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Adaptive agents must act in intrinsically uncertain environments with complex latent structure. Here, we elaborate a model of visual foraging-in a hierarchical context-wherein agents infer a higher-order visual pattern (a "scene") by sequentially sampling ambiguous cues. Inspired by previous models of scene construction-that cast perception and action as consequences of approximate Bayesian inference-we use active inference to simulate decisions of agents categorizing a scene in a hierarchically-structured setting. Under active inference, agents develop probabilistic beliefs about their environment, while actively sampling it to maximize the evidence for their internal generative model. This approximate evidence maximization (i.e., self-evidencing) comprises drives to both maximize rewards and resolve uncertainty about hidden states. This is realized via minimization of a free energy functional of posterior beliefs about both the world as well as the actions used to sample or perturb it, corresponding to perception and action, respectively. We show that active inference, in the context of hierarchical scene construction, gives rise to many empirical evidence accumulation phenomena, such as noise-sensitive reaction times and epistemic saccades. We explain these behaviors in terms of the principled drives that constitute the expected free energy, the key quantity for evaluating policies under active inference. In addition, we report novel behaviors exhibited by these active inference agents that furnish new predictions for research on evidence accumulation and perceptual decision-making. We discuss the implications of this hierarchical active inference scheme for tasks that require planned sequences of information-gathering actions to infer compositional latent structure (such as visual scene construction and sentence comprehension). This work sets the stage for future experiments to investigate active inference in relation to other formulations of evidence accumulation (e.g., drift-diffusion models) in tasks that require planning in uncertain environments with higher-order structure.

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Sleep abnormalities have widespread and costly public health consequences, yet we have only a rudimentary understanding of the events occurring at the cellular level in the brain that regulate sleep. Several key signaling molecules that regulate sleep across taxa come from the family of neuropeptide transmitters. For example, in Drosophila melanogaster, the neuropeptide Y (NPY)-related transmitter short neuropeptide F (sNPF) appears to promote sleep. In this study, we utilized optogenetic activation of neuronal populations expressing sNPF to determine the causal effects of precisely timed activity in these cells on sleep behavior. Combining sNPF-GAL4 and UAS-Chrimson transgenes allowed us to activate sNPF neurons using red light. We found that activating sNPF neurons for as little as 3 s at a time of day when most flies were awake caused a rapid transition to sleep that persisted for another 2+ hours following the stimulation. Changing the timing of red light stimulation to times of day when flies were already asleep caused the control flies to wake up (due to the pulse of light), but the flies in which sNPF neurons were activated stayed asleep through the light pulse, and then showed further increases in sleep at later points when they would have normally been waking up. Video recording of individual fly responses to short-term (0.5-20 s) activation of sNPF neurons demonstrated a clear light duration-dependent decrease in movement during the subsequent 4-min period. These results provide supportive evidence that sNPF-producing neurons promote long-lasting increases in sleep, and show for the first time that even brief periods of activation of these neurons can cause changes in behavior that persist after cessation of activation. We have also presented evidence that sNPF neuron activation produces a homeostatic sleep drive that can be dissipated at times long after the neurons were stimulated. Future studies will determine the specific roles of sub-populations of sNPF-producing neurons, and will also assess how sNPF neurons act in concert with other neuronal circuits to control sleep.

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We recently developed a conditioned place preference (CPP) procedure, commonly used to study rewarding drug effects, to demonstrate that dominant sexually-experienced CD-1 male mice form CPP to contexts previously associated with defeating subordinate male C57BL/6J mice. Here we further characterized conditioned and unconditioned aggression behavior in CD-1 mice. In Exp. 1 we used CD-1 mice that displayed a variable spectrum of unconditioned aggressive behavior toward younger subordinate C57BL/6J intruder mice. We then trained the CD-1 mice in the CPP procedure where one context was intruder-paired, while a different context was not. We then tested for aggression CPP 1 day after training. In Exp. 2, we tested CD-1 mice for aggression CPP 1 day and 18 days after training. In Exp. 3-4, we trained the CD-1 mice to lever-press for palatable food and tested them for footshock punishment-induced suppression of food-reinforced responding. In Exp. 5, we characterized unconditioned aggression in hybrid CD-1 × C57BL/6J D1-Cre or D2-Cre F1 generation crosses. Persistent aggression CPP was observed in CD-1 mice that either immediately attacked C57BL/6J mice during all screening sessions or mice that gradually developed aggressive behavior during the screening phase. In contrast, CD-1 mice that did not attack the C57BL/6J mice during screening did not develop CPP to contexts previously paired with C57BL/6J mice. The aggressive phenotype did not predict resistance to punishment-induced suppression of food-reinforced responding. CD-1 × D1-Cre or D2-Cre F1 transgenic mice showed strong unconditioned aggression. Our study demonstrates that aggression experience causes persistent CPP and introduces transgenic mice for circuit studies of aggression.

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LoVo adenocarcinoma cells are fairly sensitive to cytostatic drugs, e.g. doxorubicin, but can develop drug resistance by expression of a P-glycoprotein-mediated MDR1 phenotype. LoVo cells respond with apoptosis to nanomolar concentrations of okadaic acid and micromolar concentrations of cantharidic acid. Interestingly, LoVoDx cells which had become about 10-fold less sensitive to doxorubicin by incubation in increasing concentrations of this cytostatic drug were also less sensitive to the toxicity of okadaic acid. Resistance to both agents was lost or significantly reduced by incubation in drug-free medium for about 4 months. On the other hand, LoVoDx cells did not lose responsiveness to the structurally different phosphatase inhibitor cantharidic acid but were about twofold more sensitive to the cytotoxic effect of this agent. Thus, MDR expression protects LoVo cells from the toxicity of phosphatase inhibitors that presumably are substrates of the P-glycoprotein, e.g. okadaic acid and its derivatives but not cantharidic acid, despite the fact that both agents are potent inducers of apoptotic cell death via ser/thr phosphatase inhibition.

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Plant height can be regulated by manipulation of day (DT) and night temperatures (NT). Traditionally, commercial flower crops are grown with a DT higher than the NT, which results in greater internode length than when the regimen is reversed. Because temperature manipulation is a popular height-control tool among growers, the influence of DT/NT regimens of 16/16, 19/19, 22/22, 16/19, 19/22, 16/22, 19/16, 22/19, and 22/16°C on foliage susceptibility to Botrytis cinerea was investigated. After a minimum 3-week temperature treatment, seed geraniums (Pelargonium × hortorum), petunias (Petunia × hybrida), and impatiens (Impatiens wallerana) were inoculated with 2.7 × 105 B. cinerea conidia per ml of water and incubated at 20°C for the duration of the experiment. When averaged over two experiments, the maximum proportion of geranium, petunia, and impatiens foliage infected was 81.5, 35.5, and 27.0%, respectively. The maximum proportion of leaves supporting sporulating B. cinerea was 59.5% for geraniums, 25.5% for petunias, and 5.5% for impatiens. Area under the disease progress curve data indicated that susceptibility of bedding plant foliage was not influenced by the difference in DT/NT regimens. Results suggest that growers that use higher NT than DT to limit plant height do not increase host susceptibility to B. cinerea. However, more rigorous disease management strategies are needed for production of seed geraniums than for petunias or impatiens.

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Sixty agoraphobics were treated by behavioural therapy (self-exposure in vivo) either with their partner involved in all aspects of treatment or without their partner. The two treatment formats were about equally effective. Behavioural treatment directed at the agoraphobia resulted in improvement irrespective of marital quality and partner involvement in the therapy. The effects of treatment led neither to a deterioration of the marriage nor to adjustment problems in the partner. Avoidance behaviour, intropunitivity and overprotection were found to predict treatment response. The partners of agoraphobics were not found to have psychological problems themselves.

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