Behavioral neuroscience最新文献

Video exposure is known to affect brain function, yet its impact on neurodevelopmental processes remains unclear. This study aimed to investigate whether exposure to a video depicting social behavior induces behavioral and neurological changes in socially isolated mice. On Postnatal Day (PND) 21, male mice were separated from their dams and randomly assigned to three groups: socially grouped mice; socially isolated mice (ISO), where mice were housed without any social stimulation; and social video-exposed mice (SVE), where mice were exposed to a social video played on a tablet from PND21 to PND56 under socially isolated conditions. On PND56, all animals underwent behavioral tests. Compared to the socially grouped mice and ISO group, the SVE group showed an attenuated response to amphetamine treatment. In the social cognition test, the ISO group exhibited decreased affiliative behavior and increased offensive and defensive behavior. However, the SVE group showed a partial improvement in social cognition, including increased affiliative behaviors and decreased defensive behaviors, although no changes in offensive behaviors were observed. Furthermore, the SVE group exhibited elevated levels of tyrosine hydroxylase and dopamine transporter in key social cognition regions-namely the prefrontal cortex, retrosplenial cortex, and hippocampus. This neurochemical shift implies that socially isolated mice can acquire social behaviors through exposure to video-based social interactions. These effects may be related to the compensatory response of the dopamine system, which is implicated in various psychiatric disorders. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Sexual behavior in female rats varies depending on sexual history and the combination of ovarian hormones administered to induce receptivity. Experiment 1 tested whether paced mating behavior differed in sexually experienced rats when receptivity was induced with sequential estradiol benzoate (EB) and progesterone (P) or EB-Alone. Rats gained paced mating experience under EB/P (10 μg EB 48 hr + 1 mg P 4-6 hr before mating) and then were primed with EB-Alone (2 μg EB for 6 days). Rats primed with EB-Alone were fully receptive but returned to the male more slowly, spent less time with the male, had longer interintromission intervals, showed fewer proceptive behaviors and more rejection behaviors, and had significantly longer test durations compared to when rats were primed with EB/P. Experiment 2 tested whether sexual experience-induced changes to paced mating behavior occur under both EB/P and EB-Alone hormone priming regimens. Rats received EB/P or EB-Alone prior to four paced mating tests. With sexual experience under either hormone regimen, rats showed shorter contact-return latencies to intromission, shorter interintromission intervals, and more proceptive behaviors. However, relative to EB/P-primed rats, EB-Alone-primed rats exited the male compartment more frequently after mounts and intromissions, spent less time with the male, had longer interintromission intervals, displayed fewer proceptive behaviors and more rejection behaviors, and had longer test durations, indicating lower sexual motivation. Collectively, these data illustrate that experience-enhanced paced mating behavior occurs with either EB/P or EB-Alone priming, but progesterone further facilitates mating behavior. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Individuals diagnosed with stress-related psychiatric disorders in adulthood are likely to have experienced early life stress, suggesting that early adversity is an important vulnerability factor in the subsequent development of trauma- and anxiety-related psychiatric illness. It is important to develop animal models of psychiatric dysfunction to determine evident vulnerability considerations, potential biomarkers, and novel treatment avenues to improve the human condition. In our model of acute early life stress (aELS), 15 footshocks are delivered in a single session on postnatal day 17. The following experiments investigated the persistent impacts of our aELS procedure on stress-enhanced fear learning, anxiety-related behaviors, maintenance of fear, and resistance to extinction in adult male and female rats. The findings from these experiments demonstrate that our aELS procedure yields enhanced fear learning and increased anxiety. This enhanced fear is maintained over time, yet it extinguishes normally. Taken together, these results demonstrate that exposure to 15 footshocks during a single session early in life (postnatal day 17) recapitulates a number of important features of trauma- and anxiety-related disorder symptomatology, but not others. Future studies are needed to determine the persistent physiological phenotypes resulting from aELS and the neurobiological mechanisms that mediate these long-term changes. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Prodromal signs of Parkinson's disease (PD), including vocal communication deficits, are poorly understood and do not respond adequately to current pharmacologic treatments. Norepinephrine dysfunction is involved early in PD; thus, drug therapies targeting norepinephrine may be useful as a treatment of prodromal signs. This study used a validated, translational rodent model of prodromal PD, the male Pink1-/- rat, which exhibits ultrasonic vocalization (USV) deficits as early as 2 months of age. The purpose of this preclinical study was to investigate a dose-dependent (2.5, 5.0, 7.5, 10 mg/kg) response of methylphenidate on USV parameters with the hypothesis that methylphenidate would increase vocalization output. Because methylphenidate is a psychostimulant with known adverse side effects, we also hypothesized that potential side effects including anxietylike behavior and spontaneous activity would be increased in a dose-dependent manner. To accomplish this, wild-type (WT) and Pink1-/- rats were administered a dose of a vehicle (saline) and a methylphenidate dose in a randomized within-subjects design and then assessed for USVs, anxiety behavior (open field), and limb motor (cylinder) activity. The results suggest that methylphenidate does not alter USV emissions in Pink1-/- rats; however, methylphenidate increased the total number of vocalizations and duration of frequency-modulated calls in WT rats. Methylphenidate dose dependently influenced spontaneous movements in both WT and Pink1-/- rats, as expected, while methylphenidate increased anxiety in Pink1-/- rats and not WT rats. This study demonstrates a difference in response to a psychostimulant between Pink1-/- rats and WT rats. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

The posterior parietal cortex (PPC) is an associative neocortical region that integrates multiple streams of information and is implicated in spatial cognition and decision making. In some cases, however, the PPC is not required for these functions. One possibility is that the PPC is recruited when spatial complexity is high. Yet, few studies of PPC function have explicitly manipulated environmental complexity, complexity of spatial changes, or the temporal structure of spatial tasks. To examine whether task complexity recruits PPC function, we tested rats with neurotoxic damage to the dorsal PPC on a series of tasks varying in spatial and temporal complexity. Recognition memory was first assessed in standard exploration tasks, including object recognition, object location, and object in place, as well as a more complex object task in which spatial changes occurred across multiple delays. Spatial navigation was assessed in the circular hole board maze (Barnes maze), and temporal processing was assessed in a temporal order task. PPC damage spared performance on standard recognition memory tasks but caused deficits on tasks involving changes in object configuration or multiple changes across time. PPC damage spared acquisition on the Barnes maze but impaired retention and decreased efficiency of search strategies. PPC damage did not impact temporal order memory. Overall, these results suggest that the PPC is necessary when spatial complexity of the task increases attentional and long-term memory demands. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Anxiety is highly common, and stress is a major trigger for anxiety. Anxiety includes heightened threat assessment and avoidance, but we do not fully understand which components are sensitive to stress. Rodents show a balance of exploration and avoidance that incorporates threat assessment prior to making the relatively risky decision to explore an open area. The purpose of this study was to determine if stress impacts risk assessment and if this is tied to the effects of stress on exploration. The present study used elevated plus maze (EPM) to test the effects of repeated social defeat stress (RSDS) on risk assessment behaviors in adult male rats. We then tested the effects of diazepam, an anxiolytic that reduces the impact of stress on EPM exploration, to further clarify the relationship between risk assessment and risky behavior in the EPM. We found that RSDS decreased time in the open arm, similar to prior studies. We also found that RSDS increased the likelihood of the primary risk assessment behavior, stretch and attend posture (SAP), increased SAP prior to entering an open arm, and decreased the likelihood that a rat would enter an open arm after SAP. Diazepam ameliorated the effects of RSDS on both SAP and exploratory behavior, further linking risk assessment and subsequent exploratory behaviors. These results suggest that increased risk assessment and reduced risky choices after risk assessment are tied to effects of stress on exploration and provide novel insight into how stress may increase avoidance by effects on risk assessment. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

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).

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 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).

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).