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Biomedical subjects

C Rauca

Publications and source records attributed to C Rauca.

At least 19 recordsLinked to original sources
PubMed2000

Does fucose or piracetam modify the effect of hypoxia preconditioning against pentylenetetrazol-induced seizures?

To clarify the question whether the duration of hypoxia exposure has an influence on the point in time or the strength of hypoxic preconditioning, hypoxia exposure of rats lasting 1 and 8 h was tested regarding the modification of susceptibility to acute pentylenetetrazol-induced seizures. Following the short-lasting (1 h) hypoxia, the maximum level of preconditioning action was observed 7 days after hypoxia, whereas the longer-lasting hypoxia (8 h) produced the maximum level of protection 14 days after hypoxia. We investigated the influence of fucose and piracetam on the effect of hypoxia preconditioning by the application of the substances 20 min before the beginning of hypoxia exposure. Fucose did not modify the result of hypoxia preconditioning. But after the treatment with piracetam, the preconditioning effect was prevented following hypoxia lasting 1 and 8 h. We suggest that the radical scavenger properties of piracetam are responsible for the absence of protection against pentylenetetrazol-evoked seizures.

Animals↗
PubMed2000

The importance of free hydroxyl radicals to hypoxia preconditioning.

Hypoxia preconditioning states that a sublethal hypoxia period will afford neuroprotection against a second harmful event. In our experiments, we carried out a procedure for the development of hypoxia preconditioning in adult male Wistar rats using hypoxic exposure (9% O(2); 91% N(2)) for 1 h. The protection against pentylenetetrazol (PTZ)-induced seizures was studied. For this, rats were tested by a single injection of PTZ (55 mg/kg i.p.) on days 1-21 after hypoxia exposure. The hypoxia exposure significantly prevented the development of acute PTZ convulsion at different times after hypoxia. The present study was designed to determine the effect of N-t-butyl-alpha-phenylnitrone (PBN), an electron-trapping agent and free radical scavenger, on hypoxia preconditioning against PTZ seizures 7 days after hypoxia exposure. PBN abolished the protective action of hypoxia exposure. The generation of free hydroxyl radicals in the brains of animals exposed to hypoxia was determined in a second experiment. For this purpose, the rats were i. p. pretreated with 30 mg/kg PBN and NaCl, respectively, 20 min before the start of hypoxia exposure. Forty-five minutes later the rats were i.p. injected with 300 mg/kg sodium salicylate and once again exposed to hypoxia for 15 min. Immediately after that the animals were decapitated and the free hydroxyl radicals and the salicylate content were estimated in the whole brain without cerebellum. Hypoxia preconditioned animals pretreated with NaCl showed a significantly higher extent of free hydroxyl radicals in the brain compared with PBN-injected preconditioned animals and with naive and sham exposed controls. The results pointed out that the generation of free reactive oxygen species under hypoxic conditions in the brain is involved in the development of the hypoxic preconditioning phenomenon.

Animals↗
PubMed2000

Hypothermia inhibits pentylenetetrazol kindling and prevents kindling-induced deficit in shuttle-box avoidance.

In this study, we evaluated the effects of hypothermic exposure on pentylenetetrazol (PTZ) kindling and the resulting deficit of shuttle-box avoidance learning in rats. Additionally, to acknowledge neuronal cell loss, we estimated the number of toluidine blue-positive cells in different brain regions after PTZ kindling and hypothermia exposure in comparison to different normothermic and hypothermic controls. To obtain hypothermic conditions over a period of up to about 3 h, 30 min after PTZ application the animals were treated with 5 mg/kg chlorpromazine (CP) and 25 min later exposed to 15 degrees C cold water for 5 min. Under these conditions the rectal and the striatal temperature were reduced up to a maximum of 5 degrees C. The additional injection of CP did not influence the development of PTZ kindling. Animals treated with PTZ/CP and exposed to hypothermia did not reach the criterion for kindling. Furthermore, this group of animals did not demonstrate any learning deficit. Forty-eight hours after the last kindling application the number of toluidine blue-stained cells was decreased in the investigated brain regions (hippocampal CA1 and CA3 sector, hilus, and cingular cortex) of kindled rats. Hypothermia protected from cell damage in the hippocampal CA3 sector and in the hilus. Results suggest that the inhibiting effect of hypothermia on the development of kindling and the following learning deficit possibly resulted from the suppression of cell damage in distinct brain structures on PTZ-kindled rats.

Animals↗
PubMed1999

Formation of free hydroxyl radicals after pentylenetetrazol-induced seizure and kindling.

The present study indicates that free radicals have been implicated in pentylenetetrazol (PTZ)-induced seizure and kindling. In our experiments we used a method in which free hydroxyl radicals (* OH) are trapped by systemically applied salicylate in vivo, resulting in the stable and quantifiable products, 2, 3-dihydroxybenzoic acid (DHBA) and 2,5-DHBA. We investigated the formation of both 2,3- and 2,5-DHBA in the whole brain (without cerebellum) of rats treated with an acute seizure-inducing dose of 48 mg/kg PTZ and in PTZ-kindled animals which were injected with the kindling dose of 37.5 mg/kg PTZ at different times after the last PTZ injection. An increase of * OH was observed in kindled rats compared with acutely convulsing animals when the PTZ application was performed 1 min after the salicylate treatment. The amount of DHBAs increased significantly in both convulsed groups 30 min after the application of PTZ compared with animals treated with NaCl instead of PTZ. Sixty minutes after PTZ the DHBA levels normalized to NaCl control values.

Animals↗
PubMed1999

Effects of somatostatin, octreotide and cortistatin on ischaemic neuronal damage following permanent middle cerebral artery occlusion in the rat.

This study investigated whether peptides acting at somatostatin receptors, such as somatostatin-14, octreotide or cortistatin-14, can influence the extent of brain damage after focal ischaemia in rats. The intracerebroventricular application of 0.1 or 1.0 nmol somatostatin-14 5 min after middle cerebral artery occlusion significantly reduced the infarct size assessed 7 days after the insult (by 47% and 57% of the saline control), whereas 10.0 nmol had no significant protective effect (9% reduction). A similar dose/response relationship was obtained after intracerebroventricular injection of octreotide. The lower doses of 0.1 or 1.0 nmol afforded significant neuroprotection (reduction of the infarct size by 72 and 57%), whereas 10 nmol actually increased the infarct size up to 348%. Cortistatin-14 (10 nmol) decreased the ischaemic damage by 52%. For comparison with the neuropeptides acting on somatostatin receptors, the kappa opiate agonist enadoline (10 nmol) also had a significant protective effect against the development of focal ischaemia; the extent of the brain damage was reduced by 60% after intracerebroventricular injection.

Animals↗
PubMed1998

(S)-4C3HPG reduces infarct size after focal cerebral ischemia.

This study investigated whether the metabotropic glutamate receptor ligand (S)-4C3HPG can reduce brain damage after focal ischemia in rats. Application of 1 micromol of (S)-4C3HPG (intracerebroventricularly) 5 min after occlusion of the middle cerebral artery significantly reduced the infarct size by 72.3% of the saline control.

Animals↗
PubMed1997

Does a moderate hypoxia induce manganese-superoxide dismutase or heat shock proteins to act as possible protective factors?

Male Wistar rats were kept in a hypoxia chamber (9% O2) for eight hours. Control animals breathed room air in the same chamber for a similar period of time. One week later the brains of all rats were prepared for the immunohistochemical demonstration of Mn-superoxide dismutase (Mn-SOD). In comparison with the sham-exposed controls, the hypoxia-treated animals showed an increase in the number of Mn-SOD-immunoreactive neurons in several hippocampal structures. The 72 kD heat shock protein was not found to be induced one week after a moderate hypoxia.

Animals↗
PubMed1997

Effect of age on pentylenetetrazol-kindling and kindling-induced impairments of learning performance.

Epileptogenesis during ontogeny may not be linearly related to time. It is known that the behavioral manifestations of seizures are age-dependent, but more research is needed to clarify ontogenetic aspects of epilepsies and related alterations, including cognitive deficits. Kindling is an accepted animal model for the study of the convulsive component of epilepsy and its consequences on behavior. Recently, we demonstrated an impairment in acquisition of a conditioned reaction in young adult kindled rats, using pentylenetetrazol (PTZ) as the kindling stimulus. The present study was undertaken to investigate the dependence on age of alterations in the induction of PTZ kindling in rats. We started the kindling protocol in 4-, 6-, and 8-week- and 6-, 12-, 18-, and 24-month-old rats. The PTZ kindling showed an age-dependent decrease in expression of convulsions. The diminished kindling capacity was already seen in 6-month-old rats. In contrast, kindling-related impairment effects on cognitive functions increased with age. Thus, the correlation between learning impairment and occurrence of tonic-clonic seizures that we had demonstrated in 8-week-old rats was abolished in older rats. On the other hand, when the kindling procedure was started in 6-week-old rats, no impairment was found in fully kindled rats.

Aging↗
PubMed1996

Neuropeptide Y and somatostatin immunoreactivity in the rat hippocampus after moderate hypoxia.

Transient moderate hypoxia has been previously shown to exert a potent protective role to subsequently applied convulsant drugs. We now investigated neuropeptide Y and somatostatin immunoreactivities seven days after moderate hypoxia (9% O2 in N2 for two times 8 h) in the hippocampus of the rat. A slight reduction of somatostatin immunoreactive cells was observed in the hilus of the dorsal and ventral hippocampus. At the same time, the total number of neuropeptide Y immunoreactive neurons was increased in this area due to a pronounced increase in staining of presumable basket cells. There was also increased staining of neuropeptide Y positive fibers in the outer molecular layer. Our data suggest activation of neuropeptide Y containing interneurons after a moderate or a mild transient hypoxia. Activation of these inhibitory neurons may contribute to the protective effect of this treatment.

Animals↗
PubMed1995

Moderate hypoxia reduces pentylenetetrazol-induced seizures.

Mice were exposed to an atmosphere consisting of 7% O2 and 93% N2 or 5.5% O2 and 94.5% N2 for 60 min. The susceptibility of the mice to the convulsive effect of pentylenetetrazol (PTZ) was decreased, in comparison to that of naive or sham-exposed controls, 1 and 7 days after exposure to 7% O2. A significant protective effect against PTZ-induced seizures was not observed in mice exposed to 5.5% O2. N-methyl-D-aspartate (NMDA) administrated immediately after exposure to the hypoxic atmosphere, had no significant influence on the protective effect of hypoxia. Treatment of naive or sham-exposed mice with NMDA resulted in protection against PTZ-induced seizures when they were tested 7 days later. Dizolcipine (MK 801), at a dose of 0.01 mg/kg injected i.p. 10 min before hypoxia, abolished the protective effect of hypoxia; higher doses (0.1 or 0.3 mg/kg) of MK 801 were not effective. The adenosine A1 receptor antagonist 1,3-diethyl-8-phenylxanthine (DPX), administered at a dose of 0.1 mg/kg s.c. before hypoxia, blocked the decrease in the susceptibility to the convulsive effect of PTZ. DPX also blocked the protective effect, seen after 7 days, of NMDA given to control mice. These results suggest that both NMDA and adenosine A1 receptor-mediated processes were involved in the protective effect of moderate hypoxia against PTZ-evoked seizure.

Animals↗
PubMed1995

Effect of BCH 325 (Pro-D-Phe-Pro-Gly) on central dopaminergic functions.

Three behavioral models were used to characterize the pharmacological action of BCH 325 on central dopaminergic transmission. The effect of acute SC treatment with BCH 325 upon dopaminergic mechanisms affecting motor activity was studied on the climbing behavior of mice. It was shown that the beta-casomorphin analogue evoked a dose-dependent increase in apomorphine (APO)-induced hypoactivity that was reversed by sulpiride (SULP). In in vitro studies on slices of nucleus accumbens of mice it could be demonstrated that 10(-6) M APO caused a reduction of K(+)-stimulated [14C]dopamine (DA) release that was potentiated following simultaneous incubation with 10(-6) M BCH 325. To prove a postsynaptic influence in D1 receptor-mediated behavior pattern, the action of BCH 325 was studied on bromocriptine (BROMO)-evoked yawning behavior of rats after pretreatment with reserpine (RES) or saline. The peptide could not influence the BROMO yawning after saline administration, but it was able to normalize the number of yawns, which were reduced after RES. To investigate the effect of BCH 325 on postsynaptic D2 receptors, jerking behavior on RES-pretreated rats after a high dose of BROMO was used. Following RES pretreatment only, the number of BROMO-induced jerks was decreased by treatment of rats with 0.5 mumol/kg BCH 325. In contrast, the jerking behavior was enhanced by 0.5 mumol/kg BCH 325 in rats that were additionally treated with alpha-methyl-p-tyrosine (MPT). In biochemical studies on slices of the nucleus accumbens of mice, the in vivo pretreatment with RES caused a reduction of K(+)-stimulated [14C]DA release that was blocked by the SC administration of 0.5 mumol/kg BCH 325.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Hypoxia protects against the neurotoxicity of kainic acid.

A normobar hypoxia (9% oxygen) of 8 h reduces the neurotoxicity of a subcutaneous injection of 10 mg/kg kainic acid given one week later. Both seizures and degenerative changes, including cell death of hippocampal and cortical neurons are markedly decreased by hypoxia. It is also shown that hypoxia also markedly reduced the extensive depletion of zinc from mossy fiber terminals normally induced by kainic acid. This suggests that a protective mechanism induced by hypoxia may affect the glutamatergic transmission in these synapses and prevent excessive synaptic excitation. The possible involvement of adenosine and/or GABA in this protective mechanism is discussed.

Animals↗
PubMed1986

The effect of beta-casomorphins on the apomorphine- and amphetamine-induced turning after nigral lesions in rats.

To characterize the action of derivatives of beta-casomorphin their influence on the apomorphine- or amphetamine-induced turning behaviour following unilateral lesion of the substantia nigra with 6-hydroxydopamine was investigated. The beta-casomorphins studied, (D-Pro4-beta-casomorphin1-5, D-Phe3-beta-casomorphin1-5, Des-Tyr1-D-Pro4-beta-casomorphin2-5 or Des-Tyr1-D-Phe3-beta-casomorphin2-5), did not change postsynaptic dopaminergic processes in the striatum of the rat after intraperitoneal injection of apomorphine. On the contrary, the turning induced by amphetamine was modified by beta-casomorphins. Increased amphetamine-evoked turning could be observed after intrastriatal application of tyrosine-containing beta-casomorphins (D-Pro4-beta-casomorphin1-5 or D-Phe3-beta-casomorphin1-5), whereas presynaptic dopaminergic mechanisms were inhibited by injection of the corresponding des-tyrosine beta-casomorphin analogs (Des-Tyr1-D-Pro4-beta-casomorphin2-5 or Des-Tyr1-D-Phe3-beta-casomorphin2-5) into the striatum after administration of amphetamine.

Amphetamine↗
PubMed1986

Effects of intrastriatal microinjection of beta-casomorphins and its Des-tyrosine derivatives on rat motor behaviour.

After unilateral striatal application the tyrosine-containing and Des-tyrosine analogues of beta-casomorphin were investigated with regard to the properties inducing rotational behaviour in rats. The tyrosine-containing beta-casomorphins (D-Pro4)-beta-casomorphin1-5, (D-Phe3)-beta-casomorphin1-5 or (D-Pip4)-beta-casomorphin1-5 produced contralateral rotations like apomorphine, whereas the Des-tyrosine-beta-casomorphins brought about an ipsilateral haloperidol-like asymmetry; (Des-Tyr1-D-Pip4)-beta-casomorphin2-5 did not evoke a lateralization of motor behaviour. The contralateral turning following unilateral apomorphine application into striatum was increased by striatal administration of tyrosine-containing beta-casomorphin analogues and antagonistically influenced by (Des-Tyr1-D-Pro4)-beta-casomorphin2-5 or (Des-Tyr1-D-Phe3)-beta-casomorphin2-5; however, (Des-Tyr1-D-Pip4)-beta-casomorphin2-5 has no effect on apomorphine-induced rotation behaviour. The time course of the animals' asymmetric motor behaviour after striatal apomorphine administration was antagonistically influenced by haloperidol, (Des-Tyr1-D-Phe3)-beta-casomorphin2-5 or (Des-Tyr1-D-Pro4)-beta-casomorphin2-5; quantitative differences were observed as far as the strength and the duration of the apomorphine antagonistic effect of Des-Tyr-beta-casomorphins are concerned.

Animals↗
PubMed1985

The influence of enhanced K+-concentration on the uptake and acetylation of choline in hippocampus slices of rats.

The effect of K+-evoked acetylcholine (ACh) release on uptake and acetylation of choline (Ch) in hippocampus slices of rats was studied by use of two different temporal schedules of incubation with labeled precursor and K+-stimulation of tissue. When the incubation with labeled Ch was performed before K+-stimulation, a significant increase of ACh release up to about 400% could be observed. From hippocampus tissue Ch and ACh were extracted as free, labile bound and stable bound fractions. Immediately after the end of potassium stimulation only the ACh radioactivity of the labile bound fraction was decreased, whereas the Ch radioactivities were not changed. In a second series of experiments the K+-evoked ACh release was finished immediately, 10 or 25 min before incubation with labeled precursor. At this time the ACh radioactivity in the incubation medium was normalized. On the other hand, the Ch and ACh radioactivities in the hippocampus tissue increased and returned to control values by different time courses. 30 min after potassium stimulation the ACh radioactivities were still increased, whereas the Ch radioactivities were already normalized to control level. The calculation of the totals of released ACh radioactivity and Ch and ACh radioactivities of tissue suggests that the potassium evoked release leads to a higher uptake and acetylation irrespective of whether the stimulation was carried out before or after the incubation with labeled precursor.

Acetylcholine↗
PubMed1980

Choline uptake and permanent memory storage.

The uptake of 3H-choline and its incorporation into 3H-acetylcholine was studied in vitro on hippocampus slices obtained from animals showing a good or poor long-term memory. The animals were selected on the basis of their retention performance when tested by a brightness discrimination model. The 3H-choline uptake and the incorporation of 3H-choline into 3H-acetylcholine was higher in hippocampus slices from animals showing good retention compared to those from animals with poor retention. The level of high affinity uptake of choline into hippocampus slices may serve as an indicator of the cholinergic activity in this structure under in vitro conditions. The present findings suggest that individual differences in the activity level of the hippocampal cholinergic system do exist and are capable of influencing the retention of the individual animals to a variable degree.

Acetylcholine↗