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Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 235 records · Page 13Linked to original sources

Modulation of passive avoidance behaviour of rats by intracerebroventricular administration of cholecystokinin octapeptide sulfate ester and nonsulfated cholecystokinin octapeptide.

The effects of intracerebroventricular administration of different doses of cholecystokinin octapeptide sulfate ester (CCK-8-SE) and nonsulfated cholecystokinin octapeptide (CCK-8-NS) were tested on the latency of passive avoidance behaviour in rats. Treatments were carried out prior to learning trial, immediately after electroshock and prior to testing 24 h retention. Both CCK-8-NS and CCK-8-SE enhanced the latency of passive avoidance after all forms of treatment while showing different dose-response patterns depending on time of administration. These data indicate that CCK-8-SE and CCK-8-NS might play a role in the regulation of memory consolidation and retrieval.

Animals↗

Regulation of brain prostaglandins by sexual steroids.

Hypothalamic PGF2 alpha content was determined by radioimmunoassay in rats. The male animals had significantly higher PGF/2 alpha level than the females. The hypothalamic PGF2alpha content increased following orchidectomy (GDX), while ovariectomy alone or combined with oestrone (100 microgram/kg or 1mg/kg i.m.) resulted in a significant i.m.) alone was ineffective. Testosterone (1 or 5 mg/kg i.m.) in GDX animals restored the hypothalamic PGF2 alpha content to the control level. The synthesis and breakdown of prostaglandins were also studied in the microsomal and cytosol fraction of brain homogenate. The PGD2 was the main product of the arachidonate cascade in rat brain microsomes. OVX increased the formation of PGD2 and diminished the biosynthesis of PGF2 alpha. Oestrone administration to OVX rats enhanced the formation of PGF2 alpha. Progesterone injection decreased the biosynthesis of PGF2 alpha and PGD2 alpha and PGD2 in OVX animals. Combined administration of progesterone and oestrone to OVX rats failed to restore the PGF2 alpha synthesis. In orchidectomized animals the arachidonate cascade was found to be depressed, further the synthesis of prostaglandins was normalized after testosterone substitution. The inactivation of 3H-PGF2 alpha by rat brain cytosol fraction was negligible.

Animals↗

Effects of prostaglandins on catecholamine metabolism of the central nervous system in rats.

The effects of 5 microgram prostaglandin (PG) A1, E1, E2 and F2 alpha injected intracerebroventricularly (i.c.v.) into conscious male rats were studied on the catecholamine contents of certain brain areas at different times after administration. PGE2 led to increased dopamine (DA) contents in the hypothalamus 10, 20 and 60 min, and in the septal region 20, 60 and 90 min following injection. PGE1 raised DA levels in the hypothalamus 20 min, and in the septum 20 and 60 min after i.c.v. administration. PGA1 and PGF2 alpha proved to be ineffective as regards the DA contents, while none of the PGs studied altered the noradrenaline (NA) contents of different brain areas. Disappearance of DA was significantly enhanced in the hypothalamus and in the septum, while NA disappearance rate was increased only in the hypothalamus after PGE1 and PGE2 i.c.v. injection in alpha-methyl-p-tyrosine treated rats.

Alprostadil↗

Intraventricular administration of vasopressin and oxytocin effects the steady-state levels of serotonin, dopamine and norepinephrine in rat brain.

The effect of lysine-8-vasopressin (LVP) and oxytocin (OXT) has been studied on the steady-state level of serotonin (5-HT),dopamine(DA) and norepinephrine (NE) in various brain areas four hours after intraventricular microinjection of the neuropeptides. LVP (50 microU) diminished in content of 5-HT and NE in the mesencephalon, the content of 5-HT in the septum as well as the content of DA and NE in the dorsal hippocampus. OXT (500 microU), on the other hand, decreased the content of 5-HT, DA and Ne in the hypothalamus, as well as the content of DA in the mesencephalon. In contrast, the septal NW level was increased following OXT treatment. The data indicate that both LVP and OXT are capable of influencing the 5-HT and catecholamine levels as late as 4 h after their administration. Therefore, our findings support the previous notion that posterior pituitary neuropeptides affect behavioral processes via interacting with the cerebral monoaminergic neurotransmission.

Animals↗

Effect of cholecystokinin antiserum on the brain monoamine content in rats.

The effects of intracerebroventricular administration of cholecystokinin (CCK) antiserum )specific for COOH-terminal four amino acids) of CCK were tested in three dilutions on the dopamine (DA), norepinephrine (NE) and serotonin (5-HT) contents of the hypothalamus, amygdala, septum, striatum and cerebral cortex in rats 24 h following application. CCK antiserum decreased the DA and NE contents in the hypothalamus, mesencephalon, amygdala and septum, while it increased the DA content and decreased the NE content of the striatum. It had a slight effect on the 5-HT contents of the amygdala, septum and striatum.

Amygdala↗

Effect on memory processes of anti-vasopressin serum microinjected into the dorsal raphe nucleus: the role of catecholaminergic neurotransmission.

Anti-arginine8-vasopressin serum was microinjected into the mesencephalic dorsal raphe nucleus immediately after the learning trial, in a one-trial learning passive avoidance reaction. The treatment attenuated passive avoidance behavior 24 h after treatment, suggesting a role of the endogenous vasopressin of this area in memory processes. On the other hand, the antiserum did not influence passive avoidance behavior if 6-hydroxydopamine was microinjected into the raphe region. The data suggest that the antiserum may have primarily interacted with catecholaminergic terminals, which enter the dorsal raphe nucleus.

Animals↗

Hereditary diabetes insipidus in rats. Altered cerebral indolamine and catecholamine metabolism.

Compared to heterozygous Brattleboro animals, homozygous (diabetes insipidus) rats exhibited higher steady-state levels of serotonin in the mesencephalon, septum and striatum. These differences disappeared upon the administration of pargyline, suggesting accumulation of serotonin. The norepinephrine level was higher in the mesencephalon, while the disappearance rate (alpha-met hyl-p-tyrosine) was accelerated in the septum and decreased in the hypothalamus. The lower striatal dopamine level was associated with a decreased disappearance rate. The data suggest that the altered monoamine metabolism might be associated with the known endocrine and behavioral disturbances of the homozygous rats.

Animals↗

The effect of neurohormones on the brain and the endocrine system.

The review article summarizes the results obtained in the author's laboratory during the last few years concerning the action of number of neurohormones such as ACTH, vasopressin, oxytocin, TRH and TRH analogues, human chorionic gonadotropin (HCG) LH-RH, gastrin and gastrin C-terminal fragments and cholecystokinin octapeptide on certain behavioural reactions and brain transmitters. The results obtained suggests that in some of the behavioural reactions elicited by these peptide hormones are brought about by modulatory action of these peptide on brain transmitters. These neurohormones, including gastrointestinal peptide hormones have a time dependent, locus and transmitter specific action on the brain function.

Adrenocorticotropic Hormone↗

Effect of electroconvulsive treatment on brain monoamine content, pituitary-adrenal function and plasma prolactin.

The effect of electroconvulsive therapy used in psychiatry was investigated in rats. Electroconvulsion significantly increased the plasma prolactin, and decreased the hypothalamic dopamine content. The adrenal response (increase in plasma corticosterone) did not differ from the control groups. The results indicate that the prolactin response elicited by electroconvulsion is due to monoaminergic influence and not to the stress reaction.

Animals↗

Effects of ACTH on the synthesis and metabolism of prostaglandin in rat kidney.

Prostaglandin (PG) synthetase activity of rat kidney medulla microsomal fraction was determined in vitro using I-14C-arachidonic acid as substrate. Natural ACTH resulted in a dose dependent suppression of PGE2 formation in vitro. The biosynthesis of PGE2 alpha was enhanced in the presence of ACTH (cortrophin). ACTH4--10 (1-Phe7 or d-Phe7) resulted in decreased PGE2 synthesis. The ratio of PGF2 alpha/PGE2 increased in proportion to the concentration of natural ACTH. The increase in the ratio of PG-s was more pronounced when ACTH4--10 fragments were applied. Natural ACTH in a dose dependent manner inhibited the prostaglandin dehydrogenase activity of kidney cytosol fraction in vitro. Prostaglandin inactivation was suppressed only by high doses of ACTH4--10 (d-Phe7). The data indicate that the natural ACTH and ACTH4--10 fragments might have a physiological role in the regulation of the prostaglandin system of a non-steroidogenic tissue.

Adrenocorticotropic Hormone↗

Effect of ACTH on prostaglandin induced vascular permeability.

Increased vascular permeability was induced by prostaglandin E2 (PGE1), arachidonic acid and compound 48/80 in male rats. Natural ACTH in a dose-dependent manner inhibited Evans blue exudation elicited by arachidonic acid or compound 48/80, however, it was ineffective against PGE1. ACTH4--10 (d-Phe7 and 1-Phe7) injected together with the prophlogistic agents depressed the arachidonic acid and compound 48/80 induced vascular reaction. Indomethacin pretreatment inhibited the effect of arachidonic acid on vascular permeability suggesting that arachidonic acid evoked its vascular activity by means of affecting the endogenous synthesis of prostaglandins and, on the other hand, the prostaglandin system played a role in the vascular permeability inducing effect of compound 48/80. ACTH4--10 peptide fragments free of steroidogenic action and natural ACTH inhibited locally the in vivo formation of PGS from arachidonic acid in the rat skin, resulting in a nonspecific decrease of local inflammation.

Adrenocorticotropic Hormone↗

Action of posterior pituitary neuropeptides on the nigrostriatal dopaminergic system.

The effect of vasopressin, oxytocin and the C-terminal tripeptide of oxytocin, prolyl-leucyl-glycinamide (PLG), were tested on rotational behavior, following unilateral 6-OHDA-enduced lesion of the dopaminergic cell bodies in the substantia nigra. Intraventricular injection of lysine8-vasopressin, oxytocin or PLG caused ipsilateral (towards the lesioned side) rotation, as did peripheral administration of amphetamine. Direct local microinjection of the peptides into the substantia nigra on the intact side was without effect. The data suggest that posterior pituitary neuropeptides (vasopressin and oxytocin) caused presynaptic activation of the nigrostriatal dopaminergic terminals.

Amphetamine↗

In vitro effects of a synethetic enkephalin analogue (D-Met2,Pro5)-enkephalinamide on the hypothalamus-pituitary--testis function in rats.

The effects of (D-Met2,Pro5)-enkephalinamide, a synthetic analogue of the natural opioid pentapeptides, were investigated on the hypothalamus-pituitary-testis axis using in vitro tissue and isolated cell incubation systems. (D-Met2,Pro5)-enkephalinamide in a concentration range 10(-7)--10(-5) M did not alter the testosterone production and the troph-hormone sensitivity of the isolated Leydig cells, or the gonadotroph hormone release and the luteinizing-hormone--releasing hormone (LH-RH) sensitivity of the isolated anterior pituitary cells. However 10(-5)--10(-5) M synthetic enkephalin analogue induced a dose-dependent inhibition of LH-RH content and release of the mediobasal hypothalamus, which was prevented by equimolar concentrations of naloxone.

Animals↗