The prefrontal cortex plays an important role in reward processing in humans and nonhuman primates. In the current study we examined reward modulation in the single cell activity of the avian analog of the prefrontal cortex, the nidopallium caudolaterale (NCL). Pigeons had to peck at stimuli that represented either no reward, a small reward, or a large reward in a no-choice condition (only one stimulus presented) or a choice condition (two stimuli presented simultaneously). Of the 92 recorded cells, 34 cells showed some form of reward modulation, either during the stimulus presentation or the delay activity preceding the delivery of reward in the no-choice or choice condition. Latencies to peck at the stimulus revealed that the differences in reward amount were behaviorally significant to the pigeons. Moreover, a majority of cells (approximately 70%) showed activity during the actual reward phase. Our results show that cells in the NCL modulate their response as a function of the amount of reward.

The neurophysiology underlying temporal perception significantly overlaps with areas of dysfunction identified in schizophrenia. Patients commonly exhibit distorted temporal perception, which likely contributes to functional impairments. Thus, study of temporal perception in animal models of the disease may help to understand both cognitive and neurobiological factors involved in functional impairments in patients. As maternal immune activation (MIA) has been shown to be a significant etiological risk factor in development of schizophrenia and other developmental psychiatric diseases, we tested interval timing in a rat model of MIA that has previously been shown to recapitulate several behavioural and neurophysiological impairments observed in the disease. Rats were tested on a temporal-bisection task, in which temporal duration stimuli were categorized as either “short” or “long” by responding to a corresponding lever. Data from this task were modeled to provide estimates of accuracy and sensitivity of temporal perception. Parameter estimates derived from the model fitting showed that MIA rats significantly overestimated the passage of time compared to controls. These results indicate that the MIA rat paradigm recapitulates timing distortions that are phenotypical of schizophrenia. These findings lend further support to the epidemiological validity of this MIA rat model, supporting its relevance for future research into the role of maternal immune activation in producing neurobiological and behavioural impairments in schizophrenia.

It has recently been recognized that orbitofrontal cortex has 2 subdivisions that are anatomically and functionally distinct. Most rodent research has focused on the lateral subdivision, leaving the medial subdivision (mOFC) relatively unexplored. We recently showed that inhibiting mOFC neurons eliminated the differential impact of reward probability cues on discrimination accuracy in a sustained attention task. In the present study, we tested whether increasing mOFC neuronal activity in rats would accelerate acquisition of reward contingencies. mOFC neuronal activity was increased using the DREADD (Designer Receptors Exclusively Activated by Designer Drugs) method, in which clozapine-N-oxide administration leads to neuronal modulation by acting on synthetic receptors not normally expressed in the rat brain. We predicted that rats with neuronal activation in mOFC would require fewer sessions than controls for acquisition of a task in which visual cues signal the probability of reward for correct discrimination performance. Contrary to this prediction, mOFC neuronal activation impaired task acquisition, suggesting mOFC may play a role in learning relationships between environmental cues and reward probability or for using that information in adaptive decision-making. In addition, disrupted mOFC activity may contribute to psychiatric conditions in which learning associations between environmental cues and reward probability is impaired. (PsycINFO Database Record

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Maternal immune activation (MIA) during gestation is a significant risk factor for development of schizophrenia and other neurodevelopmental diseases. In animal models of this risk factor, MIA during pregnancy can produce offspring that recapitulate certain aspects of the behavioral and neurophysiological impairments seen in schizophrenia. Here, the authors tested the effect of polyinosinic-polycytidylic acid (poly I:C)-induced MIA in a task that explicitly assays the interaction between motivation and cognition. In our paradigm, discrimination accuracy during a sustained-attention task is differentially impacted by environmental cues that signal the probability of reward for accurate performance. Cognition-motivation interactions are implicated in producing functional impairments in patients. Therefore, to the extent that this MIA model recapitulates such impairments, the authors predicted impaired ability of reward-associated signals to modulate cognitive performance in MIA rat offpsring. Adult offspring of dams in which MIA was induced displayed impaired prepulse inhibition relative to controls, verifying a functional effect of poly I:C induction. Despite this deficit, there were no differences between MIA and control rats in any aspects of task learning or performance, including under extinction and reacquisition conditions. These results indicate that MIA spares functioning of some of the cognitive, motivational, and decision-making processes that are impacted in schizophrenia and suggest that MIA as an isolated manipulation does not model the full range and nuance of the cognitive and motivational impairments in the disease. The authors suggest that some aspects of the functional impairment in schizophrenia and other neurodevelopmental diseases may be better modeled using multiple "hit" models of disease risk. (PsycINFO Database Record