WAG/Rij rats given placebo showed a depression-like state as compared with normal Wistar rats (lacking convulsive pathology); this was analogous to the state previously seen in rats of this line, with decreased investigative activity in the open field test, increased immobility in the forced swimming test, and decreased consumption and preference for sucrose solution (anhedonia). Chronic administration of the tricyclic antidepressant imipramine (15 mg/kg, i.p., 15 days) had therapeutic (antidepressant) effects on depression-like behavior in WAG/Rij rats. After withdrawal of antidepressant therapy, the behavior of WAG/Rij rats was not significantly different from that of Wistar rats. Acute (single-dose) administration of the selective dopamine D2/D3 receptor antagonist raclopride (100 microg/kg, i.p., 15 min before the start of behavioral testing) increased the symptoms of depression-like behavior and suppressed the antidepressant effect of chronic administration of imipramine in WAG/Rij rats. Raclopride had no significant effect on behavior in Wistar rats. Administration of the dopamine D2/D3 receptor agonist parlodel (a therapeutic form of bromocriptine) cured the depression-like behavior of WAG/Rij rats and had no significant effect on behavior in Wistar rats, with the exception of a reduction in the duration of immobility in the forced swimming test. Imipramine and raclopride had no significant effect on the levels of total movement activity and anxiety in either WAG/Rij or Wistar rats. These results demonstrate the dopamine-dependent nature of depression-like behavior in WAG/Rij rats and show the possible involvement of dopamine D2 receptors in mediating the antidepressant effect of imipramine on genetically determined depression-like behavior in WAG/Rij rats.

Presentation of sensory stimuli of various modalities to rats immediately before their decapitation led to a significant increase in the level of succmate dehydrogenase in the hippocampus, the magnitude of the increase being dependent on the number of stimuli presented. In each individual case, this enzyme's activity was proportional to the amplitude of the population spike recorded in the hippocampus of the same rat. An inverse relationship was noted between the rate of plastic processes in the hippocampus upon rhythmic stimulation and succinate dehydrogenase activity.Key Words: sensory stimulation; hippocampus; succinate dehydrogenase; population spike; frequency facilitationThe regulation of cell-cell interactions is inextricably bound up with assimilation-dissimilation processes. It has been shown that a major part of the glutamate secreted from nerve terminals becomes involved in energy metabolism [10][11][12]14,15]. Most of the glutamate is taken up by astrocytes [13]. The oxidation of exogenous glutamate provides an external energy source for astrocytes during neuronal excitation [5]. The remaining glutamate is taken up by neurons [13].These findings have enabled a hypothesis to be formulated concerning astro-neuronal interactions during functional activity.A convenient structure for verifying the validity of this hypothesis is the hippocampus. The main pathways in the latter are known to be glutamatergic [8]. Presentation of sensory stimuli should be accompartied by an elevation of glutamate secretion in the hippocampus and, according to the above hypothesis, will lead to increased uptake of glutamate by astrocytes followed by its entry into the Krebs cycle. This is bound to activate enzymes for the subsequent reactions, ff so, then glutamate should be expected to influence primarily the level of succihate dehydrogenase (SDH). Indeed, as shown in several studies [1,3,5], glutamate has an activating effect on succinate oxidation, and such activation is usually explained by elimination of oxaloacetic acid, which inhibits SDH [1].The purpose of this study was to elucidate the possible reasons for alterations in the level of SDH in response to sensory stimulation of different types. MATERIALS AND METHODSFour groups of Wistar rats were used for the experiments. Control rats were decapitated without being exposed to any stimulation. The second group were presented 15 light flashes immediately before decapitation, the third group was exposed to 15 electrocutaneous stimuli, and the fourth group,

Behavior in the light-dark choice, open-field, sucrose consumption/preference and forced swimming tests, monoamines and their metabolites level in 6 brain structures (prefrontal cortex, nucleus accumbens, striatum, hypothalamus, hippocampus, amygdala), and density of D2-like dopamine receptors in 21 brain regions were studied in WAG/Rij and Wistar rats. WAG/Rij rats exhibited symptoms of depression-like behavior such as increased immobility in the forced swim test and decreased sucrose consumption/preference (anhedonia). Substantial changes in behavior indicating increased anxiety in WAG/Rij rats were not revealed. Neurochemical abnormalities suggesting hypofunction of the mesolimbic dopaminergic brain system were found in "depressive" WAG/Rij rats compared with "normal" Wistar rats: decreased levels of noradrenaline, dopamine, 3,4-dihydroxyphenylacetic acid, 3-methoxytyramine in the nucleus accumbens, and increased density of D2-like dopamine receptors in the nucleus accumbens and ventral tegmental area. Reduced levels of dopamine were also observed in the prefrontal cortex and striatum. No substantial changes in the content of monoamines and their metabolites have been revealed in the hypothalamus, hippocampus and amygdala as well as in the content ofserotonin and its metabolite 5-hydroxyindolacetic acid in all studied brain structures with the exception of increased level ofserotonin in the amygdala. Results suggest that hypofunction of the mesolimbic dopaminergic brain system (nucleus accumbens) is a neurochemical mechanism of depression-like behavior in WAG/Rij rats.

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