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1.
Neuroscience Bulletin ; (6): 16-28, 2022.
Article in English | WPRIM | ID: wpr-922663

ABSTRACT

Chronic stress leads to many psychiatric disorders, including social and anxiety disorders that are associated with over-activation of neurons in the basolateral amygdala (BLA). However, not all individuals develop psychiatric diseases, many showing considerable resilience against stress exposure. Whether BLA neuronal activity is involved in regulating an individual's vulnerability to stress remains elusive. In this study, using a mouse model of chronic social defeat stress (CSDS), we divided the mice into susceptible and resilient subgroups based on their social interaction behavior. Using in vivo fiber photometry and in vitro patch-clamp recording, we showed that CSDS persistently (after 20 days of recovery from stress) increased BLA neuronal activity in all the mice regardless of their susceptible or resilient nature, although impaired social interaction behavior was only observed in susceptible mice. Increased anxiety-like behavior, on the other hand, was evident in both groups. Notably, the CSDS-induced increase of BLA neuronal activity correlated well with the heightened anxiety-like but not the social avoidance behavior in mice. These findings provide new insight to our understanding of the role of neuronal activity in the amygdala in mediating stress-related psychiatric disorders.


Subject(s)
Animals , Mice , Amygdala , Anxiety/etiology , Anxiety Disorders , Avoidance Learning , Mice, Inbred C57BL , Social Behavior , Stress, Psychological/complications
2.
Acta Physiologica Sinica ; (6): 235-242, 2020.
Article in Chinese | WPRIM | ID: wpr-827064

ABSTRACT

Gliomas are malignant tumors with strong invasiveness. The current treatment strategy is surgical treatment assisted by a variety of radiotherapies, chemotherapies and immunotherapies. However, the curative efficacy is limited. Adrenergic receptor (AR) is an important stress hormone receptor, which is highly involved in the regulation of the tumorigenesis and progression of various tumors by activating different downstream signal transduction pathways. Recent studies have shown that AR is dysregulated in glioma cells and tissues, and plays an important role in a series of biological behaviors such as tumorigenesis, invasion and metastasis of glioma. This article reviews the research progress of AR in the field of glioma in recent years, which provides a theoretical basis for the prevention and treatment of glioma targeting the AR.


Subject(s)
Humans , Brain Neoplasms , Pathology , Carcinogenesis , Cell Line, Tumor , Cell Proliferation , Gene Expression Regulation, Neoplastic , Glioma , Pathology , Neoplasm Invasiveness , Neoplasm Metastasis , Receptors, Adrenergic , Physiology , Signal Transduction
3.
Journal of Southern Medical University ; (12): 1754-1756, 2006.
Article in Chinese | WPRIM | ID: wpr-232790

ABSTRACT

<p><b>OBJECTIVE</b>To understand the role of KCNE2 in functional regulation of Kv4.3, the major alpha subunit of transient outward current (I(to)) in human heart.</p><p><b>METHODS</b>The cDNAs of Kv4.3 or Kv4.3 plus KCNE2 were transfected into COS-7 cells and 24-36 h after the transfection, the channel proteins were expressed in the surface membrane of the cells and the channel currents were recorded with patch-clamp technique in whole-cell mode.</p><p><b>RESULTS</b>KCNE2 played an important role in modulating the channel function. The recorded current density was decreased in cells co-expressing KCNE2 and Kv4.3 to 152.96-/+33.71 pA/pF (n=16) as compared with Kv4.3-expressing cells with a mean current density of 375.13-/+112.87 pA/pF (n=11). At the recording voltage of 60 mV, KCNE2 increased the time to peak (TTP) of the current. TTP in only Kv4.3-expressing cells was 4.82-/+0.32 ms (n=11), significantly shorter than the TTP of 20.41-/+2.13 ms (n=16) in cells co-expressing Kv4.3 and KCNE2 (P<0.05). In the presence of KCNE2, the voltage-dependent inactivation of Kv4.3 showed a positive shift. The voltage of half maximum inactivation (V(0.5)) was decreased significantly from -53.62-/+1.24 mV (n=8) in Kv4.3 group to -46.58-/+1.6 mV (n=10) in KCNE2 co-expression group (P<0.05). KCNE2 accelerated the recovery of the channel from inactivation, reducing the recovery time constant (tau) from 193.43-/+17.98 ms to 137.71-/+18.29 ms.</p><p><b>CONCLUSION</b>KCNE2 might serve as an important beta subunit and play a role in the regulation of I(to) function in human heart.</p>


Subject(s)
Animals , Humans , COS Cells , Chlorocebus aethiops , Kv Channel-Interacting Proteins , Genetics , Metabolism , Membrane Potentials , Physiology , Patch-Clamp Techniques , Potassium Channels, Voltage-Gated , Genetics , Metabolism , Physiology , Shal Potassium Channels , Genetics , Metabolism , Physiology , Transfection
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