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Inositol 1,3,4,5‐tetrakisphosphate enhances long‐term potentiation by regulating Ca 2+ entry in rat hippocampus
Author(s) -
Szinyei Csaba,
Behnisch Thomas,
Reiser Georg,
Reymann Klaus G.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0855u.x
Subject(s) - long term potentiation , chemistry , biophysics , excitatory postsynaptic potential , inositol , intracellular , biochemistry , biology , receptor
1 The effect of inositol 1,3,4,5‐tetrakisphosphate (Ins P 4 ) on long‐term potentiation (LTP) was investigated in the CA1 region of rat hippocampal slices. Intracellular application of Ins P 4 and EPSP recordings were carried out using the whole‐cell configuration. 2 Induction of LTP in the presence of Ins P 4 (100 μM) resulted in a substantial enhancement of the LTP magnitude compared with control potentiation. Using an intrapipette perfusion system, it was established that application of Ins P 4 was required during induction of potentiation for this enhancement to occur. An enhancement of LTP was not observed if a non‐metabolizable inositol 1,4,5‐trisphosphate (Ins P 3 ) analogue (2,3‐dideoxy‐1,4,5‐trisphosphate, 100 μM) was applied intracellularly. 3 Current‐voltage relations of NMDA receptor‐mediated EPSCs were not altered by Ins P 4 application. The presence of Ins P 4 was slightly effective in relieving a D‐(‐)‐2‐amino‐5‐phosphonopentanoic acid (D‐APV)‐induced block of LTP. 4 The peak current amplitude of voltage‐gated calcium channels (VGCCs) was increased by Ins P 4 . ω‐Conotoxin GVIA inhibited the Ins P 4 ‐induced LTP facilitation. 5 These data indicate that Ins P 4 can modify the extracellular Ca 2+ entry through upregulation of VGCCs, which may in turn contribute to the observed enhancement of LTP induced by Ins P 4 . 6 To investigate the possible involvement of intracellular Ca 2+ release in the facilitatory effect of Ins P 4 on LTP, different inhibitors of the endoplasmic reticulum‐dependent Ca 2+ release were applied (heparin, ryanodine, cyclopiazonic acid). The results suggest that Ins P 4 activates postsynaptic Ins P 3 ‐dependent Ca 2+ release which normally does not contribute to the calcium‐induced calcium release‐dependent LTP.