Knockout of 5-HT7 receptor in the mouse mildly modifies the structure and function of dorsal raphe neurons

The serotonin (5-HT) type 7 receptor (5-HT7R) mediates numerous physiological actions of 5-HT in the brain. Mice with a targeted disruption of the 5-HT7R-coding gene are characterized by an altered behavioral phenotype. Modifications of the serotonergic modulation of brain development and of the activity of the 5-HT system in adulthood that are related to ablation of functional 5-HT7Rs might, potentially, underlie the behavioral phenotype described in the literature. The present study was aimed at finding the consequences of 5-HT7R deficiency for the structure and function of single 5-HT neurons of the midline region of the dorsal raphe nucleus (DRN). It was found that while the amplitude of spontaneous excitatory postsynaptic currents recorded from tryptophan hydroxylase-immunoreactive DRN neurons was elevated in 5-HT7R-deficient animals, the excitability of these cells was mildly reduced. A lack of 5-HT7Rs was accompanied by a minor modification of DRN 5-HT neuron morphology. Our findings support the hypothesis that ablation of the 5-HT7R results in an alteration of the function of mouse DRN projection neurons. Further experiments are needed to fully elucidate the effects of the knockout of the 5-HT7R coding gene on the brain 5-HT system.