Emotional events often lead to particularly strong memory formation. Corticosterone, the final product of hypothalamic-pituitary-adrenal (HPA)-axis activation, has been suggested to play a critical role in this effect. Although a great deal of work has implicated the amygdala as a necessary structure for the effects of corticosterone, other studies have suggested a critical role for the hippocampus in determining the involvement of corticosterone. The current experiments examined this question by disrupting corticosterone synthesis with administration of metyrapone (25 or 100 mg/kg) prior to training in either dorsal hippocampus-independent delay fear conditioning or dorsal hippocampus-dependent trace fear conditioning. Metyrapone administration 2 hrs prior to training significantly attenuated corticosterone secretion during training, but these effects were transient as corticosterone levels were similar to control subjects following the test session. As hypothesized, only trace fear conditioning was impaired. This suggests that only fear conditioning tasks that are dependent on the dorsal hippocampus require HPA-axis activation in order to be learned.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2852175 | PMC |
| http://dx.doi.org/10.1037/a0018911 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Possible effects of radiofrequency electromagnetic radiation on contextual fear conditioning, hippocampal perivascular space, apoptosis and adrenal gland microarchitecture in rats.
Behav Brain Res
January 2025
Division of Biotechnology, School of Life Sciences, Manipal Academy of Higher Education, Manipal- 576104, India.
Whilst the world sees the tremendous growth of mobile phone technology, radiofrequency electromagnetic radiation (RF-EMR) induced possible health effects have emerged as a topic of recent day debate. The current study is designed to test the hypothesis that chronic 900MHz radiation exposure would potentially dysregulate the stress response system (HPA axis) in vivo, via, its non-thermal mechanisms, leading to alterations in the microarchitecture of the adrenal gland, vulnerable brain regions such as the hippocampus which may results in altered behaviours in rats. Male albino Wistar rats aged four weeks, weighing 50-60g were subjected to 900MHz radiation from a cellphone for four weeks at a rate of one hour per day.
View Article and Find Full Text PDFThe role of clock control of DRP1 activity involved in postoperative cognitive dysfunction.
Exp Neurol
January 2025
School of Public Health, Nanjing Medical University, Nanjing 211166, China. Electronic address:
Postoperative cognitive dysfunction (POCD) is a prevalent clinical issue following anesthesia and surgery. The onset of POCD, which is closely linked to circadian rhythm disturbance in previous studies, yet the underlying mechanism remains elusive. There is increasing evidence showed that mitochondrial architecture is coordinated by the circadian clock which DRP1 playing a crucial role.
View Article and Find Full Text PDFLearning to fear novel stimuli by observing others in the social affordance framework.
Neurosci Biobehav Rev
January 2025
Department of Psychology, University of Turin, Turin, Italy; Department of Medical and Clinical Psychology, Tilburg University, Netherlands; Centro Linceo Interdisciplinare "Beniamino Segre", Accademia Nazionale dei Lincei, Roma, Italy. Electronic address:
Fear responses to novel stimuli can be learned directly, through personal experiences (Fear Conditioning, FC), or indirectly, by observing conspecific reactions to a stimulus (Social Fear Learning, SFL). Although substantial knowledge exists about FC and SFL in humans and other species, they are typically conceived as mechanisms that engage separate neural networks and operate at different levels of complexity. Here, we propose a broader framework that links these two fear learning modes by supporting the view that social signals may act as unconditioned stimuli during SFL.
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 PDFBackground: While the formation of β-amyloid plaques and neurofibrillary "tau" tangles are considered hallmarks of AD pathology, therapeutic targeting of these pathways has been unsuccessful, highlighting the necessity to define the underlying molecular mechanisms driving AD progression. Previous studies from our lab demonstrated that mitochondrial calcium (Ca) overload through neuronal ablation of the mitochondrial Na/Ca exchanger (NCLX) is sufficient to trigger 'AD-like' pathology, including mitochondrial dysfunction, amyloid deposition and tau pathology, and cognitive decline. In addition, we found significant proteomic remodeling of components of the mitochondrial calcium uniporter channel (mtCU), the primary mediator of Ca uptake, in frontal cortex samples isolated post-mortem from patients diagnosed with non-familial/sporadic AD.
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!