Concordant neurophysiological signatures of cognitive control in humans and rats

Robble, Mykel A.; Schroder, Hans S.; Kangas, Brian D.; Nickels, Stefanie; Breiger, Micah; Iturra-Mena, Ann Mary; Perlo, Sarah; Der-Avakian, Andre; Barnes, Sarah; Leutgeb, Stefan; Risbrough, Victoria B.; Vitaliano, Gordana; Bergman, Jack; Carlezon, William A.; Pizzagalli, Diego A.

doi:10.1038/s41386-021-00998-4

Cited by 28 publications

(9 citation statements)

References 49 publications

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“…scalp vs. dura). Still, increasing evidence suggests comparable midfrontal cortical structures (Balsters et al 2020; Schaeffer et al 2020) and confirms empirical similarities in EEG responses between humans and rodents (Narayanan et al 2013; Ehlers et al 2014, 2020; Warren et al 2015; Featherstone et al 2018; Robble et al 2021). There are also inherent differences between species in task experience, motivation, and difficulty.…”

Section: Discussionsupporting

confidence: 61%

Amphetamine alters an EEG marker of reward processing in humans and mice

Cavanagh

Olguin

Talledo

et al. 2021

Preprint

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The development of pro-cognitive therapeutics for psychiatric disorders has been beset with difficulties. This is in part due to the absence of pharmacologically-sensitive cognitive biomarkers common to humans and rodents. Here, we describe a cross-species translational measure of reward processing that is sensitive to the dopamine agonist, d-amphetamine. Motivated by human electroencephalographic (EEG) findings, we recently reported that frontal midline delta-band power is also an electrophysiological biomarker of reward surprise in mice. Here, we determined the impact on this reward-related EEG response from humans (n=23) and mice (n=28) performing a probabilistic learning task under parametric doses of d-amphetamine (human: placebo, 10 mg, 20 mg; mice: placebo, 0.1 mg/kg, 0.3 mg.kg, 1.0 mg/kg). In humans, d-amphetamine boosted the Reward Positivity event-related potential (ERP) component as well as the spectral delta-band representation of this signal. In mice, only the Reward Positivity ERP component was significantly boosted by d-amphetamine. In sum, the present results confirm the role of dopamine in the generation of the Reward Positivity, and support the first pharmacologically valid biomarker of reward sensitivity across species.

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Section: Discussionsupporting

confidence: 61%

Amphetamine alters an EEG marker of reward processing in humans and mice

Cavanagh

Olguin

Talledo

et al. 2021

Preprint

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“…Computational modeling allows such differentiation, including regressing the same computational parameters to, for example, fMRI activation in humans and neuronal recordings in non-human primates or rodents (e.g., [39,42,269]. We argue that, even if tasks across species are not identical due to practical limitations, showing that an intervention (e.g., a given pharmacological manipulation) affects a computational process in similar ways across species greatly reduces the translational divide (for recent examples, see [29,[270][271][272]). Eventually, we believe these approaches and those highlighted in the current review will help reduce the translational divide and accelerate the development of much-needed novel treatments for depression.…”

Section: Conclusion Future Directions and Clinical Implicationsmentioning

confidence: 94%

Prefrontal cortex and depression

Pizzagalli

Roberts

2021

Neuropsychopharmacol.

300

127

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The prefrontal cortex (PFC) has emerged as one of the regions most consistently impaired in major depressive disorder (MDD). Although functional and structural PFC abnormalities have been reported in both individuals with current MDD as well as those at increased vulnerability to MDD, this information has not translated into better treatment and prevention strategies. Here, we argue that dissecting depressive phenotypes into biologically more tractable dimensionsnegative processing biases, anhedonia, despair-like behavior (learned helplessness)affords unique opportunities for integrating clinical findings with mechanistic evidence emerging from preclinical models relevant to depression, and thereby promises to improve our understanding of MDD. To this end, we review and integrate clinical and preclinical literature pertinent to these core phenotypes, while emphasizing a systems-level approach, treatment effects, and whether specific PFC abnormalities are causes or consequences of MDD. In addition, we discuss several key issues linked to cross-species translation, including functional brain homology across species, the importance of dissecting neural pathways underlying specific functional domains that can be fruitfully probed across species, and the experimental approaches that best ensure translatability. Future directions and clinical implications of this burgeoning literature are discussed.

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“…The ERN has a rich literature in psychopathology research as well as in basic human research (23). Despite the robust findings of abnormally enhanced ERN in OCD, only a handful of studies has investigated ERN-analogs in animal models (24)(25)(26), which limits the translation of insights only possible in animal research (e.g., gene knockout) (27) to human research (28).…”

Section: Introductionmentioning

confidence: 99%