[The effect of the dopamine D2 receptor agonist cabergoline on the content of catecholamines and expression of BDNF mRNA in the rat midbrain and hypothalamus]. / Vliianie agonista dofaminovykh D2-retseptorov kabergolina na soderzhanie katekholaminov i ékspressiiu mRNK BDNF v srednem mozge i gipotalamuse v éksperimente.

AIM: To study an effect of cabergoline on dopamine and noradrenaline concentration and BDNF mRNA level in the rat midbrain and hypothalamus. MATERIAL AND METHODS: Twenty adult male Wistar rats were used in a single treatment paradigm: animals of the treatment group (n=10) received cabergoline (i.p., 0.5 mg/kg) and the control group (n=10) received an equivalent volume of the solvent. Quantitative analysis for the dopamine (DA) and noradrenaline (NA) was carried out using high-performance liquid chromatography (HPLC) coupled with electrochemical detection. BDNF mRNA levels were studied using quantitative RT-PCR. RESULTS AND CONCLUSION: Cabergoline significantly increases NA concentration in the midbrain 24 hours after injection: 639.2±64.5 ng/g in the treatment group versus 398.0±66.0 ng/g in the control group (p<0.05), while mean content of DA is not significantly changed (211.4±16.3 ng/g vs 169.7±54.6 ng/g, respectively). Cabergoline does not affect hypothalamic DA and NA levels. The drug increases BDNF mRNA levels by 2-times in the midbrain, but not in the hypothalamus, 24 hours after injection.

Biochemical resistance to development of morphine-dependence in rats: biogenic amines, its receptors and antibodies.

The level of norepinephrine (NE), epinephrine (E) and dopamine (DA) in hypothalamus and blood plasma along with antibodies to NE, DA and serotonin (5-HT) and characteristics of alpha 1-, alpha 2-adrenergic, D2-dopaminergic and S2-serotoninergic receptors in synaptic brain membranes were studied in two groups of rats predisposed or resistant to the formation of physical morphine dependence. The resistant animals were characterized by a significant elevation of DA levels in blood plasma, elevation of antibodies to NE, and by higher concentration of alpha 2-adrenergic receptors in the brain cortex and of D2-receptors in striatum. The affinity of D2-receptors to dopamine in resistant rats also was higher than in predisposed animals. The other parameters studied did not differ significantly between the two groups. These findings suggest that the increased activity of DA and NE neurotransmitter systems can be a cause for the genetic resistance of some individuals among Wistar rats to the formation of physical dependence on morphine.