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N B Saul'skaia

Publications and source records attributed to N B Saul'skaia.

At least 19 recordsLinked to original sources
PubMed2006

[NO-synthase dependent increase in citrulline extracellular level in the nucleus accumbens during acquisition and expression of conditioned emotional response].

In Sprague-Dawley rats, by means of in vivo microdialysis combined with HPLC analysis, it was shown that acquisition and expression of conditioned emotional response resulted in increase in extracellular level of citrulline: a nitric oxide co-product, in the nucleus accumbens. The rise extracellular citrulline caused by the acquisition of the response was significantly reduced by intraaccumbens infusion of 7-nitroindasole (0.5 mM), a selective inhibitor of neuronal NO-synthase, and completely prevented by intraaccumbens infusion of N-nitroarginine (0.5 mM): a nonselective NO-synthase inhibitor. The increase in citrulline extracellular level cased by expression of the conditioned emotional response is completely prevented by infusion of both NO-synthase inhibitors. The data obtained suggest that the acquisition and the expression of the conditioned emotional response increase the production of nitric oxide in the n. accumbens, predominantly due to activation of the neuronal NO-synthase.

Animals↗
PubMed2004

[Tetrodotoxine-dependent glycine release in the rat nucleus accumbens during correction of feeding behaviour].

Presence of a tone previously paired with a foot-shock in rats during food intake increases the glycine extracellular level in the n. accumbens. The increase will be completely prevented by intra-accumbal infusion of Na-channel blocking agent tetrodotoxine. The findings suggest that glycine mechanisms in the n. accumbens are involved in the correction of feeding behaviour.

Animals↗
PubMed2001

[Effects of motivational and emotional factors on glutamate release in the nucleus accumbens of rats during feeding].

Food intake was shown to decrease the glutamate extracellular level in the nucleus accumbens in both deprived and non-deprived Spraque-Dawly rats. Feeding combined with presentation of a tone previously paired with foot shock caused an increase in the glutamate extracellular level in deprived rats only, whereas the tone alone had no effect. The data suggest that emotional and motivational variations exert co-operative effect on the glutamate release in the nucleus accumbens during feeding.

Animals↗
PubMed2000

[Dopamine-dependent inhibition of glycine release in the rat nucleus accumbens during feeding].

Food intake decreased the glycine extracellular level in the rat n.accumbens. Tetrodotoxin prevented the decrease, whereas D,L-threo-beta-hydroxyaspartic acid exerted no effect. Raclopride (D2 dopamine receptor antagonist) increased the glycine extracellular level in food intake. The data obtained suggest that during feeding the glycine release in the n.accumbens is controlled by the D2 dopamine receptors.

Animals↗
PubMed2000

[Intercellular integration in the central nervous system].

A humoral mechanism of the intercellular communication in the CNS based on diffusion of neuroactive compounds within the brain extracellular space, was studied. The leading role of the volume transmission was shown in the early stage of ontogeny. Structural basis of this mechanism was studied in adult mammals, and the data on extrasynaptic receptors and release of classical neurotransmitters into the extracellular space was reviewed.

Animals↗
PubMed1996

[Monoamine metabolism in the rat striatum during actions on the nucleus accumbens].

In vivo microdialysis in conscious rats combined with HPLC-EC analysis was used to monitor extracellular levels of 3, 4-dihydroxyphenilacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) in the dorsal striatum (STR) during infusions of procain and apomorphine into the nucleus accumbens (N.acc). It was shown that apomorphine infused into the N.acc (2 x 10(-5) M) caused a decrease in striatal extracellular levels of DOPAC, HVA, and 5-HIAA. Infusions of procain into the N.acc (10(-5) M) produced an increase in extracellular DOPAC, and HVA in the STR. Data indicated that the N.acc exerts an inhibitory influence on the metabolism of dopamine in the STR, the influence being under control of dopaminergic system of the N.acc.

Anesthetics, Local↗
PubMed1994

[The participation of the glutaminergic input of the nucleus accumbens in regulating the synaptic release of dopamine during associative learning].

The effect of MK-801 on basal and conditioned dopamine release in the rat n. accumbens, was studied. Exposure of the rats to the box where they had been given electrical shock, caused an immediate long lasting increase in the dopamine release. Administration of the MK-801 into the n. accumbens abolished the delayed increase in the dopamine release while exerting no effect on the immediate increase.

Animals↗
PubMed1992

[The effect of 6-hydroxydopamine injections into the nucleus accumbens and substantia nigra on rat behavior].

Bilateral infusion of 6-hydroxydophamine (15 mg/ml) into the n. accumbens and substantia nigra accelerated the avoidance conditioning and increased the dopamine and 3,4-dihydroxiphenylacetic acid levels in the striatum as compared with the rats which had only been injected the same agent in the substantia nigra alone. Infusion of this agent into the n. accumbens can be used to compensate for the nigrostriatal deficit.

Animals↗
PubMed1991

[Changes in the synaptic release of catecholamines in the rat striatum with multiple microinjections into it of fenamine and haloperidol].

The dopamine (DA) and noradrenaline (NA) levels of the synapses of the rat rostral striatum was studied with the aid of radioenzymatic and microdialysis techniques. Two weeks after the starting of 45 g amphetamine daily intrastriatal microinjections, the level of DA was 3-5-fold higher than in the control whereas NA level still was unchanged. The next amphetamine injection did not potentiate the synaptic DA level whereas NA level was increased. In contrast to behavioral deviation (the avoidance conditioning lost), the haloperidol intrastriatal microinjections did not affect the DA synaptic level in rostral neostriatum.

Amphetamine↗
PubMed1990

[The effect of the simultaneous dopamine- and glutamatergic stimulation of the nucleus accumbens on synaptic dopamine release in the striatum of freely moving rats].

The influence of n. accumbens on the striatal synaptic dopamine release was investigated in freely moving male Sprague-Dawley rats using in vivo intracranial dialysis followed by radioenzymatic analysis. It was shown that amphetamine or glutamic acid dialysis infusion in the n. accumbens resulted in a decrease in striatal extracellular dopamine level while simultaneous infusion of these drugs led to increase in striatal level of extracellular dopamine. It is suggested that there exist an influence of the n. accumbens on dopamine release in the striatum, the sign of this influence being mediated by dopamine-glutamic acid interaction in the n. accumbens.

Amphetamine↗
PubMed1984

[The striatonigral dopaminergic system and its role in adaptive conditioned reflex behavior].

Neurochemical and pharmacological techniques helped to study the role of the nigro-strial dophaminergic system in adaptive conditioned behaviour of rats and dogs. The avoidance technique revealed that dophamine content in the rat neostriatum increased in a more complicated task performance, and administration of 3 micrograms of dophamine into the rostral neostriatum accelerated and improved the conditioning. Nonadaptive forms of behaviour were accompanied by a drop of the dophamine level in the neostriatum. Stimulation of the caudate nucleus' dophamine-reactive system in dogs by means of administration of dophamine (60 micrograms) and phenamine led to deterioration of conditioned and unconditioned components of feeding behaviour. The effects of the dophaminomimetics were suppressed by administration of haloperidol (10 micrograms) and naloxon (0.8 micrograms) into the same area of the caudate nucleus which attested a functional interrelationship between the dophamine- and enkephalin-containing systems of the neostriatum in regulation of feeding behaviour. The data obtained and literature references gave ground for discussing the role of the nigro-strial dophaminergic system in the positive modulation of adaptive conditioned behaviour under natural conditions.

Adaptation, Physiological↗
PubMed1981

[Dopamine concentration in the nigro-striatal system during elaboration and performance of conditioned avoidance reactions of various complexity in rats].

Experiments in rats revealed that complication of the avoidance conditioning induced a concomitant increase of the dopamine content in the striatum. The dopamine content changes were biphasic in the subst. nigra; its increase in the unilateral avoidance shifted to a decrease in the bilateral avoidance conditioning. Actualization of both simple and complicated avoidance responses was followed by a similar increase of the dopamine content in the striatum.

Animals↗
PubMed1979

[Dopamine concentration in the nigrostriatal system during electrical stimulation of the head of the caudate nucleus].

The high-frequency (50/sec) stimulation of the caudate nucleus head increases the level of dophamine in the area under stimulation with simultaneous drop of dophamine content in the rest of the nucleus. The dophamine content, however, does not change in the black substance or in the putamen. The 2/sec stimulation has no effect upon the dophamine content in the area under stimulation or in the black substance but increases its level in the rest of the caudate nucleus with simultaneous decrease of the dophamine in the putamen.

Animals↗
PubMedDate not supplied

[The enhancement of glutamate release in the nucleus accumbens of rats with a destroyed hippocampal formation during an emotional conditioned response].

It was shown by means of in vivo microdialysis combined with HPLC/EC analysis that the exocytotoxic lesions of the hippocampal formation impaired the emotional conditioning and led to additional glutamate release in the n. accumbens during acquisition and performance of the conditioned response. Thus, it was shown that the disruption of glutamatergic synaptic transmission in the n. accumbens results in a compensatory increase in the volume glutamatergic transmission in this structure.

Animals↗