内源性丝氨酸蛋白酶抑制剂调节癫痫活动和海马体长期增强效应。
Endogenous serine protease inhibitor modulates epileptic activity and hippocampal long-term potentiation.
作者信息
Lüthi A, Van der Putten H, Botteri F M, Mansuy I M, Meins M, Frey U, Sansig G, Portet C, Schmutz M, Schröder M, Nitsch C, Laurent J P, Monard D
机构信息
Pharma Division, Preclinical Research, F. Hoffmann-La Roche Limited, CH-4002 Basel, Switzerland.
出版信息
J Neurosci. 1997 Jun 15;17(12):4688-99. doi: 10.1523/JNEUROSCI.17-12-04688.1997.
Abstract
Protease nexin-1 (PN-1), a member of the serpin superfamily, controls the activity of extracellular serine proteases and is expressed in the brain. Mutant mice overexpressing PN-1 in brain under the control of the Thy-1 promoter (Thy 1/PN-1) or lacking PN-1 (PN-1-/-) were found to develop epileptic activity in vivo and in vitro. Theta burst-induced long-term potentiation (LTP) and NMDA receptor-mediated synaptic transmission in the CA1 field of hippocampal slices were augmented in Thy 1/PN-1 mice and reduced in PN-1-/- mice. Compensatory changes in GABA-mediated inhibition in Thy 1/PN-1 mice suggest that altered brain PN-1 levels lead to an imbalance between excitatory and inhibitory synaptic transmission.
摘要
蛋白酶抑制因子-1（PN-1）是丝氨酸蛋白酶抑制剂超家族的成员之一，可控制细胞外丝氨酸蛋白酶的活性，并在大脑中表达。发现在Thy-1启动子（Thy 1/PN-1）控制下大脑中过表达PN-1或缺乏PN-1（PN-1-/-）的突变小鼠在体内和体外都会出现癫痫活动。在Thy 1/PN-1小鼠中，海马切片CA1区的theta爆发诱导的长时程增强（LTP）和NMDA受体介导的突触传递增强，而在PN-1-/-小鼠中则减弱。Thy 1/PN-1小鼠中GABA介导的抑制作用的代偿性变化表明，大脑中PN-1水平的改变导致兴奋性和抑制性突触传递之间的失衡。
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