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J Neurophysiol 92: 1077-1087, 2004; doi:10.1152/jn.00602.2003
0022-3077/04 $5.00
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Presynaptic Activity and Ca2+ Entry Are Required for the Maintenance of NMDA Receptor–Independent LTP at Visual Cortical Excitatory Synapses

Hong Nian Liu, Tohru Kurotani, Ming Ren, Kazumasa Yamada, Yumiko Yoshimura and Yukio Komatsu

Department of Visual Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan

Submitted 25 June 2003; accepted in final form 29 March 2004

We have shown that some neural activity is required for the maintenance of long-term potentiation (LTP) at visual cortical inhibitory synapses. We tested whether this was also the case in N-methyl-D-aspartate (NMDA) receptor–independent LTP of excitatory connections in layer 2/3 cells of developing rat visual cortex. This LTP occurred after 2-Hz stimulation was applied for 15 min and always persisted for several hours while test stimulation was continued at 0.1 Hz. When test stimulation was stopped for 1 h after LTP induction, only one-third of the LTP instances disappeared, but most did disappear under a pharmacological suppression of spontaneous firing, indicating that LTP maintenance requires either evoked or spontaneous activities. LTP was totally abolished by a temporary blockade of action potentials with lidocaine or the removal of extracellular Ca2+ after LTP induction, but it persisted under a voltage clamp of postsynaptic cells or after a temporary blockade of postsynaptic activity with the glutamate receptor antagonist kynurenate, suggesting that LTP maintenance requires presynaptic, but not postsynaptic, firing and Ca2+ entry. More than one-half of the LTP instances were abolished after a pharmacological blockade of P-type Ca2+ channels, whereas it persisted after either L-type or Ni2+-sensitive Ca2+ channel blockades. These results show that the maintenance of NMDA receptor–independent excitatory LTP requires presynaptic firing and Ca2+ channel activation as inhibitory LTP, although the necessary level of firing and Ca2+ entry seems lower for the former than the latter and the Ca2+ channel types involved are only partly the same.


Address for reprint requests and other correspondence: Y. Komatsu, Dept. of Visual Neuroscience, Research Inst. of Environmental Medicine, Nagoya Univ., Furo-Cho, Chikusa-ku, Nagoya 464-8601, Japan (E-mail: komatsu{at}riem.nagoya-u.ac.jp).




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