Behavioral neuroscience最新文献

A previous study reported lateral habenula (LHb) lesions decelerated appetitive extinction. Therefore, we examined whether LHb activation accelerated appetitive extinction. In this study, rats received appetitive Pavlovian conditioning, pairing a conditioned stimulus (CS, light) with an unconditioned stimulus (food pellets), followed by CS-alone presentations. Chemogenetic LHb activation accelerated the decline in conditioned food-cup responses during extinction. The present results and the reports of previous LHb lesion studies suggest that LHb mediates appetitive extinction. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

People are more likely to engage in various suboptimal behaviors such as overeating, addictive behaviors, and short-sighted financial decision-making when they are under stress. Traditional dual-process models propose that stress can impair the ability to engage in goal-directed behavior so that people have to rely on habitual behavior. Support for this idea comes from a study by Schwabe and Wolf (2010), in which stressed participants continued to perform a learned instrumental behavior leading to a liquid after the liquid was devalued with a satiation procedure. Based on these findings, suboptimal behavior under stress is often seen as habitual. In the present study, we conducted a conceptual replication of the study by Schwabe and Wolf (2010). Instead of using a satiation procedure to achieve the outcome devaluation, we devalued outcomes through taste aversion. We did not replicate the pattern of findings by Schwabe and Wolf (2010). Our results indicate instead that stressed participants were sensitive to outcome values when the outcomes became truly aversive and hence that their behavior was goal-directed. This suggests either that (a) habitual processes are subject to boundary conditions or (b) the processes responsible for the findings of Schwabe and Wolf (2010) were never habitual to begin with. This may have far-reaching implications for explaining suboptimal behavior under stress in general. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The nociceptin/orphanin FQ receptor (NOP receptor) has wide expression in the nervous system and is involved in neurotransmitter release. However, the role of the NOPR in depression is not widely recognized. This study aims to evaluate behavioral and biochemical effects of the NOPR agonist Ro 65-6570 in mice submitted to social defeat protocol. The open-field test, social interaction test, and tail suspension test were applied to evaluate depressive behavior in male Swiss mice. Blood and brain tissue samples were obtained to evaluate the oxidative stress. The NOP agonist, Ro 65-6570 (1 mg/kg), or the social defeat stress reduced exploration rate in the open-field test. The social defeat stress and/or the NOP agonist also increased immobility time in the tail suspension test and the grooming time, as well as reduced the social interaction on the last day of social defeat protocol. Seven days after the end of the protocol, only the drug alone was able to affect the animals' interaction. Additionally, the NOP agonist increased the concentration of carbonyl groups (CGs) in hippocampus and malondialdehyde in serum. The stress of social defeat and the NOP agonist, together, increased malondialdehyde in animals' serum and prefrontal cortex, as well as increased the CGs concentration in the prefrontal cortex. These findings indicate a chronic depressive effect induced by the NOPR activation, sometimes regardless of the social defeat stress. We suggest that the NOPR signaling can activate pathways involved in cellular oxidative stress, contributing to the depression pathology. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The amygdala and orbitofrontal cortex (OFC) are interconnected regions that serve as key nodes in brain circuits supporting social and affective behaviors. An important question that has come into focus is whether these regions also play a fundamental role in responding to novelty. One possibility is that these regions are important for discriminating novel from familiar stimuli. An alternative possibility is that these regions contribute to affective responses to stimuli in novelty-based tasks. For example, the amygdala and OFC could contribute to assessing novel stimuli as being threatening or previously selected stimuli as having reward value. The present study tested rhesus macaque monkeys with damage to the amygdala or OFC, along with sham-operated control monkeys, across six variants of novelty-based memory tasks. The results showed that monkeys with damage to the amygdala or OFC performed better overall than control monkeys across the tasks. The results indicated that neither region was essential for discriminating novel from familiar stimuli. Instead, the findings suggested that the improved performance observed in novelty-based tasks following damage to these regions was more likely attributable to influences on affect. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The main psychoactive compound within the cannabis plant, Δ9-tetrahydrocannabinol (THC), is thought to drive both the sensation of "high" and the cognitive impairments associated with cannabis consumption. Researchers keen to understand how cannabis impairs cognition have, therefore, studied the behavioral effects of systemic injections of THC in animal models. However, cannabis contains multiple other cannabinoids which may critically modulate the resulting cognitive effects. Users also typically eat or smoke cannabis, leading to concern over the translational validity of pure THC injections. We, therefore, tested whether acute oral administration of two different commercially available cannabis extracts, marketed as C. indica or C. sativa, decreased male Long-Evans rats' willingness to exert greater cognitive effort in order to maximize reward earned, as expected from previous experiments using injected THC. Both oils were matched for THC and cannabidiol content. While both cannabis products slowed response times at higher doses, only C. indica oil at the highest dose administered (10 mg/kg THC) decreased the number of trials on which rats chose to complete high-effort/high-reward trials. Repeated dosing with a medium dose of either cannabinoid product (3 mg/kg THC) did not influence choice. Ex vivo analyses confirmed comparable levels of brain THC after C. indica or C. sativa administration. Although controversial in the field, these results support the suggestion that products marketed as different cannabis cultivars have dissociable cognitive effects that may not resemble pure THC and emphasize the importance of the route of administration in experimental design. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Do we preferentially learn from outcomes that confirm our choices? In recent years, we investigated this question in a series of studies implementing increasingly complex behavioral protocols. The learning rates fitted in experiments featuring partial or complete feedback, as well as free and forced choices, were systematically found to be consistent with a choice-confirmation bias. One of the prominent behavioral consequences of the confirmatory learning rate pattern is choice hysteresis: that is, the tendency of repeating previous choices, despite contradictory evidence. However, choice-confirmatory pattern of learning rates may spuriously arise from not taking into consideration an explicit choice (gradual) perseveration term in the model. In the present study, we reanalyze data from four published papers (nine experiments; 363 subjects; 126,192 trials), originally included in the studies demonstrating or criticizing the choice-confirmation bias in human participants. We fitted two models: one featured valence-specific updates (i.e., different learning rates for confirmatory and disconfirmatory outcomes) and one additionally including gradual perseveration. Our analysis confirms that the inclusion of the gradual perseveration process in the model significantly reduces the estimated choice-confirmation bias. However, in all considered experiments, the choice-confirmation bias remains present at the meta-analytical level, and significantly different from zero in most experiments. Our results demonstrate that the choice-confirmation bias resists the inclusion of a gradual perseveration term, thus proving to be a robust feature of human reinforcement learning. We conclude by pointing to additional computational processes that may play an important role in estimating and interpreting the computational biases under scrutiny. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The mechanisms underlying chronic psychiatric-like impairments after traumatic brain injury (TBI) are currently unknown. The goal of the present study was to assess the role of diet and the gut microbiome in psychiatric symptoms after TBI. Rats were randomly assigned to receive a high-fat diet (HFD) or calorie-matched low-fat diet (LFD). After 2 weeks of free access, rats began training on the rodent gambling task (RGT), a measure of risky decision-making and motor impulsivity. After training, rats received a bilateral frontal TBI or a sham procedure and continued postinjury testing for 10 weeks. Fecal samples were collected before injury and 3-, 30-, and 60 days postinjury to evaluate the gut microbiome. HFD altered the microbiome, but ultimately had low-magnitude effects on behavior and did not modify functional outcomes after TBI. Injury-induced functional deficits were far more robust; TBI substantially decreased optimal choice and increased suboptimal choice and motor impulsivity on the RGT. TBI also affected the microbiome, and a model comparison approach revealed that bacterial diversity measured 3 days postinjury was predictive of chronic psychiatric-like deficits on the RGT. A functional metagenomic analysis identified changes to dopamine and serotonin synthesis pathways as a potential candidate mechanism. Thus, the gut may be a potential acute treatment target for psychiatric symptoms after TBI, as well as a biomarker for injury and deficit severity. However, further research will be needed to confirm and extend these findings. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

As a hallmark characteristic of schizophrenia, abnormal perception of time is thought to arise from cognitive impairment; however, the absence of translational models indexing this pathological relationship creates barriers to understanding the functional and biological bases of timing impairments. Here, we investigate the relationship between timing and cognition using the maternal immune activation (MIA) rat model of schizophrenia. We additionally investigate the role of prefrontal cortex L-arginine metabolism in these processes via high-performance liquid chromatography and liquid chromatography/mass spectrometry. Results revealed that MIA rats exhibit greater underestimation of interval durations (2-8 s); greater underestimation corresponded with declines in sustained attention capacity. Working memory impairments were not found to contribute to timing deficits. These findings represent the first direct identification of a timing-attention relationship within rodents and are discussed with respect to the dopamine hypothesis of temporal pace. We also found that MIA exposure altered aspects of arginine metabolism as observed in schizophrenia, and we present preliminary evidence suggesting that these changes have functional consequences for cognition. These findings support the MIA rat model as a valuable tool for future investigations exploring the biological instantiation of interrelated timing and cognitive deficits in schizophrenia. (PsycInfo Database Record (c) 2023 APA, all rights reserved).