Mismatch negativity (MMN) is a well-defined component of human event-related potentials that reflects the pre-attentive, stimulus-discrimination process and is associated with involuntary switching of attention. MMN-like responses detected in animal models provide an opportunity to investigate the neural mechanisms of this process that involves several neurotransmitter and neuromodulator systems. Trace amines are believed to play a significant role in neuromodulation of synaptic transmission. The present study aimed to determine the role of trace amine-associated receptor 5 (TAAR5) in the MMN-like response in rats. First, using a bioluminescence resonance energy transfer (BRET) cAMP biosensor, we performed unbiased screening of TAAR5 ligands from a commercially available compound library (661 compounds) and identified 2-(alpha-naphthoyl)ethyltrimethylammonium iodide (alpha-NETA) as a potent (EC 150 nM) TAAR5 agonist. Then, we recorded auditory event-related potentials during an oddball paradigm in awake freely moving rats that were intraperitoneally injected with a vehicle or two doses of the putative TAAR5 agonist alpha-NETA. The MMN-like response was increased by alpha-NETA 3 mg/kg dose, but not by 1 mg/kg dose or 0.9% saline solution. These results suggest that the MMN-like response in rats may be modulated, at least in part, through TAAR5-dependent processes.

Word acquisition could be mediated by the neurocognitive mechanism known as fast mapping (FM). It refers to a process of incidental exclusion-based learning and is believed to be a critical mechanism for the rapid build-up of lexicon, although its neural mechanisms are still poorly understood. To investigate the neural bases of this key learning skill, we used event-related potentials (ERPs) and employed an audio-visual paradigm that included a counterbalanced set of familiar and novel spoken word forms presented, in a single exposure, in conjunction with novel and familiar images. To define learning-related brain dynamics, passive auditory ERPs, known to index long-term memory trace activation, were recorded before and after the FM task. Following the single FM learning exposure, we found a significant enhancement in neural activation elicited by the newly trained word form, which was expressed at ~200–400 ms after the word onset. No similar amplitude increase was found either for the native familiar word used as a control stimulus in the same learning paradigm or for similar control stimuli which were not subject to training. Topographic analysis suggested a left-lateral shift of the ERP scalp distribution for the novel FM word form, underpinned by fronto-temporal cortical sources, which may indicate the involvement of pre-existing neurolinguistic networks for mastering new word forms with native phonology. Overall, the near-instant changes in neural activity after a single-shot novel word training indicate that FM could promote rapid integration of newly learned items into the brain’s neural lexicon, even in adulthood.

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Performance of certain cognitive tasks either during physical load or in rest pauses between boosts might lead to slowing of muscle fatigue and fatigue related decline in performance. Seventeen right-handed healthy volunteers (age 24±1.4, 8 males) participated in this study, aiming to investigate the effect of the level of the cognitive information processing -1) passive perception of audio stimuli, 2) active stimuli discrimination, 3) active stimuli discrimination following motor response -on motor task performance (handgrip test 30% and 7% of MVC) and muscle fatigue development. Cognitive tasks show the following effects on motor work: i) Perceived fatigue during 30 % MVC (fatiguing) condition developed slower if participant pressed button in response to deviant acoustic stimuli, as compared to passive listening. Counting task, an active task without motor component, took the intermediate position and did not differ significantly from two other cognitive tasks. ii) MVC after 30% MVC (fatiguing) condition tended to decrease stronger when accompanied with passive listening in comparison with both active tasks. iii) Motor task performance during 30% MVC (fatiguing) condition was better for active cognitive task with motor component than for passive task. Active task without motor component took the intermediate position and did not differ significantly from both the other cognitive tasks.

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The trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor widely expressed in the mammalian brain, particularly in limbic system and monoaminergic areas. It has proven to be an important modulator of dopaminergic, serotoninergic, and glutamatergic neurotransmission and is considered to be a potential useful target for the pharmacotherapy of neuropsychiatric disorders, including schizophrenia. One of the promising schizophrenia endophenotypes is a deficit in neurocognitive abilities manifested as mismatch negativity (MMN) deficit. This study examines the effect of TAAR1 partial agonist RO5263397 on the MMN-like response in freely moving C57BL/6 mice. Event-related potentials (ERPs) were recorded from awake mice in the oddball paradigm before and after RO5263397 administration. The RO5263397 (but not saline) administration increased the N40 amplitude in response to deviant stimuli. That provided the MMN-like difference at the 36–44 ms interval after the injection. The pitch deviance-elicited changes before the injection and in the control paradigm were established for the P68 component. After TAAR1 agonist administration the P68 amplitude in response both to standard and deviant stimuli was increased. These results suggest that the MMN-like response in mice may be modulated through TAAR1-dependent processes (possibly acting through the direct or indirect glutamate NMDA receptor modulation), indicating the TAAR1 agonists potential antipsychotic and pro-cognitive activity.