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长期增强过程中磷脂酰肌醇 -4,5-二磷酸水解增加。

Increased hydrolysis of phosphatidylinositol-4,5-bisphosphate in long-term potentiation.

作者信息

Lynch M A, Clements M P, Errington M L, Bliss T V

机构信息

Division of Neurophysiology and Neuropharmacology, National Institute for Medical Research, London, U.K.

出版信息

Neurosci Lett. 1988 Feb 3;84(3):291-6. doi: 10.1016/0304-3940(88)90523-x.

Abstract

Inositol phospholipid hydrolysis was examined in slices and synaptosomes prepared from area CA3 of control hippocampi and hippocampi in which long-term potentiation (LTP) was induced in vivo. In both synaptosomes and slices, LTP was associated with an increase in [3H]inositol labelling of inositol phosphates but not phosphoinositides. Glutamate (10(-3) M) significantly increased labelling of inositol phosphates in slices obtained from control tissue but had no effect either in slices obtained from potentiated tissue or in synaptosomes obtained from control or potentiated tissue. The finding that glutamate had no significant effect in slices prepared from potentiated tissue suggests that glutamate-mediated stimulation of inositol phospholipid hydrolysis in a postsynaptic compartment may be saturated in LTP. The possibility that the increase in phospholipid hydrolysis associated with LTP which we report here may be linked with the previously reported increase in transmitter release is discussed.

摘要

在从对照海马体和在体内诱导了长时程增强(LTP)的海马体的CA3区制备的切片和突触体中检测了肌醇磷脂水解。在突触体和切片中,LTP均与肌醇磷酸的[3H]肌醇标记增加有关,但与磷酸肌醇无关。谷氨酸(10^(-3) M)显著增加了从对照组织获得的切片中肌醇磷酸的标记,但对从增强组织获得的切片或从对照或增强组织获得的突触体均无影响。谷氨酸对从增强组织制备的切片无显著影响这一发现表明,在突触后区室中谷氨酸介导的肌醇磷脂水解刺激在LTP中可能已饱和。本文报道的与LTP相关的磷脂水解增加可能与先前报道的递质释放增加有关,对此可能性进行了讨论。

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