Cation-chloride co-transporters mRNA expression in mice CA1 region after lithium-pilocarpine induced status epilepticus [Farelerde lityum-pilokarpin i̇le oluşturulan status epilepticus sonrasi{dotless} CA1 bölgesinde katyon-klorür mRNA yardi{dotless}mci{dotless}-taşi{dotless}yi{dotless}ci{dotless}lari{dotless}ni{dotless}n bulunuşu]

Objective: intracellular chloride concentration of a given cell within the central nervous system is determined by a delicate balance between the cl- extrusion system and the claccumulation system. in this study,we aim to investigate the expression profiles of cationchloride cotransporters (cccs) mrna in the mice model of lithium-pilocarpine induced status epilepticus (pise) and the possible relationships between cccs and epileptogenesis. methods: male adult balb/c mice were randomly divided into two groups: the pise group and the control. we used the mice of pise group to establish the animal model of pise and the pise group could be subdivided into three time points: 1 d,14 d and 45 d. real-time fluorescence quantitative pcr (polymerase chain reaction) was used to explore the expression of cccs family members mrna in ca1 region. results: these cccs members all showed distinctive expression patterns. the expression levels of nkcc1 (sodium potassium cation-chloride cotransporter 1),kcc1 (potassium cation-chloride cotransporter 1),kcc3 (potassium cation-chloride cotransporter 3) and cip1 (ccc-interacting protein type 1)mrna were up-regulated while those of kcc2 (potassium cation-chloride cotransporter 2) and ccc9 (cation-chloride cotransporter) mrna were downregulated after pise. the expression of kcc4 (potassium cation-chloride cotransporter 4) remained unchanged. conclusions: these data lead us to conclude that cccs expression as a whole is under very strict transcriptional control in this model. deregulation of their expression might break the balance of intracellular and extracellular chloride concentration which contributed to the mechanism of hyperexcitability that led to seizures. this may be due to some form of genetic program activated in response to epileptic seizure in the brain and may highlight which biological pathways are modulated.