Abstract
Chronic stress results in neurochemical, physiological, immune, molecular, cellular, and structural changes in the brain and often dampens the cognition. The hippocampus has been one major focus in studying the stress responsivity and neural mechanisms underlying depression. Both acute and chronic stress stimuli lead to dynamic changes in excitatory transmission in the hippocampus. The present study examined the potential effects of spontaneous recovery after chronic stress on spatial memory function and glutamatergic transmission in the hippocampus. The results showed that chronic unpredicted mild stress transiently increased AMPA receptor GluA2/3 subunit expression, together with elevated PICK-1 protein expression. Spontaneous recovery restored the behavioral deficits in Barnes maze test, as well as the glutamate receptor expression changes. In conclusion, spontaneous recovery acts as an important mechanism in system homeostasis.
Highlights
Chronic stress results in neurochemical, physiological, immune, molecular, cellular, and structural changes in the brain and often dampens the cognition [1,2,3,4]
Chronic stress alters glia homeostasis [8,9,10], such as triggering microglial cell proliferation and activation, suppresses astrocyte proliferation, and decreases the expression of GFAP protein and excitatory amino acid transporters (EAATs) in astrocytes, which might contribute to the altered excitatory transmission of hippocampal neurons following chronic stress
We reported that the expression of AMPAR subunits were increased following chronic stress, which decreased to baseline following a period of recovery, in line with the behavioral restoration
Summary
Chronic stress results in neurochemical, physiological, immune, molecular, cellular, and structural changes in the brain and often dampens the cognition [1,2,3,4]. The hippocampus is believed to be responsible for the decreased learning and memory abilities following chronic stress. It has been found that chronic stress decreases adult hippocampal neurogenesis, blocks LTP induction, downregulates expression of neurotrophic factors, and exacerbates neuronal apoptosis in the hippocampus [5,6,7]. Chronic stress alters glia homeostasis [8,9,10], such as triggering microglial cell proliferation and activation, suppresses astrocyte proliferation, and decreases the expression of GFAP protein and excitatory amino acid transporters (EAATs) in astrocytes, which might contribute to the altered excitatory transmission (e.g., glutamatergic) of hippocampal neurons following chronic stress. AMPA receptors are composed of GluA1–4 subunits, which bind to scaffolding proteins postsynaptically to be functional on the membrane. PICK-1 and PSD-95 interact with the glutamatergic receptors, regulating their membrane distribution and functions [12,13,14]
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