Ecological decoding of visual aesthetic preference with oscillatory electroencephalogram features-A mini-review.

In today's digital information age, human exposure to visual artifacts has reached an unprecedented quasi-omnipresence. Some of these cultural artifacts are elevated to the status of artworks which indicates a special appreciation of these objects. For many persons, the perception of such artworks coincides with aesthetic experiences (AE) that can positively affect health and wellbeing. AEs are composed of complex cognitive and affective mental and physiological states. More profound scientific understanding of the neural dynamics behind AEs would allow the development of passive Brain-Computer-Interfaces (BCI) that offer personalized art presentation to improve AE without the necessity of explicit user feedback. However, previous empirical research in visual neuroaesthetics predominantly investigated functional Magnetic Resonance Imaging and Event-Related-Potentials correlates of AE in unnaturalistic laboratory conditions which might not be the best features for practical neuroaesthetic BCIs. Furthermore, AE has, until recently, largely been framed as the experience of beauty or pleasantness. Yet, these concepts do not encompass all types of AE. Thus, the scope of these concepts is too narrow to allow personalized and optimal art experience across individuals and cultures. This narrative mini-review summarizes the state-of-the-art in oscillatory Electroencephalography (EEG) based visual neuroaesthetics and paints a road map toward the development of ecologically valid neuroaesthetic passive BCI systems that could optimize AEs, as well as their beneficial consequences. We detail reported oscillatory EEG correlates of AEs, as well as machine learning approaches to classify AE. We also highlight current limitations in neuroaesthetics and suggest future directions to improve EEG decoding of AE.

Dual control of dopamine synthesis and release by presynaptic and postsynaptic dopamine D2 receptors.

Dysfunctions of dopaminergic homeostasis leading to either low or high dopamine (DA) levels are causally linked to Parkinson's disease, schizophrenia, and addiction. Major sites of DA synthesis are the mesencephalic neurons originating in the substantia nigra and ventral tegmental area; these structures send major projections to the dorsal striatum (DSt) and nucleus accumbens (NAcc), respectively. DA finely tunes its own synthesis and release by activating DA D2 receptors (D2R). To date, this critical D2R-dependent function was thought to be solely due to activation of D2Rs on dopaminergic neurons (D2 autoreceptors); instead, using site-specific D2R knock-out mice, we uncover that D2 heteroreceptors located on non-DAergic medium spiny neurons participate in the control of DA levels. This D2 heteroreceptor-mediated mechanism is more efficient in the DSt than in NAcc, indicating that D2R signaling differentially regulates mesolimbic- versus nigrostriatal-mediated functions. This study reveals previously unappreciated control of DA signaling, shedding new light on region-specific regulation of DA-mediated effects.

Absence of dopamine D2 receptors unmasks an inhibitory control over the brain circuitries activated by cocaine.

Cocaine is a psychostimulant and a drug widely abused by humans. Cocaine elicits its effects primarily by blocking the activity of the dopamine (DA) transporter, leading to elevated levels of extracellular DA in areas receiving dopaminergic innervation, with the consequent activation of DA receptors. Cocaine, however, also elevates other neurotransmitter levels, leading to a general activation of interconnected brain circuitries. Studies aimed at unraveling the molecular mechanisms underlying the effects of cocaine have shown a leading role of DA D1 receptors in the cascade of cellular events elicited by this drug. In this study, we have analyzed the acute response to cocaine in animals deleted for the expression of DA D2 receptors (D2R), an inhibitor of DA signaling. Importantly, we show that although D1 receptor-mediated functions are preserved and even enhanced in D2R-/- mutants, the behavioral response to acute cocaine administration is severely altered. In addition, c-fos response to acute cocaine administration, in contrast to wild-type mice, is absent in D2R-/- mutants. Our findings show that the absence of D2R, very likely through a presynaptic mechanism, uncovers an inhibitory signaling pathway normally masked by the activity of this receptor on brain circuitries engaged by abused drugs.