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Biomedical subjects

G Telegdy

Publications and source records attributed to G Telegdy.

At least 55 records · Page 3Linked to original sources
PubMed1998

Vasoactive intestinal polypeptide induces analgesia and impairs the antinociceptive effect of morphine in mice.

Vasoactive intestinal polypeptide (VIP) has numerous regulatory roles in peripheral, endocrine organs and in the central nervous system. The present study related to the effects of centrally (intracerebroventricularly) administered VIP on pain sensitivity and on opiate tolerance and dependence in intact male CFLP mice. VIP was analgesic when administered alone centrally. Naloxone treatment abolished this analgesic effect. VIP decreased the analgesic effect of a single subcutaneous morphine injection and the development of chronic tolerance to morphine. Morphine withdrawal signs were not significantly affected after VIP pretreatment. These findings indicate that VIP may play a role in pain sensitivity and that an opiate component may participate in this effect.

Analgesics, Non-Narcotic↗
PubMed1997

Platelet eicosanoids and the effect of captopril in blood pressure regulation.

We investigated the eicosanoid synthesis of platelets of Wistar and of Okamoto spontaneously hypertensive rats (SHR), and the effect of captopril in vitro, using [14C]arachidonic acid as a tracer substrate and chromatographic determination. Lipoxygenase activity was elevated, while the formation of cyclooxygenase products was reduced in SHR platelets, compared to those of Wistar rats. This difference might play a role in the pathomechanism of hypertension in SHR. In SHR with lower blood pressure, captopril reduced thromboxane synthesis, while in SHR with higher blood pressure thromboxane synthesis was unchanged, but the synthesis of prostaglandin D2, a potent vasodilator, and of 12-L-hydroxy-5,8,10-heptadecatrienoic acid, a stimulator of endothelial prostacyclin formation, was increased. We may conclude that, in spite of the missing angiotensin converting enzyme in platelets, a direct effect on platelet eicosanoid synthesis could contribute to the blood pressure decreasing effect of captopril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

The effects of brain and C-type natriuretic peptides on corticotropin-releasing factor in brain of rats.

The central corticotropin-releasing factor (CRF)-ergic system plays a critical role in anxiety and other behavioral stress responses. It has been shown that atrial (ANP), brain (BNP) and C-type (CNP) natriuretic peptides exert anxiolytic-like effects in behavioral studies. Our previous findings demonstrated that various doses of centrally administered ANP selectively altered the CRF content in different brain areas. In the present study, CRF immunoreactivity was determined in hypothalamic and extrahypothalamic brain regions after central injection of BNP or CNP in rats. A high dose (400 ng) of BNP significantly increased the CRF-like immunoreactivity (CRF-LI) in the hypothalamus and amygdala, while only a tendency towards an increase was found in the hippocampus. In the hypothalamus, the CRF-LI decreased after a high dose (400 ng) of CNP. The CRF-LI increased in the basal forebrain after a low dose (100 ng) of CNP. These results suggest that CRF may be involved in the mediation of some neuroendocrine and behavioral responses to BNP and CNP.

Animals↗
PubMed1997

Time-dependent alterations in corticotropin-releasing factor-like immunoreactivity in different brain regions after acute cocaine administration to rats.

Recent data from various laboratories suggest that the activation of endogenous corticotropin-releasing factor (CRF) may contribute to the behavioral and neuroendocrine effects of cocaine. In the present study, the time-dependent variations in CRF-like immunoreactivity (CRF-LI) in the hypothalamus and several extrahypothalamic brain regions were determined after acute cocaine administration to handled rats. The intraperitoneal injection of 7.5 mg/kg cocaine led to a significantly decreased CRF-LI level in the basal forebrain and to a significantly increased CRF-LI level in the amygdala 60 min after administration, while the CRF-LI content was decreased in the hypothalamus and in the hippocampus 180 min after cocaine treatment. These results suggest that the durations of the effects of cocaine on CRF-LI are in the brain region-specific, which might contribute to the mediation of the diverse behavioral and neuroendocrine effects of cocaine.

Amygdala↗
PubMed1997

Role of different neurotransmitter systems in the cholecystokinin octapeptide-induced anxiogenic response in rats.

The possible involvement of different neurotransmitter systems in the anxiogenic action of cholecystokinin octapeptide sulphate ester (CCK-8) was investigated in rats. Intracerebroventricularly (i.c.v.) administered CCK-8 induced an anxiogenic response in an elevated plus-maze test. Pretreatment with dopaminergic, muscarinergic acetylcholine receptor blockers and an opiate receptor antagonist blocked the anxiogenic response to CCK-8. The alpha and beta adrenoreceptor, the GABA receptor and the 5-hydroxytryptamine (5-HT) receptor blockers were not able to modulate the 'anxiogenic-like' effect of CCK-8. The results suggest that the anxiogenic effects of CCK-8 are mediated via different neurotransmitters and the anxiogenic action can be prevented by receptor blockers to these transmitters.

Adrenergic alpha-Antagonists↗
PubMed1996

The effects of atrial natriuretic peptide (ANP1-28) on corticotropin releasing factor in brain of rats.

We have shown that ANP has anxiolytic-like effects in behavioral studies. Since CRF is thought to be involved in emotional state of the brain, the present study was undertaken to follow the possible alterations in corticotropin-releasing factor-like immunoreactivity (CRF-LI) in different regions of the brain in rats following ANP treatment. CRF-LI immunoreactivity was determined in hypothalamic and extrahypothalamic brain areas after central injection of atrial natriuretic peptide 1-28 (ANP1-28) in rats. After various doses of ANP1-28 administration the CRF-LI significantly increased in the hypothalamus, the hippocampus and the frontal cortex. In the amygdala, ANP caused a marked but nonsignificant CRF-LI enhancement. In the basal forebrain, the CRF-LI decreased. These results suggest that ANP1-28 may moderate activation of the CRF-ergic system in the brain which could be related to the neuroendocrine and behavioral action.

Animals↗
PubMed1996

The effects of amylin on motivated behavior in rats.

The effects of administration of amylin into the lateral brain ventricle on active and passive avoidance behavior and open field activity were studied in rats. Amylin increased the latency of passive avoidance behavior in a dose-dependent manner between 250 ng and 1 microgram, but 50 and 100 ng and 2 micrograms were ineffective when given immediately after passive avoidance conditioning. As concerns active avoidance behavior, the extinction was facilitated in a dose-dependent manner. The locomotion in an open field was inhibited at 3 h at 500 ng and 1 microgram doses and at 6 h at 250 and 500 ng and 1 microgram doses. However, the action was still present 24 h after administration of a large dose (1 microgram). The rearing activity was increased 3 and 6 h after administration of 1 microgram. Smaller doses (50, 100, 250, and 500 ng) were ineffective. Twenty-four hours following administration, none of the doses used exhibited any effect. The grooming activity was increased 3, 6, and 24 h after administration of 1 microgram amylin. Other doses were ineffective. The results suggest that amylin influences the behavioral reaction in these paradigms mainly by acting on locomotion, and not by modifying learning and memory processes.

Amyloid↗
PubMed1996

The effect of bradykinin and substance P on the arachidonate cascade of platelets.

Several peptide receptors are expressed on the surface of platelets, including B1 and NK1, through which Bk and SP might influence platelet functions including their arachidonate cascade. The metabolites of the arachidonate cascade might play a regulatory role in the inter- and intracellular functions of platelets. Platelets were separated from fresh rat blood by differential centrifugation. Platelets (10(8) ml-1 in each sample) were preincubated with Bk or SP. The arachidonate cascade was investigated with [1-14C]arachidonic acid, as tracer substrate. The synthesised [14C]eicosanoids were isolated and quantitatively determined. Bradykinin elicited a biphasic dose-response curve in the formation of the vasoconstrictor and platelet aggregating thromboxane A2 (TxA2). Bk both inhibited (10(-8) mol/l), and elevated (10(-6) mol/l) the synthesis of TxA2 in the thrombocytes. The 12-HETE synthesis was inhibited by Bk (10(-8), 10(-7), 10(-5) mol/l); 12-HETE is an endogenous regulator of prostacyclin synthesis. The formation of 12-HETE in platelets was stimulated by SP (10(-11), 10(-9), 10(-8) mol/l). The synthesis of TxA2 in platelets was either attenuated (10(-12) mol/l), or stimulated (10(-9) mol/l) by SP. According to our observations Bk and SP might play a regulatory role in the activation or deactivation of platelets.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1996

Effects of brain natriuretic peptide on effects of morphine in mice.

Brain natriuretic peptide (BNP) is a member of the natriuretic peptide family. The effects of intracerebroventricularly administered BNP (in 0.002-200 ng doses) on the analgesic, tolerance-inducing and dependence-inducing actions of morphine were investigated in adult male CFLP mice. Graded doses of BNP centrally did not affect pain sensitivity itself in a tail-flick test. However, different doses of BNP depressed the acute nociceptive effect of a single subcutaneous dose of morphine (5 mg/kg), and BNP attenuated the development of acute and chronic tolerance to morphine. Withdrawal signs were studied by injecting naloxone (1 mg/kg s.c.). There was no significant difference in symptoms between the tolerant group and animals treated with BNP. The data obtained indicate that BNP can modify the analgesic action of morphine.

Analgesics↗
PubMed1996

Effect of receptor blockers on brain natriuretic peptide and C-type natriuretic peptide caused anxiolytic state in rats.

Effect of different doses of centrally administered brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) were examined in rats with respect to anxiolytic properties in an elevated plus-maze model. BNP in doses of 100, 200 and 400 ng, and CNP in doses of 100 and 200 ng abolished the normal preference for the closed arms of the maze, and increased the percentage time spent in the open arms; this is consistent with an 'anxiolytic-like' effect. Doses of 50 and 1000 ng BNP, and of 25, 50, 400 and 1000 ng CNP produced no behavioural effects in the elevated plus-maze model. Pretreatment with an alpha-adrenoreceptor antagonist or a muscarinergic cholinergic blocker, antagonized the effect of 200 ng BNP in the elevated plus-maze test. The 'anxiolytic-like' effects of a BNP were not modulated by a dopaminergic blocker, an alpha-adrenoreceptor antagonist, a GABA receptor antagonist, a 5-HT receptor antagonist or an opiate antagonist. The 'anxiolytic-like' effect of CNP was prevented by a dopamine receptor antagonist, or an alpha- or beta-adrenoreceptor blocker but not by a muscarinergic cholinergic blocker, a GABA receptor, a 5-HT receptor antagonist or an opiate receptor antagonist. These results suggest that multiple neurotransmitter system activation might be responsible for the BNP and CNP-induced 'anxiolytic-like' activity.

Animals↗
PubMed1996

The involvement of nitric oxide (NO) in the CGRP-induced behavior of rats.

The possible role of nitric oxide (NO) in CGRP-induced passive avoidance, active avoidance, and open field behavior was tested in rats. A specific NO synthase inhibitor, N omega-nitro-L-arginine (L-NA), was used to disrupt NO synthesis. ICV administration of 5 micrograms of L-NA reversed the action of CGRP in passive and active avoidance tests. In an open field, L-NA prevented the action of CGRP on locomotion and grooming. The inactive isomer D-NA had no effect on behavior of animals. The data suggest that NO might contribute to CGRP-induced behavior in rats.

Animals↗
PubMed1995

Brain corticotropin-releasing factor mediates 'anxiety-like' behavior induced by cocaine withdrawal in rats.

Anxiety is a key symptom of the cocaine withdrawal syndrome in human addicts, and it is considered to be one of the major factors in precipitating relapse to chronic cocaine abuse. Corticotropin-releasing factor (CRF) plays an important role in the pathophysiology of anxiety and depression, and it may also be involved in the acute behavioral and neuroendocrine actions of cocaine. The role of endogenous CRF in cocaine withdrawal-induced anxiety was investigated in the present study. Animals were subjected to chronic cocaine (20 mg/kg, intraperitoneally, once a day for 14 days) administration. Rats tested 30 min after the last cocaine injection did not show withdrawal anxiety on the elevated plus maze or any alterations in brain CRF levels. Withdrawal (48 h) from chronic cocaine administration produced an intense anxiety-like behavior characterized by decreased open arm exploration. Immunoreactive CRF (CRF-LI) levels were selectively altered in the hypothalamus, in the amygdala and in the basal forebrain structures at the time of the behavioral anxiety, reflecting an increased activity of brain CRF systems. Daily intracerebroventricular (i.c.v.) pretreatment with an immunoserum raised against CRF completely prevented the development of anxiety induced by cocaine withdrawal. These data suggest that extrahypothalamic-limbic CRF hypersecretion may be involved in the development of anxiety related to cocaine withdrawal and that the CRF system may be a useful target for new pharmacotherapies for cocaine withdrawal and relapse.

Animals↗
PubMed1995

Effects of CGRP on active avoidance behavior in rats.

The effects of calcitonin gene-related peptide (CGRP) on the extinction of active avoidance behaviour was examined in rats. Three doses (250 ng, 500 ng and 1 microgram) of the peptide were administered into the lateral brain ventricle (i.c.v.). CGRP delayed the extinction of an active avoidance response in a dose-dependent manner. To reveal any role of the transmitter systems in the action of exogenously administered CGRP, the animals were pretreated with different receptor blockers. CGRP induced a delay in the extinction of an active avoidance response, which could be prevented by haloperidol, propranolol, methysergide and naloxone. Phenoxybenamine, atropine and bicuculline were ineffective. The data suggest that dopaminergic, beta adrenergic, serotonergic and opiate transmission are involved in the CGRP-induced behavioral alterations.

Animals↗
PubMed1995

Oxytocin blocks the development of heroin-fentanyl cross-tolerance in mice.

The development of cross-tolerance to an analgesic effect was observed between two mu-receptor agonists, heroin and fentanyl. Repeated treatments with heroin twice a day for 4 days resulted in a decreased nociceptive effect to fentanyl on day 5. The fentanyl dose-response line shifted to the right, and was considered to be a sign of the development of cross-tolerance. Peripheral treatment with oxytocin did not block the development of heroin-fentanyl cross-tolerance. However, intracerebroventricular administration of oxytocin blocked the development of tolerance, causing a leftward shift in the dose-response curve and supporting the assumption that oxytocin blocks the development of heroin-fentanyl cross-tolerance via CNS mechanisms.

Analgesics, Opioid↗
PubMed1995

Effects of calcitonin gene-related peptide on acute and chronic effects of morphine.

Calcitonin gene-related peptide (CGRP), which has been observed in different parts of the nervous system, is known to modify pain sensitivity to different stimuli in rats and mice. The aim of this study was to investigate the possible interaction of CGRP with morphine on nociception in adult male NMRI mice after central administration of the peptide. CGRP (20 or 200 ng) did not itself modify pain sensitivity in the tail-flick test and did not affect the acute antinociceptive action of a single dose of morphine in the same test. However, CGRP suppressed the development of rapid tolerance to morphine in a dose-dependent manner, but had no action on the development of chronic tolerance to morphine and on manifestations of naloxone-precipitated withdrawal syndrome.

Analgesics, Opioid↗
PubMed1995

C-type natriuretic peptide can modify the acute and chronic effects of morphine.

Different doses (0.2-200 ng) of C-type natriuretic peptide (CNP) were administered into the lateral brain ventricle, and morphine (5 mg/kg) was injected subcutaneously. The analgesic effect was measured in a tail-flick test, in CFLP mice. CNP administered centrally did not itself affect pain sensitivity, but it depressed the acute antinociceptive effect of morphine 30 min after icv (0.2, 2 or 20 ng) CNP administration and the 2 and 20 ng doses also decreased this action after 60 min. CNP in a 0.2 or 200 ng dose blocked the development of acute tolerance to morphine after 30 min, as did the 200 ng dose at 60 min. CNP in a 0.2 ng dose blocked the development of chronic tolerance to morphine after 30 min, but there was no effect at 60 min. Morphine withdrawal signs were studied by injecting naloxone (1 mg/kg sc). There was no significant difference in symptoms between the tolerant group and the animals treated with CNP.

Animals↗