Why Does Depression Hurt? Ancestral Primary-Process Separation-Distress (PANIC/GRIEF) and Diminished Brain Reward (SEEKING) Processes in the Genesis of Depressive Affect

Psychiatry ◽  
2011 ◽  
Vol 74 (1) ◽  
pp. 5-13 ◽  
Author(s):  
Jaak Panksepp ◽  
Douglas Watt
2019 ◽  
Author(s):  
Ivan Trujillo-Pisanty ◽  
Kent Conover ◽  
Pavel Solis ◽  
Daniel Palacios ◽  
Peter Shizgal

AbstractThe neurobiological study of reward was launched by the discovery of intracranial self-stimulation (ICSS). Subsequent investigation of this phenomenon provided the initial link between reward-seeking behavior and dopaminergic neurotransmission. We re-evaluated this relationship by psychophysical, pharmacological, optogenetic, and computational means. In rats working for direct, optical activation of midbrain dopamine neurons, we varied the strength and opportunity cost of the stimulation and measured time allocation, the proportion of trial time devoted to reward pursuit. We found that the dependence of time allocation on the strength and cost of stimulation was similar formally to that observed when electrical stimulation of the medial forebrain bundle served as the reward. When the stimulation is strong and cheap, the rats devote almost all their time to reward pursuit; time allocation falls off as stimulation strength is decreased and/or its opportunity cost is increased. A 3D plot of time allocation versus stimulation strength and cost produces a surface resembling the corner of a plateau (the “reward mountain”). We show that dopamine-transporter blockade shifts the mountain along both the strength and cost axes in rats working for optical activation of midbrain dopamine neurons. In contrast, the same drug shifted the mountain uniquely along the opportunity-cost axis when rats worked for electrical MFB stimulation in a prior study. Dopamine neurons are an obligatory stage in the dominant model of ICSS, which positions them at a key nexus in the final common path for reward seeking. This model fails to provide a cogent account for the differential effect of dopamine transporter blockade on the reward mountain. Instead, we propose that midbrain dopamine neurons and neurons with non-dopaminergic, MFB axons constitute parallel limbs of brain-reward circuitry that ultimately converge on the final-common path for the evaluation and pursuit of rewards.Author summaryTo succeed in the struggle for survival and reproductive success, animals must make wise choices about which goals to pursue and how much to pay to attain them. How does the brain make such decisions and adjust behaviour accordingly? An animal model that has long served to address this question entails delivery of rewarding brain stimulation. When the probe is positioned appropriately in the brain, rats will work indefatigably to trigger such stimulation. Dopamine neurons play a crucial role in this phenomenon. The dominant model of the brain circuitry responsible for the reward-seeking behavior treats these cells as a gateway through which the reward-generating brain signals must pass. Here, we challenge this idea on the basis of an experiment in which the dopamine neurons were activated selectively and directly. Mathematical modeling of the results argues for a new view of the structure of brain reward circuitry. On this view, the pathway(s) in which the dopamine neurons are embedded is one of a set of parallel channels that process reward signals in the brain. To achieve a full understanding of how goals are evaluated, selected and pursued, the full set of channels must be identified and investigated.


2019 ◽  
Vol 42 ◽  
Author(s):  
Davood G. Gozli ◽  
Ci Jun Gao

AbstractThe concepts want, hope, and exploration cannot be organized in relation to a single type of motive (e.g., motive for food). They require, in addition, the motive for acquiring and maintaining a stable scheme that enables reward-directed activity. Facing unpredictability, the animal has to seek not only reward, but also a new equilibrated state within which reward seeking is possible.


Author(s):  
L. Reimer

Most information about a specimen is obtained by elastic scattering of electrons, but one cannot avoid inelastic scattering and therefore radiation damage by ionisation as a primary process of damage. This damage is a dose effect, being proportional to the product of lectron current density j and the irradiation time t in Coul.cm−2 as long as there is a negligible heating of the specimen.Therefore one has to determine the dose needed to produce secondary damage processes, which can be measured quantitatively by a chemical or physical effect in the thin specimen. The survival of micro-organisms or the decrease of photoconductivity and cathodoluminescence are such effects needing very small doses (see table).


2020 ◽  
Vol 22 (1) ◽  
pp. 127-148
Author(s):  
Ulrike Körbitz

Is it possible to speak of conceptual conjunctions between Fritz Morgenthaler and Jacques Lacan? This question is explored in relation to the practical work of an analyst as she engages with their – at once completely different and yet complementary – theoretical perspectives. Both emphasize the active, demanding-desiring position of the analyst while simultaneously refusing any metapsychologically oriented interpretive technique. Both criticize the normative, denigrating impetus of too much psychoanalytic thinking, especially in the context of developmental psychology and pathologizing doctrine. They warn against too-certain knowledge on the analyst's part. Both emphasize primary-process drive-strivings and the emancipatory possibilities of psychoanalysis – as they both also attend particularly to the formal aspects of the analysand's speech.


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