Dopamine – Action, Deficiency, Excess… How to Increase Dopamine Levels?

Dopamine is one of the neurotransmitters of the catecholamine group. Of all the compounds of this group, dopamine makes up the overwhelming majority in the brains of mammals about 80%. It is produced by specialized nerve cells (though not only), which form in the brain specific concentrations of structures: the black-strap system, the mesocortholimbic system. However, it occurs in several stages. In the first of these, tyrosine is converted into L-DOPA, from which only dopamine is produced in the next stage.

Dopamine exerts its influence through highly specialized, precision-tailored receptor structures that operate on a "lock-and-key" principle within cellular signaling pathways. Upon release from the presynaptic neuron, these molecules traverse the synaptic cleft before binding to membrane-bound receptors on the target cell—whether a postsynaptic neuron or another effector cell type. The biological scope of this neurotransmitter’s activity is remarkably extensive and functionally diverse. Motor coordination, including the fluidity and accuracy of movement, is primarily governed by the *substantia nigra*-*striatal* axis, whereas cognitive functions—such as learning capacity, attentional focus, and memory consolidation—are modulated by the mesocorticolimbic pathway. Consequently, the physiological effects of dopamine are intrinsically linked to the anatomical site of its release. Any deviation from the optimal concentration—whether deficiency or excess—may precipitate significant neurobiological dysfunctions, encompassing both motor and psychological dimensions. Deliberate alteration of dopamine levels in individuals with a baseline equilibrium carries substantial risk for adverse reactions, including disruption of nervous system homeostasis.

The clinical syndrome known as Parkinson’s disease primarily stems from the progressive degeneration of dopaminergic neurons located within the *substantia nigra*. While the majority of cases emerge around the sixth decade of life, early-onset and juvenile variants also exist, affecting individuals at significantly younger ages. The pathophysiological mechanism involves the gradual deterioration of cells capable of synthesizing dopamine—a critical neurotransmitter governing motor function. Only when approximately 50–60% of these neuronal populations within the aforementioned brain structure have degenerated do the hallmark symptoms become apparent. These include motor coordination deficits (*bradykinesia*), resting tremor, heightened muscle tone (*rigidity*), and a distinctive alteration in handwriting termed micrographia—a phenomenon characterized by the progressive reduction in letter size during writing. The etiology of this neurodegenerative process remains incompletely understood; among the proposed hypotheses are environmental neurotoxins, including certain pesticides that may disrupt mitochondrial enzyme activity. The consequence of such metabolic impairments is compromised cellular energy production (ATP), ultimately culminating in apoptosis—the programmed death of neurons.

On the contrary, we have schizophrenia. On the opposite end of the spectrum, it seems that this is exactly the mechanism behind the over-activity of dopaminergic neurons in the mesocortholimbic system and its excessive excretion. However, cocaine also increases the amount of dopamine between the neurons, which is why it's effective in treating dopamine receptors. Amphetamine is also associated with high dopamine release and very intense receptor stimulation.