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Dopamine is a key regulator neurotransmitter in the important cognitive and intellectual functions of the brain. This neurotransmitter in a structure of catecholamine is responsible for motivation, movement, reward-punishment, mood, memory, attention and more functions in central nervous system. This large effect area gives dopamine high importance in the pathophysiology of neuropsychiatric diseases. Dopamine shows its effects through dopamine receptors that are G protein-coupled receptors ranging from D1 to D5. Changes in the activity of these receptors are associated with diseases like schizophrenia, Parkinson’s disease and addiction. This relationship between dopamine receptors and neuropsychiatric diseases has made these receptors main target in the strategy of clinic researches. Cognitive physiological functions of dopamine and the role of dopamine receptors in the common neuropsychiatric diseases are focused in this chapter.

Serotonin (5-HT) has an important role in the pathophysiology of the mood disorders like major depression and anxiety disorders in central nervous system. On the one hand, dorsal raphe nucleus (DRN) neurons send serotonergic projections to almost all brain regions. On the other hand, they affect themselves through 5-HT1A autoreceptors. Many electrophysiological studies have investigated the ionic mechanism of the 5-HTs effect on the DRN neurons of the rat. However, there is no study characterizing the current that mediates the 5-HTs effect on mouse DRN neurons. In the present electrophysiological study, the whole-cell patch-clamp technique was used in the neurons of the DRN from one-month-old Balb/c mice to investigate the effect of 5-HT on the DRN neurons of mice and its ionic mechanism of action. The application of 5-HT resulted in a 14.3 ± 3.1 mV hyperpolarization (n = 9, P < 0.01) of resting membrane potential and 25.7 ± 3.5 pA outward current (n = 7) in the DRN neurons. The reversal potential (E5-HT) of the current induced by 5-HT was close to the potassium equilibrium potential (EK). This current had an inward rectification feature and was blocked by quinine pretreatment (n = 5, P < 0.05). In conclusion, 5-HT inhibits the DRN neurons of mice by inducing a current that is carried by potassium ions through G-protein–coupled inward rectifier potassium channels.

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