Loss of Parvalbumin Reactive Interneuron in Area CA3 of the Kainate-Treated Mouse Hippocampal Slice Culture

Lee, Chang Hee; Kim, Soo Jin; Kim, Young Hoon; Lee, Yoon Kyung; Kim, Dong Un; Han, Seung Hoon; Chung, Seung Yun; Lee, In Goo; Whang, Kyung Tai; Kim, Myung Suk

Abstract

PURPOSE: Loss of hippocampal interneurons in area CA3 has been reported in patients with severe temporal lobe epilepsy and in animals treated with kainic acid(KA). The effects of kainic acid on the survival of parvalbumin-immunoreactive(PARV-IR) interneurons in area CA3 were investigated in organotypic hippocampal slice cultures.
METHODS
Cultured hippocampal slices from postnatal day 8-10 FVB mouse were exposed to 5 microM KA, and were analyzed at 0, 8, 24, 48, 72 hours after 1 hour KA exposure. Neuronal injury was determined by morphologic changes of PARV-IR interneuron in area CA3.
RESULTS
Untreated cultures displayed an organotypic organization and morphology of PARV-IR interneurons in the hippocampus which paralelled those reported to occur in vivo. The reduction in numbers of PARV-IR interneurons in CA3 after transient(1 hour) exposure to 5 microM KA were similar to those reported to occur in CA1 after transient exposure to 10 microM. Parvalbumin-immunoreactivity transiently was reduced from the soma and dendrites of PARV-IR interneuron within 24 hours. Transient exposure of hippocampal slice cultures to KA produced marked focal swellings of the dendrites of PARV-IR interneurons. At 5 microM KA, more than 30% of the PARV-IR interneuron dendrites in area CA3 had a beaded appearance. The presence of focal swellings was reversible with KA washout and was not accompanied by interneuronal cell death.
CONCLUSION
The results suggest that KA-induced cell death is delayed, therefore acute edema is insufficient to kill PARV-IR interneurons in area CA3.