Early-life adversity increases risk for mental illnesses including depression and substance use disorders, disorders characterized by dysregulated reward behaviors. However, the mechanisms by which transient ELA enduringly impacts reward circuitries are not well understood. In mice, ELA leads to anhedonia-like behaviors in males and augmented motivation for palatable food and sex-reward cues in females. Here, the use of genetic tagging demonstrated robust, preferential, and sex-specific activation of the paraventricular nucleus of the thalamus (PVT) during ELA and a potentiated reactivation of these PVT neurons during a reward task in adult ELA mice. Chemogenetic manipulation of specific ensembles of PVT neurons engaged during ELA identified a role for the posterior PVT in ELA-induced aberrantly augmented reward behaviors in females. In contrast, anterior PVT neurons activated during ELA were required for the anhedonia-like behaviors in males. Thus, the PVT encodes adverse experiences early-in life, prior to the emergence of the hippocampal memory system, and contributes critically to the lasting, sex-modulated impacts of ELA on reward behaviors.
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http://dx.doi.org/10.1101/2024.04.28.591547 | DOI Listing |
Behav Brain Funct
December 2024
School of Psychology, Northeast Normal University, 5268 Renmin Street, Changchun, 130024, Jilin, China.
Reward cues have long been considered to enhance creative performance; however, little is known about whether rewards can affect creative problem solving by manipulating states of flexibility and persistence. This study sought to elucidate the differential impacts of real versus hypothetical rewards on the creative process utilizing the Chinese compound remote association task. Behavioral analysis revealed a significantly enhanced solution rate and response times in scenarios involving real rewards, in contrast to those observed with hypothetical rewards.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
December 2024
Department of Psychiatry, University of Cambridge, Cambridge, UK; Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany. Electronic address:
Background: A preference for sooner-smaller over later-larger rewards, known as delay discounting, is a candidate transdiagnostic marker of waiting impulsivity and a research domain criterion. While abnormal discounting rates have been associated with many psychiatric diagnoses and abnormal brain structure, the underlying neuropsychological processes remain largely unknown. Here, we deconstruct delay discounting into choice and rate processes by testing different computational models and investigate their associations with white matter tracts.
View Article and Find Full Text PDFCurr Biol
December 2024
Department of Neurobiology, University of Utah, 20 S 2030 E, BPRB 490D, Salt Lake City, UT 84112, USA. Electronic address:
Integrative studies of diverse neuronal networks that govern social behavior are hindered by a lack of methods to record neural activity comprehensively across the entire brain. The recent development of the miniature fish Danionella cerebrum as a model organism offers one potential solution, as the small size and optical transparency of these animals make it possible to visualize circuit activity throughout the nervous system. Here, we establish the feasibility of using Danionella as a model for social behavior and socially reinforced learning by showing that adult fish exhibit strong affiliative tendencies and that social interactions can serve as the reinforcer in an appetitive conditioning paradigm.
View Article and Find Full Text PDFBehav Brain Funct
December 2024
Department of Pharmacology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
The large-conductance calcium- and voltage-activated potassium (BK) channels, encoded by the KCNMA1 gene, play important roles in neuronal function. Mutations in KCNMA1 have been found in patients with various neurodevelopmental features, including intellectual disability, autism spectrum disorder (ASD), or attention deficit hyperactivity disorder (ADHD). Previous studies of KCNMA1 knockout mice have suggested altered activity patterns and behavioral flexibility, but it remained unclear whether these changes primarily affect immediate behavioral adaptation or longer-term learning processes.
View Article and Find Full Text PDFPsychopharmacology (Berl)
December 2024
Department of Basic Medical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN, 47904, USA.
Rationale: The rise in overdose deaths from synthetic opioids, especially fentanyl, necessitates the development of preclinical models to study fentanyl use disorder (FUD). While there has been progress with rodent models, additional translationally relevant models are needed to examine excessive fentanyl intake and withdrawal signs.
Objective: The current study aimed to develop a translationally relevant preclinical mouse model of FUD by employing chronic intravenous fentanyl self-administration (IVSA).
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