Research topics

Clinical studies have shown that stress can lead to cardiovascular and emotional diseases,    such as depression. There is a numerous evidence that depression contributes to the onset of arteriosclerosis and that it is a risk factor in the development of cardiac disease.  Sympathoneural system innervates heart and other organs in the body and the first is activated in response to stress. Activation of this system produces a release of catecholamines (dopamine, noradrenaline and adrenaline) which lead to increased production of oxidative radicals and changes in cell function. Dysregulation of dopaminergic and noradrenergic neurotransmission in the brain contributes to the development of depression. The monoamine deficiency hypothesis indicates that depressive symptoms are due to insufficient levels of monoamine neurotransmitters.

This hypothesis points out that an increase of these neurotransmitters in the synapse is the first step in a series of cascade responses that lead to antidepressant activities. The frequency of depression as well as the success of antidepressant therapy are influenced by the sex, age and the individual hormonal status. Women are twice as likely to suffer from depression and have a higher prevelence of comorbid depression and heart disease. Catecholaminergic  neurotransmission is regulated by a diverse set of macromolecules including enzymes, transporters, and pre- and postsynaptic receptors. Our research focuses on the molecular mechanisms of disease development, as well as treatment with various substances in an animal model of depression, measuring the activity of various signaling pathways and the level of catecholamines, gene expression of their biosynthetic and degrading enzymes, transporters and adrenergic receptors in brain, heart and other peripheral organs in both male and female of experimental animals.