AI Article Synopsis
- - A positive mental state can influence fear emotions, suggesting that brain mechanisms allow different feelings to interact.
- - Dopamine, a key neurotransmitter involved in both reward and fear, plays a role in how these emotions affect each other, though its exact contribution was unclear until now.
- - Research shows that activating dopamine neurons in mice during rewards can effectively alter fear memories and help with their extinction, highlighting a potential approach for treating fear-related disorders.
Article Abstract
A positive mental state has been shown to modulate fear-related emotions associated with the recall of fear memories. These, and other observations suggest the presence of central brain mechanisms for affective states to interact. The neurotransmitter dopamine is important for both Reward- and fear-related processes, but it is unclear whether dopamine contributes to such affective interactions. Here, we show that precisely timed Reward-induced activation of dopamine neurons in mice potently modifies fear memories and enhances their extinction. This Reward-based switch in fear states is associated with changes in dopamine release and dopamine-dependent regulation of fear encoding in the central amygdala (CeA). These data provide a central mechanism for Reward-induced modification of fear states that have broad implications for treating generalized fear disorders.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11398482 | PMC |
| http://dx.doi.org/10.1101/2024.09.05.611495 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Re-encountering the phobic cue within days after a reconsolidation intervention is crucial to observe a lasting fear reduction in spider phobia.
Mol Psychiatry
January 2025
Department of Psychology, University of Amsterdam, Amsterdam, The Netherlands.
Memory reconsolidation interventions offer an exciting alternative to exposure treatment because they may target fear memories directly, thereby preventing relapse. A previous reconsolidation intervention for spider fear abruptly reduced avoidance behaviour, whereas changes in self-reported fear followed later. In this pre-registered placebo-controlled study, we first aimed to conceptually replicate these effects in spider phobia.
View Article and Find Full Text PDFAustralian occupational therapists' perspectives about the management of driving safety concerns for older people with dementia and mild cognitive impairment.
Aust Occup Ther J
February 2025
Caring Futures Institute, College of Nursing and Health Sciences, Flinders University, Adelaide, Australia.
Introduction: Driving safety may be compromised in people with dementia or mild cognitive impairment (MCI). Occupational therapists assess and screen for driving safety in older people with cognitive impairment. However, little is known about their perspectives relating to these assessments.
View Article and Find Full Text PDFEmotional stress increases GluA2 expression and potentiates fear memory via adenylyl cyclase 5.
Cell Rep
January 2025
Department of Cell Biology and Anatomy, LSUHSC, New Orleans, LA 70112, USA; Southeast Louisiana VA Healthcare System, New Orleans, LA 70119, USA. Electronic address:
Stress can alter behavior and contributes to psychiatric disorders by regulating the expression of the GluA2 AMPA receptor subunit. We have previously shown in mice that exposure to predator odor stress elevates GluA2 transcription in cerebellar molecular layer interneurons (MLIs), and MLI activity is required for fear memory consolidation. Here, we identified the critical involvement of adenylyl cyclase 5, in both the stress-induced increase in GluA2 in MLIs and the enhancement of fear memory.
View Article and Find Full Text PDFComputational modeling of fear and stress responses: validation using consolidated fear and stress protocols.
Front Syst Neurosci
December 2024
Universidade Federal de Goias, School of Electrical, Mechanical and Computer Engineering, Goiânia, Brazil.
Dysfunction in fear and stress responses is intrinsically linked to various neurological diseases, including anxiety disorders, depression, and Post-Traumatic Stress Disorder. Previous studies using in vivo models with Immediate-Extinction Deficit (IED) and Stress Enhanced Fear Learning (SEFL) protocols have provided valuable insights into these mechanisms and aided the development of new therapeutic approaches. However, assessing these dysfunctions in animal subjects using IED and SEFL protocols can cause significant pain and suffering.
View Article and Find Full Text PDFAerobic exercise and metformin attenuate the cognitive impairment in an experimental model of type 2 diabetes mellitus: focus on neuroinflammation and adult hippocampal neurogenesis.
Metab Brain Dis
January 2025
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER)- Kolkata, Kolkata, West Bengal, 700054, India.
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that increases the prevalence of cognitive impairment in the geriatric population. Aerobic exercise is an excellent non-pharmacological therapeutic strategy to prevent Alzheimer's disease, the most common form of dementia. The exact molecular mechanism of aerobic exercise (Exe) as an intervention to counter cognitive decline is far from clear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!