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Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 145 records · Page 8Linked to original sources
PubMed1987

Differential effect of desglycinamide9-(Arg8)-vasopressin on cognitive functions of diabetes insipidus and alcoholic patients.

Intranasal treatment with desglycinamide9-(Arg8)-vasopressin (DGAVP) improved certain aspects of cognitive functions of patients with acquired and congenital diabetes insipidus and of alcoholic patients with mild cognitive impairments. Patients with Korsakoff's syndrome, presenting with severe cognitive impairments, were resistent to DGVP treatment. DGAVP treatment did not affect blood pressure and water metabolism. The action of DGAVP on cognitive functions is probably mediated by centrally located target sites and may be expressed only in patients in whom these target sites are unimpaired.

Administration, Intranasal↗
PubMed1987

C-terminal fragments of oxytocin (prolyl-leucyl-glycinamide and Z-prolyl-D-leucine) attenuate the development of tolerance to ethanol.

Earlier it was found that oxytocin (OXT) treatment inhibited the development of tolerance to ethanol. In the present study the possibility was investigated whether the effect of OXT on ethanol tolerance was related to peptide fragments derived from the C-terminal part of the molecule. The actions of different doses of the C-terminal tripeptide (prolyl-leucyl-glycinamide, PLG) and of a synthetic dipeptide derivative (Z-prolyl-D-leucine, Z-Pro-D-Leu) on the development of tolerance to the hypothermic effect of ethanol in CFLP mice were therefore investigated. Peptide treatment did not affect body temperature in ethanol-naive animals. The acute effects (hypothermia, sleeping time) of a single ethanol injection were also unaffected by these peptides. In contrast, both PLG and Z-Pro-D-Leu inhibited the development of tolerance to the hypothermic effect of ethanol. Accordingly, it might be speculated that a sequence active in affecting ethanol tolerance is located in the C-terminal part of the OXT molecule.

Animals↗
PubMed1987

Effects of oxytocin-related peptides on acute morphine tolerance: opposite actions by oxytocin and its receptor antagonists.

The hormonally and behaviorally active nonapeptide oxytocin (OXT), its behaviorally active N-terminal octapeptide desglycinamide9-OXT and Z-prolyl-D-leucine, a synthetic analog of the C-terminal prolyl7-leucine8 sequence, inhibited the development both of a moderate and of a strong tolerance to morphine. N-alpha-Acetyl-(2-0-methyltyrosine)-OXT and (penicillamine1-2-0-methyltyrosine)- lysine8-vasopressin, both OXT receptor antagonists, facilitated the development of a moderate morphine tolerance. The i.c.v. injection of either antagonist prevented the effects of i.c.v. and s.c. OXT treatment on the development of tolerance. The effect of desglycinamide9-OXT, but not that of Z-prolyl-D-leucine was also prevented by N-alpha-acetyl-(2-0-methyltyrosine)-OXT. It is concluded that OXT and desglycinamide9-OXT, but not Z-prolyl-D-leucine, attenuate morphine tolerance by affecting putative oxytocinergic binding sites in the mouse brain. The fact that i.c.v. injection of the receptor antagonist also blocked the effect of s.c. OXT treatment argues in favor of the possibility that a minor proportion of s.c. OXT (or behaviorally active fragments thereof) may reach central nervous system target sites.

Analgesia↗
PubMed1987

Inhibition of electroshock-induced seizures by cholecystokinin-related peptides in mice.

The effects of several doses of cholecystokinin octapeptide sulphate ester (CCK-8-SE) and nonsulphated cholecystokinin octapeptide (CCK-8-NS), and two CCK-related peptide analogues Ac-Thr5-caerulein, and nonsulphated Ac-Thr5-caerulein were investigated on electroshock-(ES)-induced seizures after intraperitoneal administration in mice. As parameters, the duration of the tonic and clonic phase of the fit, and those of postictal coma and behavioural depression were measured. CCK-8-SE decreased the duration of the clonic phase; its highest dose, 3.2 mumol/kg, shortened the coma. CCK-8-NS antagonized only slightly the clonic phase of seizure. Ac-Thr5-caerulein did not influence ES-induced seizures in any dose, only increased the duration of behavioural depression. Similarly to CCK-8-NS, the nonsulphated form of Ac-Thr5-caerulein inhibited selectively the clonic phase of seizures. The reference drugs, diazepam and phenobarbital, antagonized dose-dependently and most effectively the tonic phase of ES-induced seizures, but in much higher doses than did the CCK-related peptides. Besides, diazepam increased and phenobarbital decreased the duration of postictal coma. The results showed that the tested CCK-related peptides inhibit prevalently the clonic phase of ES-induced seizures after peripheral administration.

Animals↗
PubMed1987

Effects of neurohypophyseal peptide hormones on alcohol dependence and withdrawal.

The effect of oxytocin (OXT) and vasopressin (VP) on alcohol withdrawal was investigated. CFLP mice were treated with alternating daily injections of tert-butanol and ethanol for four days, which resulted in physical dependence on ethanol. The severity of withdrawal symptoms was assessed by picrotoxin. The lowest dose (0.02 IU) of each of the peptides precipitated tonic convulsions, while higher doses resulted in different tendencies. OXT-treated mice displayed milder withdrawal symptoms in response to increasing doses of peptide (0.2-2.0 IU). VP showed a U-shaped dose-response effect. The lowest (0.02 IU) and the highest (2.0 IU) doses increased the occurrence of withdrawal convulsions and the frequency of deaths.

Alcohol Withdrawal Delirium↗
PubMed1987

D-pipecolyl-leucyl-glycinamide, a substituted tripeptide analogue of the C-terminal part of oxytocin, influences tolerance to and dependence on ethanol in mice.

The effects of graded doses of a substituted tripeptide analogue of the C-terminal part of oxytocin, D-Pip-Leu-GlyNH2 (DPLG), were investigated on the development of tolerance to the hypothermic effect of and dependence on alcohol in mice. Ethanol injection (4 g/kg i.p.) repeated on 3 consecutive days led to the development of tolerance in control and peptide-treated (0.005 microgram/mouse) animals. In the latter group, however, the level of tolerance was lower than in the control animals. The higher doses (0.05-5.0 micrograms/mouse) inhibited the development of tolerance. Repeated peptide administrations (5, 25, 125 micrograms/animal) did not affect the development of the dependence on alcohol which resulted from combined daily injections of tert-butanol (1.5 g/kg i.p.) and ethanol (3 g/kg i.p.). The severity of withdrawal was quantified via the convulsions induced with different doses of picrotoxin. When the peptide was injected only before the testing of withdrawal, DPLG markedly prolonged the onset of withdrawal signs.

Animals↗
PubMed1986

The action of peptides and proteases on the arachidonate cascade of human and rat platelets.

The arachidonate cascade of human or rat platelets were found to be modified by peptides (bradykinin, angiotensin I, angiotensin II, Asp1-Val5-angiotensin II-amide, somatostatin) and proteases (trypsin, kallikrein). The lipoxygenase pathway was not altered by angiotensin I, angiotensin II, trypsin and kallikrein, while the synthesis some of the cyclooxygenase products was selectively changed by these substances. Bradykinin and somatostatin resulted in an attenuated formation of 12-HPETE and 12-HETE - U shape dose response curve, at the same time the synthesis of cyclooxygenase metabolites was increased - bell shape dose response curve. Asp1-Val5-angiotensin II-amide increased the synthesis of lipoxygenase products and diminished the formation of TxB2. At the same time this peptide selectively induced the enzymatic release of PGD2 from platelets. These peptides and proteolytic enzymes might have physiologic significance in the "Ying-Yang" balance in one hand between lipoxygenase and cyclooxygenase metabolites and on the other between the proaggregatory and antiaggregatory substances released from platelets.

Angiotensins↗
PubMed1986

D-pipecolic acid inhibits ethanol tolerance in mice.

The effects of graded doses of D-pipecolic acid (0.005-5 micrograms/animals s.c.) on tolerance to the hypothermic effect of ethanol (4 g/kg i.p.) were investigated in mice. D-Pipecolic acid itself did not change the core temperature or the acute hypothermic response to a single dose of ethanol. Repeated D-pipecolic acid administration, however, blocked the development of tolerance to the hypothermic effect of ethanol. The development of tolerance could be observed in the control group. It is assumed that D-pipecolic acid is capable of counteracting the tolerance effect of ethanol.

Animals↗
PubMed1986

The effect on brain 5-HT of central lysine-vasopressin administration into different cerebral ventricular compartments depends on the site of injection.

The influence of lysine-8-vasopressin (LVP) on the steady-state level of serotonin was studied in different brain regions four hours after microinjection into the lateral ventricle (icv) or cisterna magna (cm). LVP (200 pg) increased the serotonin (5-HT) level in the hypothalamus and mesencephalon after cm application, while icv administration caused an opposite tendency. The findings suggest that the site of peptide administration is of decisive importance in the mediation of various effects of LVP on the transmitter metabolism. A possible link exists between opposite effects of cm versus icv injection of LVP on central serotoninergic mechanisms, as well as on behavioral and autonomic correlates of these treatment.

Animals↗
PubMed1986

Effect of oxytocin on acute enkephalin tolerance in mice.

Intracerebroventricular (i.c.v.) administration of a test dose of 0.5 microgram D-Met2-Pro5-enkephalinamide (ENK) resulted in analgesia. Acute tolerance developed if a tolerance-inducing high dose of 5 micrograms ENK was administered i.c.v. prior to the test dose. Tolerance appeared as a reduction of the analgesic effect of the test dose. Subcutaneous (s.c.) injection of oxytocin (OXT) inhibited the development of tolerance. It is suggested that OXT is able to modify the development of tolerance to enkephalins, which are ligands of delta-opiate rather than mu-opiate receptors.

Analgesia↗
PubMed1986

Somatostatin and (D-Trp8, D-Cys14)-somatostatin delay extinction and reverse electroconvulsive shock induced amnesia in rats.

In the present study the effects of somatostatin and its analogs on active avoidance behavior, electroconvulsive shock (ECS)-induced retrograde amnesia, and spatial-discrimination learning were compared in rats. (D-Trp8, D-Cys14)-somatostatin (as did the somatostatin molecule itself) delayed the extinction of active avoidance behavior, antagonized ECS-induced amnesia, and did not modify spatial-discrimination learning. Des-Asn5-(D-Trp8, D-Ser13) somatostatin and des-AA1,2,4,5,12,13,-(D-Trp8) somatostatin did not influence these behaviors. The data suggest that certain parts of the somatostatin molecule are important for its behavioral actions.

Amnesia↗
PubMed1986

Development of morphine tolerance under tonic control of brain oxytocin.

Acute morphine tolerance was induced in mice by subcutaneous (s.c.) injection of a high dose (30 or 100 mg/kg) of morphine. The degree of tolerance was estimated 5 h later. Intracerebroventricular (i.c.v.) injection of graded doses of oxytocin (OXT) dose-dependently attenuated the development of tolerance. i.c.v. injection of a specific anti-OXT serum, on the other hand, facilitated the development of tolerance. Neither OXT nor anti-OXT serum had any effect on the pain sensitivity in morphine-naive mice; nor did these treatments modify the antinociceptive action of a single morphine treatment. It is concluded that the endogenous OXT of the mouse brain is normally involved in the adaptive response of the organism, leading to the development of morphine tolerance.

Adaptation, Physiological↗
PubMed1986

Stimulatory effect of intracerebroventricularly administered dopamine on vasopressin release in rats.

Experiments were designed to investigate the effects of the intracerebroventricular administration of dopamine (DA) and a DA antagonist (pimozide) on the immunoreactive-vasopressin (IR-VP) contents of the rat magnocellular nuclei (MCN), neurohypophysis (NH) and plasma. The IR-VP levels in the MCN and NH were decreased 5 min after administration of DA in a dose of 20 nmol, but that in the plasma was increased. This effect was not observed after pretreatment with pimozide. Administration of pimozide alone did not affect the IR-VP contents of the MCN, NH or plasma. The results suggest that DA given icv. has a stimulatory effect on VP release from the neurohypophysial system.

Animals↗
PubMed1986

Effect on brain monoamines in the rat of substituted and protected analogues of the oxytocin fragment, prolyl-leucyl-glycinamide following N-terminal substitution by D- and L-pipecolic acid.

The effect of modified and substituted analogues of prolyl-leucyl-glycinamide (PLG, MIF-I) was investigated on the steady-state level of noradrenaline (NA), dopamine (DA) and serotonin (5-HT) in various brain regions. Proline was replaced by D- or L-pipecolic acid (D- or L-Pip), which analogues in turn were protected by benzoxy-carbonyl (Z) group. Substitution by D- or L-pipecolic acid caused opposite changes in the DA level of the dorsal hippocampus. These effects were absent it the N-terminal of either analogues was protected by Z-group. Following the above mentioned N-terminal modification, the amino group of the C-terminal glycine was also substituted by methyl-esther (Gly-OMe), Z-D-Pip-Leu-Gly-OMe decreased the mesencephalic DA level, while Z-L-Pip-Leu-Gly-OMe increased the 5-HT content of the mesencephalon and striatum. In general, N-terminal substitution by D-pipecolic acid decreased, whereas that by L-pipecolic acid increased the monoamine level in the brain.

Animals↗
PubMed1986

Effect of human pancreatic polypeptide (HPP) on the release of anterior pituitary hormones.

The effects of different doses of human pancreatic polypeptide (HPP) injected into the third ventricle was studied on plasma follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (Prl) and somatotropin (GH) in freely moving ovariectomized rats. Two hundred ng of HPP produced a significant decrease in plasma LH at 15, 30, and 60 min following microinjection. The LH-lowering effect of 400 and 800 ng of HPP developed at 5 min and persisted throughout the experiment. The strongest inhibition was observed at 15 and 30 min. No change in plasma FSH was detected at any time during the experimental period. Two hundred and 400 ng of HPP failed to influence the plasma Prl, while 800 ng resulted in a moderate but significant decrease in plasma Prl levels at 15 and 30 min following injection. Intraventricular microinjection of 400 ng of HPP decreased the GH level at 15 min and 800 ng caused a more pronounced decrease which was significant at 15, 30, and 60 min after the injection. The study suggested that HPP, either from the periphery if it can pass the blood brain barriers or produced in the brain, can influence pituitary function.

Animals↗
PubMed1985

Oxytocin reduces intravenous heroin self-administration in heroin-tolerant rats.

Intravenous self-administration of heroin was studied in experimentally naive rats, as compared to this behavior in animals rendered tolerant to heroin by multiple injections. The tolerant rats also exhibited mild signs of spontaneous and naloxone-precipitated heroin withdrawal. Self-administration behavior developed earlier in the tolerant rats. In heroin-naive rats, oxytocin treatment did not influence the acquisition of heroin self-administration behavior. In the tolerant rats, on the other hand, oxytocin decreased the acquisition of heroin self-administration. When maintenance of heroin self-administration was studied in the tolerant rats, graded doses of oxytocin (0.05, 0.5 and 5 micrograms s.c.) decreased heroin intake. This finding, which is in agreement with previous data indicating that oxytocin attenuates the development of tolerance to and dependence on narcotic analgesics, suggests that the neuropeptide reduced the reinforcing efficacy of heroin in the tolerant organism.

Animals↗
PubMed1985

Acute morphine treatment and morphine tolerance/dependence alter immunoreactive oxytocin levels in the mouse hippocampus.

Immunoreactive oxytocin levels were measured in the mouse hippocampal tissue (h-OXT). Acute morphine treatment increased h-OXT, which effect was reversed by naloxone. In mice rendered tolerant to and dependent on morphine h-OXT was lower than in placebo pellet-implanted control mice. In the tolerant/dependent animals naloxone resulted in precipitated withdrawal syndrome which was associated with a slight increase in h-OXT. The data indicate that h-OXT is affected by acute morphine treatment and by morphine tolerance/dependence and raises the possibility that h-OXT participates in the adaptive response of the organism towards narcotic drugs.

Animals↗