Effects of a Trace Amine-Associated Receptor TAAR5 Agonist as a Model of Schizophrenia Using Electrocorticography Data from Rats

Chronic experiments on rats were run to evaluate the effects of the substance α-NETA, a trace amine-associated receptor TAAR5 agonist, on the electrocorticogram (ECoG). Changes in the spectral power of the main ECoG rhythms were assessed, as was spatial synchronization in the γ range, because of the role of γ oscillations in the transmission of information between regions presumptively affected in schizophrenia. Adult male Wistar rats underwent implantation of six nichrome electrodes into the cerebral cortex of both hemispheres in two rows of three, with the aim of assessing the topography of the whole cortex. A total of 20 experiments were conducted: animals in 10 experiments received systemic doses of α-NETA, while in the other 10 animals received physiological saline. Injections of α-NETA increased power in the δ range (0–5 Hz) and there was a linked decrease in power in the range 5–10 Hz. The greatest differences were seen in the first 10 min. No changes occurred after administration of physiological saline. Increases in slow waves were accompanied by decreases in spatial synchronization of γ oscillations between all six recording points from the pre-injection baseline as compared with controls. All effects were more marked in the anterior zones of the cortex. The results suggest that α-NETA alters dopamine transmission via infl uences on TAAR5, which in turn disrupts glutamatergic transmission, leading to dysfunction in γ synchronization, as occurs in schizophrenia.