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S A Savel'ev

Publications and source records attributed to S A Savel'ev.

13 recordsLinked to original sources
PubMed2006

Glutamate release in the nucleus accumbens during competitive presentation of aversive and appetitive stimuli.

In vivo intracerebral microdialysis/HPLC studies on Sprague-Dawley rats showed that simultaneous presentation of food and a tone previously combined with a pain stimulus was accompanied by transient elevation of the glutamate level in the extracellular space of the nucleus accumbens, the extent of this increase being proportional to the latent period of initiation of the act of eating. Conversely, sequential presentation of the conditioned aversive signal followed by food and isolated presentation of the conditioned aversive signal alone were not accompanied by changes in the level of extracellular glutamate. It is suggested that glutamate release in the nucleus accumbens in conditions of competition between presentation of food and a tone previously combined with pain stimulation is not related to the process of selecting between the aversive and appetitive strategies of behavior, but may be associated with inhibition of preparation to perform or performance of the food-related behavior.

Animals↗
PubMed2006

Effects of local infusions of apomorphine on the extracellular citrulline level in the striatum: Involvement of D1 and D2 dopamine receptors.

Studies using vital microdialysis and high-performance liquid chromatography showed that local infusion of the NO synthase inhibitor N-nitro-L-arginine (1 mM) into the striatum decreased, while infusion of the dopamine receptor agonist apomorphine (100 microM) increased the level of citrulline (a side product of nitric oxide synthesis) in the intercellular space of this structure in Sprague-Dawley rats. The increase in the citrulline level induced by infusions of apomorphine was completely prevented by local infusions of N-nitro-L-arginine (1 mM) and raclopride (10 microm), a dopamine D2 receptor blocker, but not by infusion of SCH-23390 (50 microm), a dopamine D1 receptor blocker. These data suggest that the increase in extracellular citrulline in the striatum induced by dopaminergic stimulation results from local increases in NO synthase activity and that this effect involves D2, but not D1 dopamine receptors.

Animals↗
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↗
PubMed2005

[Influence of local administration of apomorphine on citrulline extracellular level in the striatum: participation of the dopamine D1 and D2 receptors].

By means of in vivo microdialysis combined with HPLC analysis, we have shown that local infusions of 1 mM N-nitro-L-arginine (NO-synthase inhibitors) in the rat striatum reduced, and infusions of 100 microM apomorphine (agonists of the dopamine receptors) increased the level of citrulline (a NO co-product) in extracellular space of this structure. The apomorphine-induced increase in citrulline extracellular levels in the striatum was completely prevented by infusions of N-nitro-L-arginine in this structure, and 10 microM raclopride (dopamine D2 receptor blocker), but not by infusions of 50 microM SCH-23390 (dopamine D1 receptor blocker). The data obtained suggest that the increase in citrulline extracellular levels in striatum resulted from local activation of NO-synthase, and this effect is mediated by D2 rather than D1 dopamine receptors.

Animals↗
PubMedDate not supplied

[Glutamate release in the nucleus accumbens during competitive presentation of aversive and appetitive stimuli].

By means of in vivo microdialysis combined with HPLC analysis, we have shown that extracellular glutamate level in the rat n. accumbens increases during a simultaneous presentation of a palatable diet and a tone previously paired with a footshock, the magnitude of the extracellular glutamate increase being proportional to the latency of food taking. In contrast, extracellular glutamate level remains unchanged when the diet is presented after the conditioned aversive stimulus or when the tone is given alone. These data suggest that the glutamate release evoked by the competitive presentation of the diet and the conditioned aversive stimulus appears to be related to the inhibition of a planned feeding response, whereas the choice between behavioural strategies may not contribute to this phenomenon.

Animals↗
PubMedDate not supplied

[Citrulline extracellular level in the nucleus accumbens during acquisition and extinction of classical conditioned fear response with pain reinforcement].

By means of in vivo microdialysis combined with HPLC analysis, we have shown that extracellular levels of citrulline (NO co-product) and arginine (NO precursor) increase in the rat n. accumbens during acquisition and expression of a classical fear response. The conditioned rise of citrulline and arginine levels gradually decreased in the course of extinction. The renewal of the response produced an increase in extracellular citrulline and arginine levels. These data suggest that the acquisition of conditioned fear response causes an increase in NO production in the n. accumbens that weakens during the extinction and is restored during the reinstatement of the response.

Animals↗