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During adolescence, individuals experience a broad range of dynamic environments as they strive to establish independence. Learning to respond appropriately in both new and previously encountered environments requires that an individual identify and learn the meaning of cues indicating that a behavior is appropriate, or alternatively, that it should be altered or inhibited. Although the ability to regulate goal-directed behavior continues to develop across adolescence, the specific circumstances under which adolescents experience difficulty with inhibitory control remain unclear. Here we review recent findings in our laboratory that address how adolescents learn to proactively inhibit a response. Much of our research has utilized a negative occasion setting paradigm, in which one cue (a feature) gates the meaning of a second cue (a target). The feature provides information that resolves the ambiguity of the target and indicates the appropriate behavioral response to the target. As such, we have been able to determine how adolescents learn about ambiguous stimuli, such as those whose meaning changes in accordance with other features of the surrounding environment. We consider why adolescents in particular exhibit difficulty in negative occasion setting compared to either pre-adolescents or adults. In addition, we review findings indicating that a balance in neural activity between orbitofrontal cortex and nucleus accumbens is necessary to support normal negative occasion setting. Finally, we consider aspects of associative learning that may contribute to adolescent inhibitory control, as well as provide insight into adolescent behavior as a whole. [ABSTRACT FROM AUTHOR]

A wealth of data supports the notion that the hippocampus binds objects and events together in place and time. In support of this function, a cortical circuit that includes the retrosplenial cortex (RSC) and various structures in the parahippocampal region is thought to provide the hippocampus with essential information regarding the physical and temporal context in which the object/event occurs. However, it remains unclear if and how individual components of this so-called ‘where’ circuit make unique contributions to processing context-related information. Here we focus on the RSC and the postrhinal cortex (POR; homologous with parahippocampal cortex (PHC) in primates), two of the most strongly interconnected components of the where pathway and the foci of an increasing amount of recent research. Much of the behavioral evidence to date suggests that RSC and POR/PHC work closely together as a functional unit. We begin by briefly reviewing studies that have investigated the involvement of RSC and POR/PHC in contextual and spatial learning, both of which involve learning associations and relationships between the individual stimuli that compose an environment (i.e., where information). However, we propose that potential differences have been overlooked because most studies to date have relied on behavioral paradigms and experimental approaches that are not well suited for distinguishing between different aspects of information processing. We then consider the anatomical differences between RSC and POR/PHC and emerging behavioral evidence that gives rise to a working model of how these regions may differentially contribute to hippocampal-dependent learning and memory. We then discuss experimental designs and behavioral methods that may be useful in testing the model. Finally, approaches are described that may be valuable in probing the nature of information processing and neuroplasticity in the myriad of local circuits that are nested within the where pathway. [ABSTRACT FROM AUTHOR]

Abstract: Physical exercise induces widespread neurobiological adaptations and improves learning and memory. Most research in this field has focused on hippocampus-based spatial tasks and changes in brain-derived neurotrophic factor (BDNF) as a putative substrate underlying exercise-induced cognitive improvements. Chronic exercise can also be anxiolytic and causes adaptive changes in stress-reactivity. The present study employed a perirhinal cortex-dependent object recognition task as well as the elevated plus maze to directly test for interactions between the cognitive and anxiolytic effects of exercise in male Long Evans rats. Hippocampal and perirhinal cortex tissue was collected to determine whether the relationship between BDNF and cognitive performance extends to this non-spatial and non-hippocampal-dependent task. We also examined whether the cognitive improvements persisted once the exercise regimen was terminated. Our data indicate that 4weeks of voluntary exercise every-other-day improved object recognition memory. Importantly, BDNF expression in the perirhinal cortex of exercising rats was strongly correlated with object recognition memory. Exercise also decreased anxiety-like behavior, however there was no evidence to support a relationship between anxiety-like behavior and performance on the novel object recognition task. There was a trend for a negative relationship between anxiety-like behavior and hippocampal BDNF. Neither the cognitive improvements nor the relationship between cognitive function and perirhinal BDNF levels persisted after 2weeks of inactivity. These are the first data demonstrating that region-specific changes in BDNF protein levels are correlated with exercise-induced improvements in non-spatial memory, mediated by structures outside the hippocampus and are consistent with the theory that, with regard to object recognition, the anxiolytic and cognitive effects of exercise may be mediated through separable mechanisms. [ABSTRACT FROM AUTHOR]

Abstract: Mounting evidence indicates that the retrosplenial cortex (RSP) has a critical role in spatial navigation. The goal of the present study was to characterize the specific nature of spatial memory deficits that are observed following damage to RSP. Rats with RSP lesions or sham lesions were first trained in a working memory task using an 8-arm radial arm maze. Rats were allowed 5min to visit each arm and retrieve food pellets and a 5-s delay was imposed between arm choices. Consistent with previous research, rats with RSP damage committed more errors than controls. In particular, RSP-lesioned rats committed more errors of omission (failing to visit an arm of the maze), but there were no lesion effects on errors of commission (revisiting an arm). Neither group of rats exhibited a turn bias (i.e., always turning a certain direction when choosing an arm). At the end of the training phase of the experiment, both groups had reached asymptote and committed very few errors. In the subsequent test phase, a longer delay (30-s) was imposed during some sessions. Both control and RSP-lesioned rats continued to make few errors during sessions with the standard 5-s delay, but RSP-lesioned rats were impaired at the 30-s delay and committed more errors of commission, consistent with an increase in taxing spatial working memory. [Copyright &y& Elsevier]

Abstract: The posterior parietal cortex (PPC) of rats has most recently been defined based on patterns of thalamic and cortical connectivity. The anatomical characteristics of this area suggest that it may be homologous to the PPC of primates and contribute to similar functions. This review summarizes evidence for and against a role for the rat PPC in attention and working memory and evaluates how the function of the rat PPC compares to that of primates on these dimensions. Theories of how the rat PPC contributes to behavior are presented, including the notion that PPC may serve as an interface between attention and learning. Finally, several avenues for future research are considered. [Copyright &y& Elsevier]

• Pretraining lesions of retrosplenial cortex do not impair learning a negative pattering discrimination. • However, lesions or temporary silencing of retrosplenial cortex impairs the expression negative patterning. • This pattern of findings suggests that retrosplenial cortex is normally involved in forming configural representations. The retrosplenial cortex (RSC) is positioned at the interface between cortical sensory regions and the hippocampal/parahippocampal memory system. As such, it has been theorized that RSC may have a fundamental role in linking sensory stimuli together in the service of forming complex representations. To test this, three experiments were carried out to determine the effects of RSC damage or temporary inactivation on learning or performing a negative patterning discrimination. In this procedure, two conditioned stimuli are reinforced when they are presented individually (i.e., stimulus elements) but are non-reinforced when they are presented simultaneously as a compound stimulus. Normal rats successfully discriminate between the two types of trials as evidenced by more responding to the elements compared to the compound stimulus. This is thought to reflect the formation of a configural representation of the compound stimulus; that is, the two cues are linked together in such a fashion that the compound stimulus is a wholly different, unique stimulus. Permanent lesions of RSC made prior to training (Experiment 1) had no effect on learning the discrimination. However, lesions (Experiment 2) or temporary chemogenetic inactivation (Experiment 3) of RSC made after training impaired subsequent performance of the discrimination. We argue that this pattern of results indicates that RSC may normally be involved in forming the configural representations manifested in negative patterning, but that absent the RSC, other brain systems or structures can compensate sufficiently to result in normal behavior. [ABSTRACT FROM AUTHOR]

The retrosplenial cortex (RSC) is known to contribute to contextual and spatial learning and memory. This is consistent with its well-established connectivity; the RSC is located at the interface of visuo-spatial association areas and the parahippocampal–hippocampal memory system. However, the RSC also contributes to learning and memory for discrete cues. For example, both permanent lesions and temporary inactivation of the RSC have been shown to impair sensory preconditioning, a form of higher-order conditioning. The purpose of the present experiment was to examine the role of the RSC in a closely related higher-order conditioning paradigm: second-order conditioning. Sham and RSC lesioned rats received first-order conditioning in which one visual stimulus (V1) was paired with footshock and one visual stimulus (V2) was not. Following first-order conditioning, one auditory stimulus (A1) was then paired with V1 and a second auditory stimulus (A2) was paired with V2. Although lesions of the RSC impaired the first-order discrimination, they had no impact on the acquisition of second-order conditioning. Thus, the RSC does not appear necessary for acquisition/expression of second-order fear conditioning. The role of the RSC in higher-order conditioning, as well as a possible dissociation from the hippocampus, is discussed. [ABSTRACT FROM AUTHOR]

• Examined the role of the postrhinal cortex in the retrieval of auditory fear conditioning. • Inactivation of the postrhinal cortex impaired retrieval of auditory fear conditioning following extinction. • Inactivation of the postrhinal cortex also impaired retrieval of auditory fear conditioning that had not been extinguished. The postrhinal cortex (POR), the rodent homologue of the primate parahippocampal cortex (PHC), has been implicated in contextual and spatial processing. For instance, prior studies have demonstrated that permanent lesions of POR impair contextual fear conditioning. In contrast, permanent lesions of POR, specifically prior to training, do not impact auditory fear conditioning. In the current experiments, we examined the role of POR in the expression of auditory fear conditioning by using chemogenetics to silence neural activity in POR at the time of retrieval testing. Considering that extinction is context-dependent, and POR contributes to contextual memory, we hypothesized that POR would be necessary for expression of auditory fear conditioning following extinction. We found that POR inactivation during retrieval impaired freezing to an auditory cue that was tested in the conditioning context (A) after it had been extinguished in a different context (B). However, the involvement of POR was not specific to extinction. POR inactivation also impaired freezing to an auditory fear cue that had not undergone extinction. Thus, while prior studies have identified a role for POR in contextual fear conditioning, the current findings extend the functional role of POR to include the expression of auditory fear conditioning. [ABSTRACT FROM AUTHOR]

• RSC inactivation impaired retrieval of remotely acquired delay fear conditioning (FC). • RSC inactivation did not impair retrieval of recently acquired delay FC. • RSC inactivation during encoding did not impair later retrieval of delay FC. Prior studies with permanent lesion methods have demonstrated a role for the retrosplenial cortex (RSC) in the retrieval of remotely, but not recently, acquired delay fear conditioning. To extend the generalizability of these prior findings, the present experiments used chemogenetics to temporarily inactivate the RSC during either retrieval or encoding of delay auditory fear conditioning. Inactivation of the RSC at the time of test impaired retrieval of a remotely conditioned auditory cue, but not a recently conditioned one. In addition, inactivation of the RSC during encoding had no impact on freezing during later retrieval testing for both a remotely and recently conditioned auditory cue. These findings indicate that the RSC contributes to the retrieval, but not encoding, of remotely acquired auditory fear conditioning, and suggest it has less of a role in both retrieval and encoding of recently acquired auditory fear conditioning. [ABSTRACT FROM AUTHOR]