Expression of cation chloride cotransporter (NKCC1/KCC2) in brain tissue of children with focal cortical dysplasia type Ⅱ.
10.3760/cma.j.cn112151-20220418-00300
- Author:
Yan LI
1
;
Yun Lin LI
2
;
Yong Ling LIU
1
;
Jing FU
1
;
Wei Wei ZHANG
3
;
Yue Shan PIAO
3
Author Information
1. Department of Pathology, Beijing Haidian Hospital/Peking University Third Hospital Haidian Division, Beijing 100080, China.
2. Department of Neurosurgery, Capital Institute of Pediatrics, Beijing 100020, China.
3. Department of Pathology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
- Publication Type:Journal Article
- MeSH:
Child;
Humans;
Brain/pathology*;
Cations/metabolism*;
Chlorides/metabolism*;
Epilepsy/metabolism*;
Malformations of Cortical Development, Group I/metabolism*;
Solute Carrier Family 12, Member 2/metabolism*;
Symporters/metabolism*
- From:
Chinese Journal of Pathology
2022;51(11):1123-1128
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the expression of cation chloride cotransporter (NKCC1/KCC2) in the neurons from cerebral lesions of children with focal cortical dysplasia (FCD) type Ⅱ, to provide a morphological basis for revealing the possible mechanism of epilepsy. Methods: Eight cases of FCD type Ⅱ diagnosed at Beijing Haidian Hospital, Beijing, China and 12 cases diagnosed at Xuanwu Hospital, Capital Medical University, Beijing, China from February 2017 to December 2019 were included. The expression of NKCC1 and KCC2 in FCD type Ⅱa and FCD type Ⅱb was detected using immunohistochemistry and double immunohistochemical stains. The average optical density of NKCC1 in dysmorphic neurons and normal neurons was also determined using immunohistochemical staining in FCD type Ⅱa (10 cases). Results: The patients were all younger than 14 years of age. Ten cases were classified as FCD type IIa, and 10 cases as FCD type Ⅱb. NKCC1 was expressed in the cytoplasm of normal cerebral cortex neurons and KCC2 expressed on cell membranes. In dysmorphic neurons of FCD type Ⅱa, expression of NKCC1 increased, which was statistically higher than that of normal neurons (P<0.01). Aberrant expression of KCC2 in dysmorphic neurons was also noted in the cytoplasm. In the FCD Ⅱb type, the expression pattern of NKCC1/KCC2 in dysmorphic neurons was the same as that of FCD type Ⅱa. The aberrant expression of NKCC1 in balloon cells was negative or weakly positive on the cell membrane, while the aberrant expression of KCC2 was absent. Conclusions: The expression pattern of NKCC1/KCC2 in dysmorphic neurons and balloon cells is completely different from that of normal neurons. The NKCC1/KCC2 protein-expression changes may affect the transmembrane chloride flow of neurons, modify the effect of inhibitory neurotransmitters γ-aminobutyric acid and increase neuronal excitability. These effects may be related to the occurrence of clinical epileptic symptoms.
