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Heat shock response and homeostatic plasticity
被引:18
|作者:
Karunanithi, Shanker
[1
,2
]
Brown, Ian R.
[3
]
机构:
[1] Griffith Univ, Sch Med Sci, Nathan, Qld 4222, Australia
[2] Griffith Univ, Menzies Hlth Inst Queensland, Nathan, Qld 4222, Australia
[3] Univ Toronto Scarborough, Ctr Neurobiol Stress, Dept Biol Sci, Toronto, ON, Canada
来源:
FRONTIERS IN CELLULAR NEUROSCIENCE
|
2015年
/
9卷
基金:
加拿大自然科学与工程研究理事会;
关键词:
adaptations;
temperature;
neuronal activity;
Drosophila neuromuscular junction;
synaptic homeostasis;
action potentials and neuroprotection;
FIRING RATE HOMEOSTASIS;
SYNAPTIC-TRANSMISSION;
MEDIATED THERMOPROTECTION;
CALCIUM REGULATION;
SLEEP-DEPRIVATION;
VISUAL-CORTEX;
K+ CHANNELS;
DROSOPHILA;
PROTEIN;
HSP70;
D O I:
10.3389/fncel.2015.00068
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
Heat shock response and homeostatic plasticity are mechanisms that afford functional stability to cells in the face of stress. Each mechanism has been investigated independently, but the link between the two has not been extensively explored. We explore this link. The heat shock response enables cells to adapt to stresses such as high temperature, metabolic stress and reduced oxygen levels. This mechanism results from the production of heat shock proteins (HSPs) which maintain normal cellular functions by counteracting the misfolding of cellular proteins. Homeostatic plasticity enables neurons and their target cells to maintain their activity levels around their respective set points in the face of stress or disturbances. This mechanism results from the recruitment of adaptations at synaptic inputs, or at voltage gated ion channels. In this perspective, we argue that heat shock triggers homeostatic plasticity through the production of HSPs. We also suggest that homeostatic plasticity is a form of neuroprotection.
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