PMID- 36117908
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220920
IS  - 1662-5099 (Print)
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 15
DP  - 2022
TI  - Differential synaptic mechanism underlying the neuronal modulation of prefrontal 
      cortex, amygdala, and hippocampus in response to chronic postsurgical pain with 
      or without cognitive deficits in rats.
PG  - 961995
LID - 10.3389/fnmol.2022.961995 [doi]
LID - 961995
AB  - Chronic Postsurgical Pain (CPSP) is well recognized to impair cognition, 
      particularly memory. Mounting evidence suggests anatomic and mechanistic overlap 
      between pain and cognition on several levels. Interestingly, the drugs currently 
      used for treating chronic pain, including opioids, gabapentin, and NMDAR 
      (N-methyl-D-aspartate receptor) antagonists, are also known to impair cognition. 
      So whether pain-related cognitive deficits have different synaptic mechanisms as 
      those underlying pain remains to be elucidated. In this context, the synaptic 
      transmission in the unsusceptible group (cognitively normal pain rats) was 
      isolated from that in the susceptible group (cognitively compromised pain rats). 
      It was revealed that nearly two-thirds of the CPSP rats suffered cognitive 
      impairment. The whole-cell voltage-clamp recordings revealed that the neuronal 
      excitability and synaptic transmission in the prefrontal cortex and amygdala 
      neurons were enhanced in the unsusceptible group, while these parameters remained 
      the same in the susceptible group. Moreover, the neuronal excitability and 
      synaptic transmission in hippocampus neurons demonstrated the opposite trend. 
      Correspondingly, the levels of synaptic transmission-related proteins 
      demonstrated a tendency similar to that of the excitatory and inhibitory synaptic 
      transmission. Furthermore, morphologically, the synapse ultrastructure varied in 
      the postsynaptic density (PSD) between the CPSP rats with and without cognitive 
      deficits. Together, these observations indicated that basal excitatory and 
      inhibitory synaptic transmission changes were strikingly different between the 
      CPSP rats with and without cognitive deficits.
CI  - Copyright (c) 2022 Li, He, Li, Sun, Zhang and Xiang.
FAU - Li, Zhen
AU  - Li Z
AD  - Department of Anesthesiology and Pain Medicine, Tongji Hospital of Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, China.
FAU - He, Zhigang
AU  - He Z
AD  - Department of Anesthesiology and Pain Medicine, Tongji Hospital of Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, China.
FAU - Li, Zhixiao
AU  - Li Z
AD  - Department of Anesthesiology and Pain Medicine, Tongji Hospital of Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, China.
FAU - Sun, Tianning
AU  - Sun T
AD  - Department of Anesthesiology and Pain Medicine, Tongji Hospital of Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, China.
FAU - Zhang, Wencui
AU  - Zhang W
AD  - Department of Anesthesiology and Pain Medicine, Tongji Hospital of Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, China.
FAU - Xiang, Hongbing
AU  - Xiang H
AD  - Department of Anesthesiology and Pain Medicine, Tongji Hospital of Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, China.
LA  - eng
PT  - Journal Article
DEP - 20220902
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC9478413
OTO - NOTNLM
OT  - chronic postsurgical pain
OT  - cognitive function
OT  - excitatory postsynaptic currents (EPSCs)
OT  - inhibitory postsynaptic synaptic currents (IPSCs)
OT  - postsynaptic density
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/09/20 06:00
MHDA- 2022/09/20 06:01
PMCR- 2022/01/01
CRDT- 2022/09/19 04:01
PHST- 2022/06/05 00:00 [received]
PHST- 2022/08/12 00:00 [accepted]
PHST- 2022/09/19 04:01 [entrez]
PHST- 2022/09/20 06:00 [pubmed]
PHST- 2022/09/20 06:01 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 10.3389/fnmol.2022.961995 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2022 Sep 2;15:961995. doi: 10.3389/fnmol.2022.961995. 
      eCollection 2022.