Hypersensitivity to pentylenetetrazol-induced convulsion in mice lacking the PLC-related inactive protein-1.
In the present study, we investigated the effects of pentylenetetrazol (PTZ), a chemical convulsant that interacts with the GABA(A) receptor, in mice lacking the phospholipase C (PLC)-related inactive protein-1 (PRIP-1). PRIP-1 knockout mice did not develop spontaneous behavioral seizure. PRIP-1 knockout mice had markedly shorter latencies until the first clonic convulsion (CL) and tonic extensor (TE) following PTZ administration and increased incidence of convulsion compared to those in wild-type mice. Furthermore, the mortality rate by PTZ in mice lacking the PRIP-1 was also significantly increased in comparison with that in wild-type mice. These findings suggested that mice lacking the PRIP-1 were hypersensitive to PTZ-induced convulsion, and PRIP-1 might play roles in suppressing excessive excitability via interactions with the GABA(A) receptor.
Yamaguchi
Taku
T
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Kubota
Takashi
T
Kanematsu
Takashi
T
Nakayama
Keiichi
K
Hirata
Masato
M
Yamamoto
Tsuneyuki
T
D000818:Animals; D047908:Intracellular Signaling Peptides and Proteins / Q000172:deficiency* / Q000235:genetics*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D056918:Nuclear Receptor Coactivators; D010433:Pentylenetetrazole / Q000633:toxicity*; D012640:Seizures / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D010738:Type C Phospholipases / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics
D047908:Intracellular Signaling Peptides and Proteins; C486559:NCOA6 protein, human; D056918:Nuclear Receptor Coactivators; D010738:Type C Phospholipases; C432456:phospholipase C1; D010433:Pentylenetetrazole