Behavioral Neuroscience

Chronic stressor exposure impairs extinction of fear in adolescent rats and has associated effects on perineuronal nets and parvalbumin interneurons.
Adolescents, both human and nonhuman, exhibit impairments in the extinction of learned fear, an effect that is exacerbated, at least in rodents, by exposure to chronic stress. However, we have little understanding of the mechanisms underlying this effect. Therefore, here, we examined whether corticosterone exposure, a model of chronic stress, alters the expression of inhibitory neurons expressing parvalbumin (PV) in the basolateral amygdala and prefrontal cortex, two brain regions that have been implicated in fear extinction memories, in adolescent rats. We also examined the expression of perineuronal nets (PNNs), extracellular matrix structures that encompass inhibitory interneurons, in these two regions. These structures might render fear memories resistant to extinction by applying a structural “brake” on the plasticity of fear memories. Corticosterone-exposed adolescent rats exhibited poor extinction retention, as in past work, and were also found to have reduced percentage of PV-positive cells surrounded by PNNs in the basolateral amygdala. PV cells and PNNs were unaffected by corticosterone exposure in the prefrontal cortex. Our results suggest that the altered function of amygdala interneurons may be associated with the impaired extinction performance in stress-exposed adolescent rats. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
Slight and hidden hearing loss in young rats is associated with impaired recognition memory and reduced myelination in the corpus callosum.
Slight and hidden hearing loss in children have been linked to cognitive and social difficulties, and yet the neurobiological mechanisms behind these issues remain poorly understood. Most animal models focus on severe hearing loss, leaving the effects of hidden or slight hearing loss largely unexplored. To uncover the neural mechanisms connecting slight/hidden hearing loss to cognitive and social challenges, we induced hearing loss in young (4-week-old) Wistar rats through noise exposure. We then examined cognitive function (object recognition test) and social behavior (juvenile play behavior and social interaction). Changes in brain anatomy were assessed using cortical thickness and hippocampal size measurements, while (immuno)histochemical staining investigated neuronal circuitry maturation (myelin basic protein, parvalbumin, and perineuronal nets) and neurogenesis (doublecortin). Noise-exposed rats displayed slight high-frequency hearing loss (around 20 dB) and hidden hearing loss at other tested frequencies. This slight/hidden hearing loss was associated with impaired object recognition but did not alter social behavior. Slight/hidden hearing loss was associated with reduced myelin basic protein expression in the corpus callosum but no other alterations in cortical thickness, hippocampal size, or other markers of maturation and neurogenesis were found. These findings show that even slight/hidden hearing loss can lead to subtle brain alterations tied to cognitive deficits. This study emphasizes the need for further research to fully understand the brain changes associated with slight/hidden hearing loss and to pinpoint the mechanisms connecting these changes to behavioral deficits. This information is crucial to develop interventions to prevent the cognitive and social consequences of hearing loss. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
Trait-level somatic anxiety modulates functional magnetic resonance imaging (fMRI) neural synchrony to naturalistic stimuli.
Somatic anxiety refers to the tendency to appraise situations as threatening, leading to heightened physiological arousal. Symptoms associated with higher levels of somatic anxiety that reflect autonomic arousal and perceptions of threat include elevated heartbeat perception, difficulty breathing, and palpitation. Somatic anxiety is generally associated with increased stimulus-driven attention; however, it is currently unknown how somatic anxiety modulates neural synchrony, measured by intersubject correlations (ISC), in response to complex audiovisual stimuli. The present study seeks to identify how differing levels of somatic anxiety are associated with neural synchrony during psychological processing of audiovisual stimuli, as measured by ISC and intersubject representational similarity analyses. We hypothesize that individuals with higher levels of somatic anxiety will show heightened ISC in response to an audiovisual stimulus in regions associated with stimulus-driven attention, including the superior parietal lobule, supplementary motor area, and precentral gyrus. Results from this study identified that higher levels of somatic anxiety are associated with widespread heightened ISC across the brain, including in regions associated with perceptual processing and stimulus-driven attention. Taken together, this research suggests that higher levels of somatic anxiety are associated with similar processing in brain regions involved in stimulus-driven attention and top-down processing, whereas lower levels of somatic anxiety are associated with similar processing in brain regions associated with higher level visual processing. These results collectively emphasize that somatic anxiety levels should be measured and controlled for during naturalistic functional magnetic resonance imaging paradigms, as this trait may have an influence on synchronous neurological activity. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
Effects of manipulating prefrontal activity and dopamine D1 receptor signaling in an appetitive feature-negative discrimination learning task.
Healthy cognition requires inhibitory modulation of associative learning; conversely, impaired inhibitory discrimination is implicated in behavioral disorders. The medial prefrontal cortex (mPFC) and its dopamine innervation are key to understanding inhibition and impulsivity. We therefore examined the role of prelimbic and infralimbic cortices in within-subjects appetitive feature-negative learning using microinfusions of (a) the gamma-aminobutyric acid-A receptor agonist muscimol (0.25 μg in 1.0 μl; N = 35), (b) the dopamine D1 receptor agonist SKF-81297 (0.1 μg in 1.0 μl; N = 33), and (c) the dopamine D1 receptor antagonist SCH-23390 (5 μg in 1.0 μl; N = 35). A conditioned stimulus (CS) was followed by food, but on trials on which the CS (A+) was compounded with the inhibitory cue (AX−), the food delivery was canceled. Difference scores (CS–preCS responding) were used to measure learning. All three experiments showed the feature-negative discrimination (A+/AX−), as decreased responding to AX− versus A+. This discrimination was reduced but preserved following muscimol infusions in Experiment 1. Similarly, in Experiments 2 and 3, infusions of SKF-81297 and SCH-23390 were both without effect on the acquisition of the discrimination. Like muscimol, SCH-23390 reduced difference score responding, consistent with nonspecific effects on the (expression of) learning. Thus, there was no evidence to suggest that inactivation of prelimbic or infralimbic cortices impaired feature-negative discrimination learning and no evidence for dopaminergic modulation of such learning in the medial prefrontal cortex either. These results are discussed in the context of the nonspecific effects of the infusions and the overall inconsistent performance in summation and retardation tests of conditioned inhibition. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
Taste enhances the ability to express a preference for a congruent odor in rats.
Foods that make up a typical diet are characterized by a rich set of sensory qualities that are perceived through multiple different modalities. It is well known that multisensory aspects of food are integrated to create our perception of flavor, which in turn affects our behavioral responses to food. However, the principles underlying multisensory integration of flavor-related sensory signals and how they inform perceptual judgments remain poorly understood, partly due to lack of control over flavor experience in human subjects. Here, we used rats as a model to overcome this limitation and tested the hypothesis that taste can enhance discriminability of retronasal odor cues. In a series of two-bottle tests, animals chose between two odorized solutions after learning to associate one of the odors with saccharin. When odors were highly similar, animals showed little preference for the saccharin-associated odor. When adding saccharin to both bottles—rendering one of the solutions’ congruent—animals’ preference for the saccharin-associated odor was significantly enhanced. No effect of taste was observed when using dissimilar odor pairs or novel taste stimuli. These findings suggest that congruent taste stimuli selectively enhance odor identity representations, aiding in the discriminability of perceptually similar flavors. (PsycInfo Database Record (c) 2024 APA, all rights reserved)
Memory reconsolidation and amnesia induction: Separate processes dependent on specific protein and RNA synthesis.
The reconsolidation hypothesis posits that memory retrieval initiates a phase of memory destabilization, followed by restabilization through protein synthesis-dependent processes. The disruption of reconsolidation by amnestic agents can lead to memory loss. Yet, this hypothesis leaves unanswered questions regarding the mechanisms driving amnesia induction and reversal of molecular and structural changes underlying memory retention. Our previous work proposed that amnesia induction is an active process reliant on both translation and transcription. To test this hypothesis, we explored the role of N-methyl-D-aspartate (NMDA) glutamate receptors, as well as protein and RNA synthesis in amnesia induction mechanisms in grape snails trained with conditional food aversion, during the initial hours following memory reconsolidation disruption. Our results reveal that protein synthesis inhibitor administration before the conditioned reminder stimulus caused amnesia 3 hr after the reminder, whereas NMDA glutamate receptor antagonists resulted in amnesia less than 20 min following the first conditioned reminder stimulus. Concurrent administration of an NMDA receptor antagonist and a protein synthesis inhibitor before the reminder resulted in a rapid (less than 20 min) and complete prevention of amnesia, underscoring the pivotal role of protein synthesis in NMDA-dependent amnesia induction. Conversely, RNA synthesis inhibitors did not affect memory reconsolidation but inhibited amnesia triggered by an NMDA receptor antagonist. Moreover, our study demonstrates a significant difference in the dependency of memory reconsolidation and amnesia induction “time windows” on protein synthesis. These findings lend support to our hypothesis that memory reconsolidation and amnesia represent distinct processes, each characterized by unique developmental dynamics and molecular underpinnings. (PsycInfo Database Record (c) 2024 APA, all rights reserved)

Behavioral Neuroscience - Vol 138, Iss 6