oxytocin levels in hypothalamic and limbic brain regions.

Immunoreactive arginine-8-vasopressin (AVP) and oxytocin (OXT) were measured in rat hypothalamic and limbic brain regions after the intracerebroventricular administration of beta-endorphin fragment 2-9 (beta E2-9). The peptide decreased the AVP content of the hippocampus and the OXT levels in the septum and amygdala. The present data favor the view that beta E2-9 interacts with limbic AVP- and OXT-systems.

Amygdala↗
PubMed1987

Arachidonate cascade in mesenteric blood vessels and platelets of spontaneously hypertensive rats.

The cyclooxygenase and lipoxygenase pathways of the arachidonate cascade are investigated in vitro in the mesenteric arteries and in the platelets of Wistar normotensive and Okamoto spontaneously hypertensive (SH) rats, using 1-14C arachidonic acid as substrate. The arachidonate cascade in the mesenteric arteries of both Wistar and Okamoto rats showed a sexual dependence. The lipoxygenase dominance in the mesenteric arteries increased almost in parallel with the blood pressure in female SH rats. The activities of cyclooxygenase and lipoxygenase were 4-12 times higher in female animals than in males. The lipoxygenase pathway dominated the arachidonate cascade in the platelets of both normotensive and hypertensive rats. The lipoxygenase pathway was more active in the platelets of SH animals than in the controls. Both in the mesenteric arteries and in the platelets, the arachidonate cascade might play some role in the pathogenesis of hypertension.

Animals↗
PubMed1987

Limbic oxytocin and arginine 8-vasopressin in morphine tolerance and dependence.

Immunoreactive oxytocin (OXT) and arginine8-vasopressin (AVP) levels were measured in limbic areas of the mouse brain (hippocampus, amygdala and basal forebrain). Peptides were measured by radioimmunoassay (RIA). Acute morphine treatment caused a naloxone-reversible increase in OXT content in all three brain regions. The AVP contents of the same brain areas, on the other hand, were not affected by acute morphine treatment. In mice rendered tolerant to/dependent on morphine with subcutaneous morphine pellets, the OXT levels in the limbic brain structures were in the control range (basal forebrain and amygdala) or even decreased (hippocampus). In the latter brain structure of the tolerant animals, the AVP content was also decreased. Naloxone-precipitated withdrawal syndrome in the tolerant/dependent animals resulted in abrupt increases in the OXT and AVP levels of the hippocampus and in the OXT content of the basal forebrain structures.

Amygdala↗
PubMed1987

Beta-endorphin tolerance is inhibited by oxytocin.

The repeated administration of beta-endorphin to mice resulted in the development of tolerance to the analgesic effect of the opioid peptide. While SC injections of oxytocin failed to modify the magnitude or the duration of the analgesic effect of a single intracerebroventricular (ICV) beta-endorphin injection, the development of tolerance to beta-endorphin was antagonized by SC and ICV oxytocin treatment. Since both oxytocin and beta-endorphin are endogenous peptides in the brain, the data raise the possibility that endogenous oxytocin might be involved in the sensitivity of the central nervous system towards repeated or prolonged opioid stimulation.

Analgesia↗