Yamazaki Yoshihiko, Fujii Satoshi, Nakamura Takeshi, Miyakawa Hiroyoshi, Kudo Yoshihisa, Kato Hiroshi, Ito Ken-Ichi
Department of Physiology, Yamagata University School of Medicine, 2-2-2 Iida Nishi, 990-9585, Japan.
Neurosci Lett. 2002 May 10;324(1):65-8. doi: 10.1016/s0304-3940(02)00175-1.
The perfusion of adenosine triphosphate (ATP) induces long-term potentiation (LTP) in CA1 synapses of hippocampal slices, whereas the perfusion of ATP plus ,-2-amino-5-phosphonovaleric acid (AP5) can result in the formation of long-term depression (LTD). To clarify the difference in change of intracellular calcium concentration ([Ca2+]i) corresponding to induction of LTP or LTD, we measured [Ca2+]i during the perfusion of ATP or ATP+AP5, while simultaneously recording evoked field potentials. In both cases, ATP (or ATP+AP5) perfusion transiently increased [Ca2+]i but the extent of increase of [Ca2+]i by ATP was larger than that caused by ATP+AP5. Thus, the larger rise in [Ca2+]i induces LTP but the smaller rise induces LTD. These results are consistent with the Ca2+ hypothesis as proposed by Lisman (Trends Neurosci. 17 (1994) 406).
灌注三磷酸腺苷（ATP）可在海马切片的CA1突触中诱导长时程增强（LTP），而灌注ATP加α-氨基-5-磷酸戊酸（AP5）则可导致长时程抑制（LTD）的形成。为了阐明对应于LTP或LTD诱导的细胞内钙浓度（[Ca2+]i）变化的差异，我们在灌注ATP或ATP + AP5期间测量了[Ca2+]i，同时记录诱发场电位。在这两种情况下，ATP（或ATP + AP5）灌注均使[Ca2+]i短暂升高，但ATP引起的[Ca2+]i升高幅度大于ATP + AP5引起的升高幅度。因此，[Ca2+]i的较大升高诱导LTP，而较小升高则诱导LTD。这些结果与Lisman提出的Ca2+假说一致（《神经科学趋势》17 (1994) 406）。
