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Defective hippocampal mossy fiber long‐term potentiation in endothelial nitric oxide synthase knockout mice
Author(s) -
Doreulee Nanuli,
Brown Ritchie E.,
Yanovsky Yevgeni,
Gödecke Axel,
Schrader Jürgen,
Haas Helmut L.
Publication year - 2001
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.1074
Subject(s) - long term potentiation , enos , adenylyl cyclase , knockout mouse , nitric oxide , chemistry , forskolin , stimulation , nitric oxide synthase , medicine , endocrinology , biochemistry , biology , receptor
Mossy fiber long‐term potentiation (mfLTP) was compared in hippocampal slices prepared from wild‐type mice and mice lacking functional endothelial nitric oxide synthase (eNOS ‐/‐ mice) using field potential recording. In the presence of D‐2‐amino‐5‐phosphonovaleric acid (AP5, 50 μM), the mfLTP induced by tetanic stimulation (100 Hz, 1 sec) was significantly reduced in knockouts (n = 8) in comparison with wild‐type (n = 8). Similarly, potentiation induced by forskolin (30 μM) or 8‐bromo‐cyclic adenosine monophosphate (8‐Br‐cAMP, 100 μM) was less pronounced in knockouts. However, in wild‐types the mfLTP‐induced in the presence of the nonselective pharmacological inhibitor of NOS (N‐nitro‐L‐Arginine, 100 μM, n = 6) was not significantly different from control (n = 8). Thus, eNOS is not directly involved in mfLTP, but lack of eNOS during development leads to a deficit downstream of adenylyl cyclase. Synapse 41:191–194, 2001. © 2001 Wiley‐Liss, Inc.