Antidepressant drugs are devoid of mood-elevating effects in normal (non-depressed) human subjects, thus, it is necessary to evaluate the antidepressant property of compounds (drugs) in animal models of depression. Several animal models of depression have been introduced, however, only a few have been extensively validated. In the present study we report the results of investigations into monoaminergic receptors in the brain of rats subjected to chronic unpredictable stress (CUS) procedure (one of the well validated animal models of depression). We have examined the dopaminergic (D-1, D-2), adrenergic (alpha-1, beta-1) and serotonergic (5HT-1A, 5HT-2A) receptors in different brain regions by a saturation radioligand binding method in rats subjected to CUS paradigm and control animals. CUS procedure resulted in a significant 29% increase in the D-1 receptor density in the limbic system and 52% increase of the density of 5HT-2A receptors in the cerebral cortex. The present data indicate that the increase of the density of brain D-1 and 5HT-2A receptors of rats subjected to CUS might be involved in the pathophysiology of "animal depression" (since chronic antidepressant treatment produced opposite changes i.e. decrease in the density of these receptors) and thus in pathophysiology of human depression.

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Researchers have demonstrated that lithium potentiated the 5-hydroxytryptophan induction of head twitches in rats that was abolished by pretreatment with the serotonin synthesis inhibitor -p-chlorphenylalanine [15]. This effect is thought to be brought about by lithium bringing about an increase in the tryptophane uptake inside the brain and inducing an increase in serotonin synthesis within the brain's neurons [2,8].Many authors have noted that the behavioural syndrome in rats and mice deemed 'head twitching' is induced by the administration of serotonin precursors (5-hydroxytryptophan) or serotonin agonists (e.g. DOI), and have utilized this effect as a model for response as mediated by 5-HT2 The effectiveness of lithium in the treatment of affective disorders is well documented. However, the mechanism of this effect is still unknown. The purpose of this study was to investigate the effect of lithium on serotonergic neurons. The evaluation of the serotoninergic system activity was performed on the basis of an experimental model of head twitch response triggered by direct or indirect stimulation of serotonin 5-HT2 receptors in the brain. The obtained results indicated that the lithium chloride co-applied with a direct precursor of serotonin -5-hydroxytryptophan used in a threshold dose and with carbidopa, generated head twitch response in mice. What is more, an enhancement of head twitch response in mice was observed after repeated 5-hydroxytryptophan application in head twitch-evoking doses. Moreover, inhibition of the serotonine storage in nerve endings in mice was evoked by reserpine administration. Furthermore, lithium increased the effect of 5-hydroxytryptophan given in a threshold dose and a head twitchevoking dose, respectively. In addition, when P-chlorphenylalanine (pCPA), an inhibitor of the serotonin synthesis within the serotonergic neurons, was given simultaneously with the lithium chloride, carbidopa and 5-hydroxytryptophan in the threshold dose, as well as with the lithium chloride and 5-hydroxytryptophan given at head twitchevoking dosage, pCPA administration decreased the number of head twitches responses in both experimental models, as well as in the reserpinized mice subjected to the lithium chloride and 5-hydroxytryptophan application. Finally, 5,7-dihydroxytryptamineevoked serotoninergic nerve endings destruction led to absolute inhibition of headtwitch response when observed after the lithium and 5-hydroxytryptophan application. Moreover, the increase by lithium 5-hydroxytryptophan-evoke head twitch response was inhibited by administration of the ritanserine -a 5-HT2 serotonin receptor blocking agent. In summary, our data show that lithium induced an enhancement of serotonergic neurotransmission due to its action on presynaptic serotonergic terminals.

correlation between 283G>A polymorphism of VDR gene and the BMD scores for the lumbar vertebrae in women with osteopenia and osteoporosis. Moreover, vitamin D receptor polymorphism also correlated with reduced BMD values. In conclusion, polymorphism (rs1544410) of VDR gene has been proved to be the genetic factor of postmenopausal osteoporosis.Glucocorticoids (GCs) and other preparations, e.g. dexamethasone (DEX -a synthetic GCs receptor agonist) are often used therapeutically for their potent anti-inflammatory and immunosuppressive properties in the different diseases. Chronic stress or prolonged exposure to high levels of GCs induces neuropathological alterations, which are frequently associated with cognitive deficits, such as the impairment of memory and learning. Brain injury, caused by ischemic or hemorrhagic stroke or trauma, may lead to the increased production of reactive oxygen species (ROS) and, in effect, to tissue damage via several different cellular molecular pathways. Many authors suggested the neuroprotective effect of antioxidant agent.The purpose of this study was to investigate the effect of antioxidant agent such as: spirulina (blue-green algae) in animal model of dexamethasone-induced neurotoxicity. The experiments were carried out on male Albino Swiss mice (25-30 g). Spirulina was administered ip (0.5 g and 1.0 g/kg/day) 4 h before DEX (16 mg/kg/day) for 14 days. The long-term memory acquisition, motor performance, as well as body weight and lethality were evaluated 14 days after the drugs administration. The results of our study have shown that DEX evoked deterioration of all parameters in behavioral tests. In mice treated with DEX, spirulina improved parameters of behavioral tests in a higher dose and increased reduction of body weight in mice subjected to DEX.Although the preliminary study suggests protective effect of spirulina in this experimental model, it should be confirmed in further research.http://dx.