The nucleus accumbens (Nacb) receives inputs from hippocampus and amygdala but it is still unclear how these inputs are functionally organized and may interact. The interplay between these input pathways was examined using electrophysiological tools in the rat, in vivo, under halothane anesthesia. After fornix/fimbria stimulation (Fo/Fi, subicular projection fibers to the Nacb), mono-and polysynaptically driven single units were recorded in the medial shell/core regions of the Nacb and in the ventromedial caudate putamen. Monosynaptically driven neurons by basolateral amygdala (BLA) stimulation were found in the medial shell/core and in the ventrolateral shell/core regions. In the areas of convergence (medial shell/core), paired activation of BLA followed by that of Fo/Fi resulted in an enhancement of the Fo/Fi response, whereas stimulation in the reverse order, Fo/Fi followed by BLA, led to a depression of the BLA response. In addition to these patterns of interactions, the tetanization of the Fo/Fi to Nacb pathway caused a homosynaptic decremental (long-term) potentiation in the Nacb, accompanied by a heterosynaptic (long-term) depression of the nontetanized BLA to Nacb pathway. We postulate that the hippocampal inputs may close a "gate" for the amygdala inputs, whereas the gate is opened for the hippocampus inputs by previous amygdalar activity. These opposite effects on the Nacb neuronal populations should be taken into account when interpreting behavioral phenomena, particularly with respect to the contrasting effects of the amygdala and the hippocampus in locomotion and place learning.

The orbitofrontal cortex (OBFc) has been suggested to code the motivational value of environmental stimuli and to use this information for the flexible guidance of goal-directed behavior. To examine whether information regarding reward prediction is quantitatively represented in the rat OBFc, neural activity was recorded during an olfactory discrimination "go"/"no-go" task in which five different odor stimuli were predictive for various amounts of reward or an aversive reinforcer. Neural correlates related to both actual and expected reward magnitude were observed. Responses related to reward expectation occurred during the execution of the behavioral response toward the reward site and within a waiting period prior to reinforcement delivery. About one-half of these neurons demonstrated differential firing toward the different reward sizes. These data provide new and strong evidence that reward expectancy, regardless of reward magnitude, is coded by neurons of the rat OBFc, and are indicative for representation of quantitative information concerning expected reward. Moreover, neural correlates of reward expectancy appear to be distributed across both motor and nonmotor phases of the task.It has been noted for a long time that the magnitude of a primary reinforcer exerts a profound effect on the selection and speed of behavioral responses (Black 1968;Campbell and Seiden 1974;Brown and Bowman 1995;Boysen et al. 2001;Bohn et al. 2003). Likewise, in computational neuroscience, different algorithms for reinforcement learning (RL) consider reward magnitude an important parameter to be gauged and predicted during sensorimotor processing (Sutton and Barto 1981;Schultz et al. 1997). In one of these models, in which glutamate serves as a reinforcing signal guiding synaptic modifications necessary for adapting operant behavior, reward-related information is primarily processed by glutamatergic projection neurons of the orbitofrontal cortex (OBFc), basolateral amygdala, and related limbic areas

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Drug safety alerts were generated in one third of orders and were frequently overridden. Duplicate order alerts more often resulted in order cancellation (20%) than did alerts for overdose (11%) or DDIs (2%). DDIs were most frequently overridden. Only a small number of DDIs caused these overrides. Studies on improvement of alert handling should focus on these frequently-overridden DDIs.