Discovery Mindblown Action Circuitry Floating Ball Experiment Set

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Zald, D. H., and Treadway, M. T. (2017). Reward Processing, Neuroeconomics, and Psychopathology. Annu. Rev. Clin. Psychol. 13:44957. doi: 10.1146/annurev-clinpsy-032816-044957 Berlin, I., Givry-Steiner, L., Lecrubier, Y., and Puech, A. J. (1998). Measures of anhedonia and hedonic responses to sucrose in depressive and schizophrenic patients in comparison with healthy subjects. Eur. Psychiatry 13, 303–309. doi: 10.1016/S0924-9338(98)80048-5

Salience memories formed by value, novelty and aversiveness

Trujillo-Pisanty, I., Conover, K., Solis, P., Palacios, D., and Shizgal, P. (2020). Dopamine neurons do not constitute an obligatory stage in the final common path for the evaluation and pursuit of brain stimulation reward. PLoS One 15:e0226722. doi: 10.1371/journal.pone.0226722 Coenen, V. A., Schlaepfer, T. E., Maedler, B., and Panksepp, J. (2011). Cross-species affective functions of the medial forebrain bundle—Implications for the treatment of affective pain and depression in humans. Neurosci. Biobehav. Rev. 35, 1971–1981. doi: 10.1016/J.NEUBIOREV.2010.12.009 It has been proposed that interest in the antidepressant efficacy of psychostimulants persists due to the induction of a fast-acting, but short-lived, mood elevation ( Candy et al., 2008; Malhi et al., 2016). This suggests that stimulants influence mood differently than established antidepressants, which have a delayed clinical onset of days or weeks ( Malhi et al., 2016; Harmer et al., 2017). Given that the mood elevation produced by psychostimulants is typically short lived, one may wonder whether such drugs can induce a lasting mood improvement when their bioavailability is increased. An initial answer is provided by a randomized controlled trial carried out to assess the effectiveness of an extended-release formulation of methylphenidate as an adjunct medication for treatment-resistant depression ( Patkar et al., 2006). No clinical efficacy was found. Further research is needed to evaluate whether the rapid-onset mood elevation inducted by psychostimulants can become sustained by drug formulation or dose regimen. In addition, it would be of interest to assess the efficacy of drugs that target the dopamine transporter more specifically than conventional psychomotor stimulants. At present, the prescription of stimulants for depression remains controversial: Clinicians are advised to use stimulants sparingly and only as additions to other antidepressant drugs for the purpose of improving arousal and tiredness ( Malhi et al., 2016). Leon, M. I., and Gallistel, C. R. (1998). Self-stimulating rats combine subjective reward magnitude and subjective reward rate multiplicatively. J. Exp. Psychol. Anim. Behav. Process. 24, 265–277. doi: 10.1037//0097-7403.24.3.265 Pritzel, M., Huston, J. P., and Buscher, W. (1983). Hypothalamic self-stimulation in rats with one hemisphere isolated anterior to the midbrain and the other hemisphere devoid of the telencephalon. Exp. Neurol. 81, 426–445. doi: 10.1016/0014-4886(83)90273-xBUILD WORKING GIZMOS AND GADGETS with the Action Circuitry Electronic Experiment Set from Discovery #MINDBLOWN! You can build kinetic sculptures and spinning robots, and even exciting toys that launch and levitate objects! The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Publisher’s Note

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Hernandez, G., Trujillo-Pisanty, I., Cossette, M.-P., Conover, K., and Shizgal, P. (2012). Role of dopamine tone in the pursuit of brain stimulation reward. J. Neurosci. 32, 11032–11041. doi: 10.1523/JNEUROSCI.1051-12.2012Preclinical laboratory-animal studies can make use of powerful, invasive methods crucial to linking changes in behavior and psychological processes to the underlying neural circuitry, thereby shedding light on the mechanisms underlying successful clinical interventions. A focus in such research on core psychological processes that have been conserved over the course of mammalian evolution can generate new approaches to intervention, such as development of novel pharmacological agents, behavioral therapies, and interventions such as deep brain stimulation ( Coenen et al., 2011; Panksepp and Yovell, 2014; Panksepp, 2016).

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One such action circuitry is the loop between prefrontal cortex and basal ganglia which is involved in gaze control 8, 9. Prefrontal cortex is known to be sensitive to object novelty 10, 11 even from childhood 12. Prefrontal cortex is also implicated in processing rewarding and aversive stimuli 13, 14, 15. Likewise selective coding of rewarding and/or punishing stimuli is observed in basal ganglia 3, 16, 17. In addition, novel objects are also known to invoke enhanced responses in areas within basal ganglia such as in caudate 18. We have previously shown that value memories shape the visual responses of objects similarly and with a remarkable granularity in vlPFC and the basal ganglia output, SNr. 19. However, it is not known whether the visual responses to objects in the corticobasal circuitry are also affected by other past experiential dimensions such as perceptual exposure (familiarity vs novelty) or aversive associations and if so whether the same neurons encode such disparate object memories across different domains. Yim, C. Y., and Mogenson, G. J. (1980). Electrophysiological studies of neurons in the ventral tegmental area of Tsai. Brain Res. 181, 301–313. doi: 10.1016/0006-8993(80)90614-9 Harmer, C. J., Duman, R. S., and Cowen, P. J. (2017). How do antidepressants work? New perspectives for refining future treatment approaches. Lancet Psychiat. 4, 409–418. doi: 10.1016/S2215-0366(17)30015-9The failure of psychomotor stimulants to serve as an effective monotherapy for depression invites reconsideration of a series-circuit model of the antidepressant effect of MFB stimulation. An alternative, analogous to the convergence model of intracranial MFB self-stimulation, would include multiple, convergent pathways. On that view, non-dopaminergic MFB components may contribute to the therapeutic effect in parallel to, in synergy with, or even instead of, a dopaminergic component. To assess those possibilities, we must look in more detail at the neuroanatomical complexity of the region where MFB stimulation is effective in relieving treatment-resistant depression and at the methods that have been used to link that effect to particular fiber bundles. Which Neurons Are Activated Directly by Therapeutically Effective Stimulation of the Medial Forebrain Bundle, and Which Are Responsible for the Antidepressant Effect? Maier-Hein, K. H., Neher, P. F., Houde, J.-C., Côté, M.-A., Garyfallidis, E., Zhong, J., et al. (2017). The challenge of mapping the human connectome based on diffusion tractography. Nat. Commun. 8:1349. doi: 10.1038/s41467-017-01285-x Grisot, G., Haber, S. N., and Yendiki, A. (2021). Diffusion MRI and anatomic tracing in the same brain reveal common failure modes of tractography. NeuroImage 239:118300. doi: 10.1016/j.neuroimage.2021.118300 While the contrast between aversive and appetitive coding is often used to argue for valence vs salience (or valence vs arousal) coding across different brain regions 3, 13, 57, our measurement of actual learned salience across three different forms of punishing outcomes (airpuff, aversive taste and time-out) showed that despite their general negative valence, aversive object can vary on magnitude and even sign of salience. While airpuff associated objects tended to have higher salience than neutral objects (positive salience), saline and time-out object had similar or slightly lower salience compared to neutral objects (negative salience) (Figs. 2, 4, Supplementary Fig. 4, 6). Thus, without actual measurements, assertions about object salience in the aversive domain and the interpretation of neural responses may be ill-founded.

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Mano, T., Albanese, A., Dodt, H.-U., Erturk, A., Gradinaru, V., Treweek, J. B., et al. (2018). Whole-Brain Analysis of Cells and Circuits by Tissue Clearing and Light-Sheet Microscopy. J. Neurosci. 38, 9330–9337. doi: 10.1523/JNEUROSCI.1677-18.2018 In an effort to alleviate treatment-resistant depression, experimental interventions are often tried. A class of such interventions focuses on neuromodulation. Among them, deep brain stimulation is a neurosurgical approach that has shown promising clinical efficacy for treatment-resistant depression ( Sironi, 2011; Döbrössy et al., 2021). At least 11 brain areas have been studied as candidate targets for relief of treatment-resistant depression by deep-brain stimulation ( Drobisz and Damborská, 2019). Particularly effective outcomes have been obtained from electrodes aimed at the medial forebrain bundle (MFB). Drobisz, D., and Damborská, A. (2019). Deep brain stimulation targets for treating depression. Behav. Brain Res. 359, 266–273. doi: 10.1016/J.BBR.2018.11.004 Research on the role of dopaminergic neurons in reward seeking has accomplished so much and achieved such prominence as to overshadow the established and potential contributions of other neural populations. The ascending dopaminergic projection from the midbrain is merely one of over 50 distinguishable components of the MFB ( Nieuwenhuys et al., 1982). Which of the others contribute to the evaluation and pursuit of rewards and in what ways? The convergence model encourages us to give greater consideration to the non-dopaminergic components, which include descending projections that pass through or near the midbrain region housing dopamine cell bodies and continue deeply into the brainstem ( Nauta et al., 1982). Hernandez, G., Breton, Y.-A., Conover, K., and Shizgal, P. (2010). At what stage of neural processing does cocaine act to boost pursuit of rewards? PLoS One 5:15081. doi: 10.1371/journal.pone.0015081Simmons, J. M., and Gallistel, C. R. (1994). Saturation of subjective reward magnitude as a function of current and pulse frequency. Behav. Neurosci. 108, 151–160. doi: 10.1037//0735-7044.108.1.151 Orgeta, V., Brede, J., and Livingston, G. (2017). Behavioural activation for depression in older people: systematic review and meta-analysis. Br. J. Psychiat. 211, 274–279. doi: 10.1192/BJP.BP.117.205021