The neural circuit of Superior colliculus to ventral tegmental area modulates visual cue associated with rewarding behavior in optical intracranial Self-Stimulation in mice.

Visual system is the most important system of animal to cognize the information in outside world, and reward-related visual cues are the key factors in the consolidation and retrieval of reward memory. However, the neural circuit mechanism is still unclear. Superior Colliculus (SC) receive direct input from the retina and belong to the earliest stages of visual processing. Recent studies identified a specific pathway from SC to ventral tegmental area (VTA) that underlie specific innate behaviors, eg. flight or freezing, approach behaviors and so on. In present research, we investigated that inhibition of SC to VTA circuit with chemogenetics suppressed light cue-associated reward-seeking behaviors, while activation of the SC-VTA circuit with chemogenetic technology triggered the reward-seeking behaviors in optical intracranial self-stimulation for VTA DA neurons (oICSS) in mice. These findings suggest that neural circuit of SC-VTA mediates the retrieval of reward memory associated with visual cues, which will provide a new field for revealing the neural mechanism of pathological memory such as addiction.

Two Distinct Neuronal Populations in the Rat Parafascicular Nucleus Oppositely Encode the Engagement in Stimulus-driven Reward-seeking.

BACKGROUND: The thalamus is a phylogenetically well-preserved structure. Known to densely contact cortical regions, its role in the transmission of sensory information to the striatal complex has been widely reconsidered in recent years. METHODS: The parafascicular nucleus of the thalamus (Pf) has been implicated in the orientation of attention toward salient sensory stimuli. In a stimulus-driven reward-seeking task, we sought to characterize the electrophysiological activity of Pf neurons in rats. RESULTS: We observed a predominance of excitatory over inhibitory responses for all events in the task. Neurons responded more strongly to the stimulus compared to lever-pressing and reward collecting, confirming the strong involvement of the Pf in sensory information processing. The use of long sessions allowed us to compare neuronal responses to stimuli between trials when animals were engaged in action and those when they were not. We distinguished two populations of neurons with opposite responses: MOTIV+ neurons responded more intensely to stimuli followed by a behavioral response than those that were not. Conversely, MOTIV- neurons responded more strongly when the animal did not respond to the stimulus. In addition, the latency of excitation of MOTIV- neurons was shorter than that of MOTIV+ neurons. CONCLUSION: Through this encoding, the Pf could perform an early selection of environmental stimuli transmitted to the striatum according to motivational level.

Navigating the complex terrain of motivated behavior: a bibliometric and neuroscientific perspective.

Over several decades, motivated behavior has emerged as a crucial study area within neuroscience. Understanding the neural substrates and mechanisms driving behaviors related to reward, addiction, and other motivation forms is pivotal for novel therapeutic interventions. This review provides a bibliometric analysis of the literature, highlighting the main trends, influential authors, and the potential future direction of the field. Utilizing a dataset comprised by 3,150 publications from the Web of Science and Scopus databases ("motivated behavior as query), we delve into key metrics like publication trends, keyword prevalence, author collaborations, citation impacts, and employed an unsupervised natural language processing technique - Latent Dirichlet Allocation - for topic modeling. From early investigations focusing on basic neural mechanism and behaviors in animal models to more recent studies exploring the complex interplay of neurobiological, psychological, and social factors in humans, the field had undergone a remarkable transformation. The last century has seen a proliferation of research dedicated to uncovering the intricacies of motivation, significantly enriching our understanding of its myriad implications for human behavior and mental health. This bibliometric analysis aims to offer comprehensive insights into this dynamic research area, highlighting the field's key contributions and potential future directions, thereby serving as a valuable resource for researchers, and hopefully give a more thorough understanding of the research area.

Less bang for my buck: Diminished anticipated enjoyment contributes to dysphoria-linked deficit in activity behavioural engagement choice.

This study experimentally investigated the role of anticipated enjoyment and effort in mediating dysphoria-related deficit in activity engagement behavioural choice. Using a novel activity information processing task (about a fictional "new" Nintendo Wii sports game called "Tornado Ball"), N = 249 participants (n = 95 High Dysphoria; n = 154 Low Dysphoria) were presented information about the benefits (enjoyable features) and costs (mental and physical effort barriers) as product reviews from another player. The order of cost vs. benefit information was manipulated such that participants either heard cost information before benefit information, or vice versa. They then rated what their anticipated enjoyment and effort will be if they were to play Tornado Ball, before being given the opportunity to choose to try it themselves or not. The High Dysphoria group reported lower anticipated enjoyment (but not higher effort) relative to the Low Dysphoria group, but only when cost information was presented first. Importantly, a moderated mediation showed that the High Dysphoria group reported lower tendency to choose activity engagement (game play) as a function of having lower anticipated enjoyment, but only when cost information was presented first. The present finding indicate that reduced anticipated enjoyment may causally contribute to dysphoria-linked deficits in activity engagement behavioural choice.

Sign-tracking to non-drug reward is related to severity of alcohol-use problems in a sample of individuals seeking treatment.

BACKGROUND: A prominent neuroscientific theory of drug addiction is the incentive sensitization model. Individual differences in the tendency to ascribe motivational salience to cues that predict reward, and involuntary "sign-tracking" (orientation towards) such cues have been identified as potentially important in understanding vulnerability to addiction and relapse. However, to date this behaviour has not been assessed in a treatment-seeking clinical population, who typically represent those most susceptible to alcohol-related harms and episodes of relapse. This highlights a significant gap in the literature pertaining to incentive sensitization and drug dependence. METHODS: Individuals accessing inpatient drug and alcohol services with alcohol as primary drug of concern were recruited to participate in a Cognitive Bias Modification (CBM) intervention. At the baseline assessment, participants completed various self-report measures (including the Alcohol Use Disorders Identification Test; AUDIT) in addition to a visual search task measuring sign-tracking to cues signalling monetary reward. At 3-month follow up, abstinence from alcohol was the primary outcome measure. All analyses and hypotheses were pre-registered. RESULTS: At baseline (57 participants), AUDIT scores correlated with sign-tracking to signals of monetary reward. In a subsequent regression analysis sign-tracking, gender and self-reported alcohol craving predicted abstinence at 3-month follow up (41 participants). CONCLUSIONS: Our work demonstrates that involuntary sign-tracking to cues signalling non-drug reward is associated with problematic alcohol use and return to use at 3-month follow up, in a treatment-seeking sample. Whether this automatic prioritisation of cues signalling reward is a consequence or vulnerability for problematic alcohol use remains to be investigated.

Choice impulsivity after repeated social stress is associated with increased perineuronal nets in the medial prefrontal cortex.

Repeated stress can predispose to substance abuse. However, behavioral and neurobiological adaptations that link stress to substance abuse remain unclear. This study investigates whether intermittent social defeat (ISD), a stress protocol that promotes drug-seeking behavior, alters intertemporal decision-making and cortical inhibitory function in the medial prefrontal cortex (mPFC). Male long evans rats were trained in a delay discounting task (DDT) where rats make a choice between a fast (1 s) small reward (1 sugar pellet) and a large reward (3 sugar pellets) that comes with a time delay (10 s or 20 s). A decreased preference for delayed rewards was used as an index of choice impulsivity. Rats were exposed to ISD and tested in the DDT 24 h after each stress episode, and one- and two-weeks after the last stress episode. Immunohistochemistry was performed in rat's brains to evaluate perineuronal nets (PNNs) and parvalbumin GABA interneurons (PV) labeling as markers of inhibitory function in mPFC. ISD significantly decreased the preference for delayed large rewards in low impulsive, but not high impulsive, animals. ISD also increased the density of PNNs in the mPFC. These results suggest that increased choice impulsivity and cortical inhibition predispose animals to seek out rewards after stress.

The role of sex on sign-tracking acquisition and outcome devaluation sensitivity in Long Evans rats.

Cues that predict rewards can trigger reward-seeking behaviors but also can, in some cases, become targets of motivation themselves. One behavioral phenomenon that captures this idea is sign-tracking in which animals, including humans, interact with reward-predictive cues even though it is not necessary to do so. Sign-tracking in rats has been studied in the domain of motivation and in how motivated behaviors can or cannot become excessive and habit-like over time. Many prior studies look at sign-tracking examine this behavior in male subjects, but there are few papers that look at this behavior in female subjects. Moreover, it is unknown where there might be sex-related variation in how flexible sign-tracking is when faced with changing reward values. Therefore, we asked if there were sex differences in the acquisition of sign-tracking behavior and if there were any sex differences in how sensitive animals were in their sign-tracking following reward devaluation. In contrast to previous reports, we found that males and females show no differences in how they acquire sign-tracking and in ultimate sign-tracking levels following training. Additionally, we found no difference in how quickly males and females learned to devalue the food reward, and we found no differences in sign-tracking levels by sex following outcome devaluation. We believe that this is primarily due to our experiment being performed in the Long Evans strain but also believe that there are many other factors contributing to differences between our study and previous work.

Hormone sensitivity predicts the beneficial effects of transdermal estradiol on reward-seeking behaviors in perimenopausal women: A randomized controlled trial.

Depression is highly prevalent during the menopause transition (perimenopause), and often presents with anxious and anhedonic features. This increased vulnerability for mood symptoms is likely driven in part by the dramatic hormonal changes that are characteristic of the menopause transition, as prior research has linked fluctuations in estradiol (E2) to emergence of depressed mood in at risk perimenopausal women. Transdermal estradiol (TE2) has been shown to reduce the severity of depression in clinically symptomatic women, particularly in those with recent stressful life events. This research extends prior work by examining the relation between E2 and reward seeking behaviors, a precise behavioral indicator of depression. Specifically, the current study utilizes a randomized, double blind, placebo-controlled design to investigate whether mood sensitivity to E2 flux ("hormone sensitivity") predicts the beneficial effects of TE2 interventions on reward seeking behaviors in perimenopausal women, and whether recent stressful life events moderate any observed associations. METHOD: Participants were 66 women who met standardized criteria for being early or late perimenopausal based on bleeding patterns. Participants were recruited from a community sample; therefore, mood symptoms varied across the continuum and the majority of participants did not meet diagnostic criteria for a depressive or anxiety disorder at the time of enrollment. Hormone sensitivity was quantified over an 8-week baseline period, using within-subjects correlations between repeated weekly measures of E2 serum concentrations and weekly anxiety (State Trait Anxiety Inventory) and anhedonia ratings (Snaith-Hamilton Pleasure Scale). Women were then randomized to receive 8 weeks of TE2 (0.1 mg) or transdermal placebo, and reward-seeking behaviors were assessed using the Effort-Expenditure for Rewards Task (EEfRT). RESULTS: Participants who were randomized to receive transdermal estradiol and who demonstrated greater anxiety sensitivity to E2 fluctuations at baseline, demonstrated more reward seeking behaviors on the EEfRT task. Notably, the strength of the association between E2-anxiety sensitivity and post-randomization EEfRT for TE2 participants increased when women experienced more recent stressful life events and rated those events as more stressful. E2-anhedonia sensitivity was not associated with reward-seeking behaviors. CONCLUSION: Perimenopausal women who are more sensitive to E2 fluctuations and experienced more recent life stress may experience a greater benefit of TE2 as evidenced by an increase in reward seeking behaviors.

Still a "hidden island"? The rodent insular cortex in drug seeking, reward, and risk.

The insular cortex (IC) is implicated in risky decision making and drug-seeking behaviors, in a manner dissociable from natural reward seeking. However, evidence from rodent studies of motivated behaviors suggests that the role of the IC is not always consistent across procedures. Moreover, there is evidence of dissociation of function between posterior (pIC) and anterior (aIC) subregions in these behaviors. Under which circumstances, and by which mechanisms, these IC subregions are recruited to regulate motivated behaviors remains unclear. Here, we discuss evidence of rodent pIC and aIC function across drug-related behaviors, natural reward seeking, and decision making under risk and highlight procedural differences that may account for seemingly conflicting findings. Although gaps in the literature persist, we hypothesize that IC activity is broadly important for selection of appropriate behaviors based on learned action-outcome contingencies and that associated risk is sufficient, but not necessary, to recruit the aIC in reward seeking without involving the pIC.

Effects of adolescent ethanol exposure on adult nondrug reward seeking behavior in male and female mice.

BACKGROUND: Adolescent alcohol use is associated with an increased likelihood of developing an alcohol use disorder in adulthood, potentially due to the effects of alcohol exposure on reward-seeking behavior. However, it remains unclear whether adolescent drinking is sufficient to alter nondrug reward seeking in adulthood. As adolescence is a period of both brain and sexual maturation, which occur in a sex-dependent manner, males and females may be differentially sensitive to the consequences of adolescent alcohol exposure. The present study investigated whether adolescent ethanol exposure affected food reward taking and seeking in male and female adult mice. METHODS: Male and female C57BL/6J mice underwent intermittent ethanol exposure (AIE) via vapor inhalation during early adolescence (28-42 days of age). At 10 weeks of age, the mice were trained in a conditioned place preference paradigm (CPP) for a food reward. We measured food consumption, CPP, and cFos expression in multiple brain regions following CPP testing. Data were analyzed using repeated measures analysis of variance with exposure (air vs. AIE), sex, and time as factors. RESULTS: AIE exposure increased food consumption during CPP training in adult male mice, but reduced pellet consumption in adult female mice. AIE exposure impaired CPP expression only in female mice. Despite these behavioral differences, exposure to the reward-paired chamber did not induce differential cFos expression following CPP testing in the prelimbic and infralimbic cortices or the nucleus accumbens core and shell. CONCLUSION: These findings indicate that adolescent ethanol exposure disrupted nondrug reward taking and seeking in adulthood in female mice and altered consumption in adult male mice.

Deep Brain Stimulation of the Medial Forebrain Bundle for Treatment-Resistant Depression: A Systematic Review Focused on the Long-Term Antidepressive Effect.

OBJECTIVE: Major depression affects millions of people worldwide and has important social and economic consequences. Since up to 30% of patients do not respond to several lines of antidepressive drugs, deep brain stimulation (DBS) has been evaluated for the management of treatment-resistant depression (TRD). The superolateral branch of the medial forebrain bundle (slMFB) appears as a "hypothesis-driven target" because of its role in the reward-seeking system, which is dysfunctional in depression. Although initial results of slMFB-DBS from open-label studies were promising and characterized by a rapid clinical response, long-term outcomes of neurostimulation for TRD deserve particular attention. Therefore, we performed a systematic review focused on the long-term outcome of slMFB-DBS. MATERIALS AND METHODS: A literature search using Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria was conducted to identify all studies reporting changes in depression scores after one-year follow-up and beyond. Patient, disease, surgical, and outcome data were extracted for statistical analysis. The Montgomery-Åsberg Depression Rating Scale (ΔMADRS) was used as the clinical outcome, defined as percentage reduction from baseline to follow-up evaluation. Responders' and remitters' rates were also calculated. RESULTS: From 56 studies screened for review, six studies comprising 34 patients met the inclusion criteria and were analyzed. After one year of active stimulation, ΔMADRS was 60.7% ± 4%; responders' and remitters' rates were 83.8% and 61.5%, respectively. At the last follow-up, four to five years after the implantation, ΔMADRS reached 74.7% ± 4.6%. The most common side effects were stimulation related and reversible with parameter adjustments. CONCLUSIONS: slMFB-DBS appears to have a strong antidepressive effect that increases over the years. Nevertheless, to date, the overall number of patients receiving implantations is limited, and the slMFB-DBS surgical technique seems to have an important impact on the clinical outcome. Further multicentric studies in a larger population are needed to confirm slMFB-DBS clinical outcomes.

Sex chromosome and gonadal hormone contributions to binge-like and aversion-resistant ethanol drinking behaviors in Four Core Genotypes mice.

Introduction: While substantial research has focused on the contribution of sex hormones to driving elevated levels of alcohol drinking in female rodents, fewer studies have investigated how genetic influences may underlie sex differences in this behavior. Methods: We used the Four Core Genotypes (FCG) mouse model to explore the contribution of sex chromosome complement (XX/XY) and gonad type [ovaries (Sry-)/testes (Sry+)] to ethanol (EtOH) consumption and quinine-resistant drinking across two voluntary self-administration tasks: limited access consumption in the home cage and an operant response task. Results: For limited access drinking in the dark, XY/Sry + (vs. XX/Sry +) mice consumed more 15% EtOH across sessions while preference for 15% EtOH vs. water was higher in XY vs. XX mice regardless of gonad type. XY chromosomes promoted quinine-resistant drinking in mice with ovaries (Sry-) and the estrous cycle did not affect the results. In the operant response task, responding for EtOH was concentration dependent in all genotypes except XX/Sry + mice, which maintained consistent response levels across all concentrations (5-20%) of EtOH. When increasing concentrations of quinine (100-500 µM) were added to the solution, FCG mice were insensitive to quinine-punished EtOH responding, regardless of sex chromosome complement. Sry + mice were further found to be insensitive to quinine when presented in water. Importantly, these effects were not influenced by sensitivity to EtOH's sedative effect, as no differences were observed in the time to lose the righting reflex or the time to regain the righting reflex between genotypes. Additionally, no differences in EtOH concentration in the blood were observed between any of the genotypes once the righting reflex was regained. Discussion: These results provide evidence that sex chromosome complement regulates EtOH consumption, preference, and aversion resistance and add to a growing body of literature suggesting that chromosomal sex may be an important contributor to alcohol drinking behaviors. Examination of sex-specific genetic differences may uncover promising new therapeutic targets for high-risk drinking.

Dissociated modulations of intranasal vasopressin on prosocial learning between reward-seeking and punishment-avoidance.

BACKGROUND: As an integral ingredient of human sociality, prosocial behavior requires learning what acts can benefit or harm others. However, it remains unknown how individuals adjust prosocial learning to avoid punishment or to pursue reward. Given that arginine vasopressin (AVP) is a neuropeptide that has been involved in modulating various social behaviors in mammals, it could be a crucial neurochemical facilitator that supports prosocial learning. METHODS: In 50 placebo controls and 54 participants with AVP administration, we examined the modulation of AVP on the prosocial learning characterized by reward and punishment framework, as well as its underlying neurocomputational mechanisms combining computational modeling, event-related potentials and oscillations. RESULTS: We found a self-bias that individuals learn to avoid punishment asymmetrically more severely than reward-seeking. Importantly, AVP increased behavioral performances and learning rates when making decisions to avoid losses for others and to obtain gains for self. These behavioral effects were underpinned by larger responses of stimulus-preceding negativity (SPN) to anticipation, as well as higher punishment-related feedback-related negativity (FRN) for prosocial learning and reward-related P300 for proself benefits, while FRN and P300 neural processes were integrated into theta (4-7 Hz) oscillation at the outcome evaluation stage. CONCLUSIONS: These results suggest that AVP context-dependently up-regulates altruism for concerning others' losses and reward-seeking for self-oriented benefits. Our findings provide insight into the selectively modulatory roles of AVP in prosocial behaviors depending on learning contexts between proself reward-seeking and prosocial punishment-avoidance.

Estrous cycle and hormone regulation of stress-induced reinstatement of reward seeking in female mice.

Women are more vulnerable to stress-induced craving, which may be associated with increased vulnerability to relapse. Susceptibility to stress-induced craving also appears to be modulated by the menstrual cycle and is negatively correlated with circulating progesterone levels in women. However, the factors that contribute to relapse vulnerability are poorly characterized in female animals. In this study, we assessed whether chronic ethanol exposure, estrous cycle, or exogenous progesterone administration modulated vulnerability to stress-induced reinstatement. To model ethanol dependence, adult female C57Bl/6J mice underwent chronic intermittent ethanol (CIE) exposure via vapor inhalation. Seventy-two hours after the final ethanol exposure, food-restricted mice began training in a conditioned place preference paradigm (CPP) for a food reward, followed by extinction training. Mice were then subjected to forced swim stress and assessed for reinstatement of their preference for the reward-paired chamber. CIE did not affect stress-induced reinstatement. However, stress-induced reinstatement was attenuated during the diestrus phase, when endogenous levels of progesterone peak in female mice. Further, administration of exogenous progesterone mimicked the attenuated reinstatement observed in diestrus. These findings indicate that circulating hormone levels modulate susceptibility to relapse-like behaviors and implicate progesterone as a potential target for treating stress-induced relapse in women.

From ensembles to meta-ensembles: Specific reward encoding by correlated network activity.

Neuronal ensembles are local, sparsely distributed populations of neurons that are reliably re-activated by a specific stimulus, context or task. Such discrete cell populations can be defined either functionally, by electrophysiological recordings or in vivo calcium imaging, or anatomically, using the expression of markers such as the immediate early gene cFos. A typical example of tasks that involve the formation of neuronal ensembles is reward learning, such as the cue-reward pairing during operant conditioning. These ensembles are re-activated during cue-presentation and increasing evidence suggests that this re-activation is the neurophysiological basis for the execution of reward-seeking behavior. Whilst the pursuit of rewards is a common daily activity, it is also related to the consumption of drugs, such as alcohol, and may result in problematic behaviors including addiction. Recent research has identified neuronal ensembles in several reward-related brain regions that control distinct aspects of a conditioned response, e.g., contextual information about the availability of a specific reward or the actions needed to retrieve this reward under the given circumstances. Here, we review studies using the activity marker cFos to identify and characterize neuronal ensembles related to alcohol and non-drug rewards with a special emphasis on the discrimination between different rewards by meta-ensembles, i.e., by dynamic co-activation of multiple ensembles across different brain areas.

The Arousal-motor Hypothesis of Dopamine Function: Evidence that Dopamine Facilitates Reward Seeking in Part by Maintaining Arousal.

Dopamine facilitates approach to reward via its actions on dopamine receptors in the nucleus accumbens. For example, blocking either D1 or D2 dopamine receptors in the accumbens reduces the proportion of reward-predictive cues to which rats respond with cued approach. Recent evidence indicates that accumbens dopamine also promotes wakefulness and arousal, but the relationship between dopamine's roles in arousal and reward seeking remains unexplored. Here, we show that the ability of systemic or intra-accumbens injections of the D1 antagonist SCH23390 to reduce cued approach to reward depends on the animal's state of arousal. Handling the animal, a manipulation known to increase arousal, was sufficient to reverse the behavioral effects of the antagonist. In addition, SCH23390 reduced spontaneous locomotion and increased time spent in sleep postures, both consistent with reduced arousal, but also increased time spent immobile in postures inconsistent with sleep. In contrast, the ability of the D2 antagonist haloperidol to reduce cued approach was not reversible by handling. Haloperidol reduced spontaneous locomotion but did not increase sleep postures, instead increasing immobility in non-sleep postures. We place these results in the context of the extensive literature on dopamine's contributions to behavior, and propose the arousal-motor hypothesis. This novel synthesis, which proposes that two main functions of dopamine are to promote arousal and facilitate motor behavior, accounts both for our findings and many previous behavioral observations that have led to disparate and conflicting conclusions.

Reversing anterior insular cortex neuronal hypoexcitability attenuates compulsive behavior in adolescent rats.

Development of self-regulatory competencies during adolescence is partially dependent on normative brain maturation. Here, we report that adolescent rats as compared to adults exhibit impulsive and compulsive-like behavioral traits, the latter being associated with lower expression of mRNA levels of the immediate early gene zif268 in the anterior insula cortex (AIC). This suggests that underdeveloped AIC function in adolescent rats could contribute to an immature pattern of interoceptive cue integration in decision making and a compulsive phenotype. In support of this, we report that layer 5 pyramidal neurons in the adolescent rat AIC are hypoexcitable and receive fewer glutamatergic synaptic inputs compared to adults. Chemogenetic activation of the AIC attenuated compulsive traits in adolescent rats supporting the idea that in early stages of AIC maturity there exists a suboptimal integration of sensory and cognitive information that contributes to inflexible behaviors in specific conditions of reward availability.

Dopamine signaling in the dorsomedial striatum promotes compulsive behavior.

Compulsive behavior is a defining feature of disorders such as substance use disorders. Current evidence suggests that corticostriatal circuits control the expression of established compulsions, but little is known about the mechanisms regulating the development of compulsions. We hypothesized that dopamine, a critical modulator of striatal synaptic plasticity, could control alterations in corticostriatal circuits leading to the development of compulsions (defined here as continued reward seeking in the face of punishment). We used dual-site fiber photometry to measure dopamine axon activity in the dorsomedial striatum (DMS) and the dorsolateral striatum (DLS) as compulsions emerged. Individual variability in the speed with which compulsions emerged was predicted by DMS dopamine axon activity. Amplifying this dopamine signal accelerated animals' transitions to compulsion, whereas inhibition delayed it. In contrast, amplifying DLS dopamine signaling had no effect on the emergence of compulsions. These results establish DMS dopamine signaling as a key controller of the development of compulsive reward seeking.

The nervous system as a solution for implementing closed negative feedback control loops.

Behavior can be regarded as the output of a system (action), as a function linking stimulus to response (reaction), or as an abstraction of the bidirectional relationship between the environment and the organism (interaction). When considering the latter possibility, a relevant question arises concerning how an organism can materially and continuously implement such a relationship during its lifetime in order to perpetuate itself. The feedback control approach has taken up the task of answering just that question. During the last several decades, said approach has been progressing and has started to be recognized as a paradigm shift, superseding certain canonical notions in mainstream behavior analysis, cognitive psychology, and even neuroscience. In this paper, we describe the main features of feedback control theory and its associated techniques, concentrating on its critiques of behavior analysis, as well as the commonalities they share. While some of feedback control theory's major critiques of behavior analysis arise from the fact that they focus on different levels of organization, we believe that some are legitimate and meaningful. Moreover, feedback control theory seems to blend with neurobiology more smoothly as compared to canonical behavior analysis, which only subsists in a scattered handful of fields. If this paradigm shift truly takes place, behavior analysts-whether they accept or reject this new currency-should be mindful of the basics of the feedback control approach.

Intermittent social stress produces different short- and long-term effects on effort-based reward-seeking behavior.

Previous studies show that intermittent social defeat (ISD) stress increases self-administration of psychostimulants, which suggests that ISD promotes reward-seeking behavior and, ultimately, increases vulnerability to develop drug abuse. The present study investigates whether ISD alters cost/benefit evaluations to promote reward-seeking behavior and whether these alterations are time-dependent. Male rats performed two different tasks that assessed their motivation to seek and consume food rewards. An effort-discounting task in which rats chose between less and more effortful options (i.e., 1 lever-press versus 2, 5, 10 or 20 lever-presses) associated with low- and high-reward (i.e., 1 sugar pellet versus 3 sugar pellets), respectively; and a progressive ratio task in which rats had to increase their effort (more lever presses) to obtain a sugar pellet. ISD consisted of exposing animals to social defeat once every three days for ten days (4 stress episodes). Rats were tested 24-48 h after stress episodes, and 1 week and 6 weeks after the last stress episode. In the effort-discounting task, stressed animals showed a decrease in their preference for high rewards associated with more effort (i.e., 10 and 20 lever-presses). These effects were transient and not maintained one week after stress. In the progressive ratio task, stressed animals showed an increase in the number of lever presses to obtain rewards that emerged six weeks after the last stress episode. These results suggest different short- and long-term effects on the motivation for rewards after ISD and indicate temporal dynamic adaptations in the function of the brain reward system.