Introduction: Depression is a mental disorder characterized by aberrant exploratory behavior. Environmental factors, such as chronic stress, are commonly used to induce depression-like behavior in rodent models. The medial prefrontal cortex (mPFC) and the basolateral amygdala (BLA) are crucial sites in subjects with chronic stress-induced depression. The transmission of amplitude information from the mPFC to the BLA was abated during exploratory behavior in depressive rats; however, the nature of the phase interaction between these two sites remains unknown.
Methods: We used chronic unpredictable mild stress (CUMS) to model depression in rats and acquired local field potentials (LFPs) via multiple electrodes implanted in the mPFC and the BLA while rats (both the control and CUMS groups, respectively) were allowed to explore freely in an open field. The weighted phase lag index (WPLI) within the mPFC and the BLA and phase transfer entropy (PTE) from the mPFC to BLA were computed for two groups of rats (control and CUMS rats) to quantify the phase information transmission.
Results: Rats subjected to CUMS showed a decrease in exploratory behavior. The WPLI within the mPFC and the BLA showed strikingly higher phase synchrony at theta frequencies (4-12 Hz) than other frequency bands during exploratory behavior in both the control and CUMS groups. The results of theta PTE from the mPFC to BLA showed that PTE was significantly decreased in the CUMS group compared with the control group.
Discussions: These findings demonstrated that attenuated phase information transfer might restrain exploratory behavior in CUMS rats.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10083315 | PMC |
http://dx.doi.org/10.3389/fnins.2023.1145721 | DOI Listing |
Neurobiol Stress
November 2024
Sagol Department of Neurobiology, University of Haifa, 3498838, Haifa, Israel.
The basolateral amygdala (BLA) is a dynamic brain region involved in emotional experiences and subject to long-term plasticity. The BLA also modulates activity, plasticity, and related behaviors associated with other brain regions, including the mPFC and hippocampus. Accordingly, intra-BLA plasticity can be expected to alter both BLA-dependent behaviors and behaviors mediated by other brain regions.
View Article and Find Full Text PDFJ Environ Sci (China)
May 2025
College of Life Science, State Key Laboratory of Medicinal Chemical Biology, The Key Laboratory of Bioactive Materials, Ministry of Education, Nankai University, Tianjin 300071, China. Electronic address:
17β-Trenbolone (17-TB) is well documented as an environmental endocrine disruptor in aquatic biological studies, but its effects on mammals remain poorly understood. Furthermore, 17-TB acts as a hormone with properties similar to testosterone, and the consequences of juvenile exposure on adult social behavior remain uncertain. Bisphenol A (BPA) acts as an estrogen-like hormone, compared to 17-TB.
View Article and Find Full Text PDFNeurobiol Dis
November 2024
Department of Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI 49503, USA; Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington DC 20007, USA. Electronic address:
Abnormal accumulation of insoluble α-synuclein (α-Syn) inclusions in neurons, neurites, and glial cells is the defining neuropathology of synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy. Accumulation of α-Syn inclusions in the amygdala has been well-documented in post-mortem studies of PD and DLB brains, as well as preclinical animal models of these conditions. Though α-Syn pathology is closely associated with neurodegeneration, there is a poor correlation between neuronal loss in the amygdala and the clinical features of PD and DLB.
View Article and Find Full Text PDFNeurosci Bull
August 2024
Department of Rehabilitation of Children's Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, 310003, China.
Anxiety disorder is a major symptom of autism spectrum disorder (ASD) with a comorbidity rate of ~40%. However, the neural mechanisms of the emergence of anxiety in ASD remain unclear. In our study, we found that hyperactivity of basolateral amygdala (BLA) pyramidal neurons (PNs) in Shank3 InsG3680 knock-in (InsG3680) mice is involved in the development of anxiety.
View Article and Find Full Text PDFSci Data
August 2024
Computational Cognitive & Systems Neuroscience Laboratory, Brain Science Institute, Korea Institute of Science and Technology, Seoul, 02792, Republic of Korea.
Responding to threats in the real world demands a sophisticated orchestration of freeze and flight behaviors dynamically modulated by the neural activity. While the medial prefrontal cortex-basolateral amygdala (mPFC-BLA) network is known to play a pivotal role in coordinating these responses, the mechanisms underlying its population dynamics remain vague. As traditional Pavlovian fear conditioning models fall short in encapsulating the breadth of natural escape behaviors, we introduce a novel dataset to bridge this gap, capturing the defensive strategies of mice against a spider robot in a natural-like environment.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!