Memories are multifaceted and can simultaneously contain positive and negative attributes. Here, we report that negative attributes of a mixed-valence memory dominate long-term recall. To induce a mixed-valence memory, running responses were randomly reinforced with either food (∼83% of trials) or footshock (∼17% of trials), or a noise conditioned stimulus (CS) was followed randomly with either food (∼80% of trials) or footshock (∼20% of trials). Control animals were consistently reinforced with only food. Mixed-valence training promoted unstable behavior (e.g., erratic approach and withdrawal from the food cup) and moderate levels of fear during the training regimens. After a 20-day retention interval, animals that were consistently reinforced with food exhibited intact approach responding, and similar responding was observed if animals were food deprived or satiated (i.e., the response was insensitive to motivation). However, animals that experienced the mixed-valence training expressed significantly enhanced and stable fear (consistent immobility) relative to the end of training, regardless of whether animals were food deprived or not, suggesting that fear transitioned to a state that was insensitive to motivation. The degree of fear expressed during long-term retention was predicted by measures of state anxiety obtained prior to the training, indicating that the enhancement of fear across the retention interval was related to individual differences in basal "anxiety." These results suggest that negative attributes of memories dominate long-term recall, particularly in animals expressing an anxious phenotype, and these observations have direct implications for the chronic nature of anxiety disorders and the exacerbation of fear that accompanies posttraumatic stress disorder. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Mental representations of stimuli that are not physically present are critical for a range of cognitive capacities, including perception, memory, and learning. Overly robust mental representations, however, can contribute to hallucinations in healthy individuals and those diagnosed with psychotic illness. Measuring the strength of mental representations can thus provide insight into how the contents of the mind influence both adaptive and maladaptive behaviors. In rodents, the robustness of mental representations has been tested using the representation-mediated learning (RML) task, in which animals respond less to a cue after a stimulus that has previously been associated with this cue has been paired with illness. This suggests that the mental representation of the cue enters into a negative association during aversive learning, even though the cue is not physically present. Here, we developed a human version of the RML task in which participants initially learned associations between two visual symbols and two different appetitive food odors. Preference for the food odors was then tested immediately before and after a session in which one symbol was paired with an aversive noise. We observed that mediated learning, in the form of selective decrease in preference for the odor previously paired with the noise-predicting symbol, was directly proportional to direct aversive learning for the symbols themselves. These findings suggest that a mental representation of the odor entered into a negative association with the sound and pave the way for future studies aimed at characterizing the neural circuits of mediated learning in the human brain. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

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).

This chapter describes the sensory systems that allow the detection and interpretation of sounds, beginning with an exploration of hearing or audition. It explains how pressure waves in the air are perceived as sound through the auditory system, including the roles of the external ear, middle ear, and inner ear in capturing, concentrating, and transducing sound energy into neural activity. It also delves into the anatomy of the cochlea and the organ of Corti, showing how vibrations are propagated and frequencies are encoded. The chapter discusses the evolutionary adaptations of various animals, from bats and owls to elephants and whales, which use sound for communication, navigation, and survival. This focus on auditory processing provides insights into how humans and animals rely on sound for interaction, reproduction, and environmental awareness.

Repetitive bouts of binge drinking can lead to neuroplastic events that alter ethanol's pharmacologic effects and perpetuate excessive consumption. The corticotropin-releasing factor (CRF) system is an example of ethanol-induced neuroadaptations that drive excessive ethanol consumption. Our laboratory has previously shown that CRF antagonist, when infused into the central amygdala (CeA), reduces binge-like ethanol consumption. The present study extends this research by assessing the effects of silencing CRF-producing neurons in CeA on binge-like ethanol drinking stemming from "Drinking in the Dark" (DID) procedures. CRF-ires-Cre mice underwent surgery to infuse Gi/o-coupled Designer Receptors Exclusively Activated by Designer Drugs (DREADD) virus or a control virus into either the CeA or basolateral amygdala (BLA). Gi/o-DREADD-induced CRF-neuronal inhibition in the CeA resulted in a 33% decrease in binge-like ethanol consumption. However, no effect on ethanol consumption was seen after DREADD manipulation in the BLA. Moreover, CeA CRF-neuronal inhibition had no effect on sucrose consumption. The effects of silencing CRF neurons in the CeA on ethanol consumption are not secondary to changes in motor function or anxiety-like behaviors as assessed in the open-field test (OFT). Finally, the DREADD construct's functional ability to inhibit CRF-neuronal activity was demonstrated by reduced ethanol-induced c-Fos following DREADD activation. Together, these data suggest that the CRF neurons in the CeA play an important role in binge ethanol consumption and that inhibition of the CRF-signaling pathway remains a viable target for manipulating binge-like ethanol consumption. (PsycInfo Database Record (c) 2022 APA, all rights reserved).