Secondary rewards acquire enhanced incentive motivation via increasing anticipatory activity of the lateral orbitofrontal cortex

The motivation to strive for and consume primary rewards such as palatable food is bound by internal satiation and devaluation mechanisms, yet secondary rewards such as money may not be bound by these regulatory mechanisms. The present study therefore aimed at determining diverging devaluation trajectories for primary (chocolate milk) and secondary (money) reinforcers on the behavioral and neural level. Satiation procedures combined with a choice (Experiment 1) and an incentive delay (Experiment 2) paradigm consistently revealed decreased hedonic value for the primary reward as reflected by decreasing hedonic evaluation and choice preference, while hedonic value and preferences for the secondary reward increased. Concomitantly acquired functional near-infrared spectroscopy (fNIRS) data during the incentive delay paradigm revealed that increasing value of the secondary reward was accompanied by increasing anticipatory activation in the lateral orbitofrontal cortex, while during the consummatory phase the secondary reinforcer associated with higher medial orbitofrontal activity irrespective of devaluation stage. Overall, the findings suggest that – in contrast to primary reinforcers - secondary reinforcers can acquire progressively enhanced incentive motivation with repeated receipt, suggesting a mechanism which could promote escalating striving to obtain secondary rewards.

Random access to palatable food stimulates similar addiction-like responses as a fixed schedule, but only a fixed schedule elicits anticipatory activation

Restricted intermittent food access to palatable food (PF) induces addiction-like behaviors and plastic changes in corticolimbic brain areas. Intermittent access protocols normally schedule PF to a fixed time, enabling animals to predict the arrival of PF. Because outside the laboratory the presence of PF may occur in a random unpredictable manner, the present study explored whether random access to PF would stimulate similar addiction-like responses as observed under a fixed scheduled. Rats were randomly assigned to a control group without chocolate access, to ad libitum access to chocolate, to fixed intermittent access (CH-F), or to random unpredictable access (CH-R) to chocolate. Only the CH-F group developed behavioral and core temperature anticipation to PF access. Both groups exposed to intermittent access to PF showed binge eating, increased effort behaviors to obtain chocolate, as well as high FosB/ΔFosB in corticolimbic areas. Moreover, FosB/ΔFosB in all areas correlated with the intensity of binge eating and effort behaviors. We conclude that both conditions of intermittent access to PF stimulate addiction-like behaviors and FosB/ΔFosB accumulation in brain reward areas; while only a fixed schedule, which provides a time clue, elicited anticipatory activation, which is strongly associated with craving behaviors and may favor relapse during withdrawal.

Individuals With Stroke Use Asymmetrical Anticipatory Postural Adjustments When Counteracting External Perturbations

The authors investigated anticipatory postural adjustments in persons with unilateral stroke using external perturbations. Nine individuals with stroke and five control subjects participated. The electromyographic activity of 16 leg and trunk muscles was recorded. The onsets of muscle activity during the anticipatory phase of postural control were analyzed. The individuals with stroke did not show an anticipatory activation of leg and trunk muscles on the affected side; instead, the muscle onsets were seen after the perturbation, during the balance restoration phase. However, an anticipatory activation of muscles on the unaffected side was seen in individuals with stroke, and it was observed earlier compared with healthy controls (p < .05). The individuals with stroke showed a distal to proximal order of anticipatory activation of muscles on the unaffected side. The outcome of the study provides a basis for future investigations regarding ways of improving balance control in people with stroke.

Movement kinematics drive chain selection toward intention detection

The ability to understand intentions based on another’s movements is crucial for human interaction. This ability has been ascribed to the so-called motor chaining mechanism: anytime a motor chain is activated (e.g., grasp-to-drink), the observer attributes to the agent the corresponding intention (i.e., to drink) from the first motor act (i.e., the grasp). However, the mechanisms by which a specific chain is selected in the observer remain poorly understood. In the current study, we investigate the possibility that in the absence of discriminative contextual cues, slight kinematic variations in the observed grasp inform mapping to the most probable chain. Chaining of motor acts predicts that, in a sequential grasping task (e.g., grasp-to-drink), electromyographic (EMG) components that are required for the final act [e.g., the mouth-opening mylohyoid (MH) muscle] show anticipatory activation. To test this prediction, we used MH EMG, transcranial magnetic stimulation (TMS; MH motor-evoked potentials), and predictive models of movement kinematics to measure the level and timing of MH activation during the execution (Experiment 1) and the observation (Experiment 2) of reach-to-grasp actions. We found that MH-related corticobulbar excitability during grasping observation varied as a function of the goal (to drink or to pour) and the kinematics of the observed grasp. These results show that subtle changes in movement kinematics drive the selection of the most probable motor chain, allowing the observer to link an observed act to the agent’s intention.

HSP-4/BiP expression in secretory cells is regulated by a lineage-dependent differentiation program and not by the unfolded protein response

Differentiation of secretory cells leads to sharp increases in protein synthesis, challenging ER proteostasis. Anticipatory activation of the unfolded protein response (UPR) prepares cells for the onset of secretory function by expanding the ER size and folding capacity. How cells ensure that the repertoire of induced chaperones matches their post-differentiation folding needs is not well understood. We find that during differentiation of stem-like seam cells, a typical UPR target, the C. elegans BiP homologue HSP-4, is selectively induced in alae-secreting daughter cells, but is repressed in hypodermal daughter cells. Surprisingly, this lineage-dependent induction bypasses the requirement for UPR signaling, and instead is controlled by a specific developmental program. The repression of HSP-4 in hypodermal-fated cells requires a transcriptional regulator BLMP-1/BLIMP1, involved in differentiation of mammalian secretory cells. The HSP-4 induction is anticipatory, and is required for the integrity of secreted alae. Thus, differentiation programs can directly control a broad-specificity chaperone that is normally stress-dependent, to ensure the integrity of secreted proteins.

Brain Responses during the Anticipation of Dyspnea

Dyspnea is common in many cardiorespiratory diseases. Already the anticipation of this aversive symptom elicits fear in many patients resulting in unfavorable health behaviors such as activity avoidance and sedentary lifestyle. This study investigated brain mechanisms underlying these anticipatory processes. We induced dyspnea using resistive-load breathing in healthy subjects during functional magnetic resonance imaging. Blocks of severe and mild dyspnea alternated, each preceded by anticipation periods. Severe dyspnea activated a network of sensorimotor, cerebellar, and limbic areas. The left insular, parietal opercular, and cerebellar cortices showed increased activation already during dyspnea anticipation. Left insular and parietal opercular cortex showed increased connectivity with right insular and anterior cingulate cortex when severe dyspnea was anticipated, while the cerebellum showed increased connectivity with the amygdala. Notably, insular activation during dyspnea perception was positively correlated with midbrain activation during anticipation. Moreover, anticipatory fear was positively correlated with anticipatory activation in right insular and anterior cingulate cortex. The results demonstrate that dyspnea anticipation activates brain areas involved in dyspnea perception. The involvement of emotion-related areas such as insula, anterior cingulate cortex, and amygdala during dyspnea anticipation most likely reflects anticipatory fear and might underlie the development of unfavorable health behaviors in patients suffering from dyspnea.