TY - JOUR
T1 - Nitric oxide acts directly in the presynaptic neuron to produce long- term potentiation in cultured hippocampal neurons
AU - Arancio, Ottavio
AU - Kiebler, Michael
AU - Lee, C. Justin
AU - Lev-Ram, Varda
AU - Tsien, Roger Y.
AU - Kandel, Eric R.
AU - Hawkins, Robert D.
N1 - Funding Information:
We thank C. de Albuquerque and L. Zablow for their generous assistance in imaging fluorescein-labeled myoglobin and synaptophysin immunofluorescence, A. MacDermott and S. Siegelbaum for their comments, C. Lam for preparing the figures, and H. Ayers and I. Trumpet for typing the manuscript. This work was supported in part by grants from the National Institute of Mental Health (MH50733) and the Howard Hughes Medical Institute. M. K. received support from the HFSPO and DFG.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 1996/12/13
Y1 - 1996/12/13
N2 - Nitric oxide (NO) has been proposed to act as a retrograde messenger during long-term potentiation (LTP) in the CA1 region of hippocampus, but the inaccessibility of the presynaptic terminal has prevented a definitive test of this hypothesis. Because both sides of the synapse are accessible in cultured hippocampal neurons, we have used this preparation to investigate the role of NO. We examined LTP following intra- or extracellular application of an NO scavanger, an inhibitor of NO synthase, and a membrane-impermeant NO donor that releases NO only upon photolysis with UV light. Our results indicate that NO is produced in the postsynaptic neuron, travels through the extracellular space, and acts directly in the presynaptic neuron to produce long-term potentiation, supporting the hypothesis that NO acts as a retrograde messenger during LTP.
AB - Nitric oxide (NO) has been proposed to act as a retrograde messenger during long-term potentiation (LTP) in the CA1 region of hippocampus, but the inaccessibility of the presynaptic terminal has prevented a definitive test of this hypothesis. Because both sides of the synapse are accessible in cultured hippocampal neurons, we have used this preparation to investigate the role of NO. We examined LTP following intra- or extracellular application of an NO scavanger, an inhibitor of NO synthase, and a membrane-impermeant NO donor that releases NO only upon photolysis with UV light. Our results indicate that NO is produced in the postsynaptic neuron, travels through the extracellular space, and acts directly in the presynaptic neuron to produce long-term potentiation, supporting the hypothesis that NO acts as a retrograde messenger during LTP.
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U2 - 10.1016/S0092-8674(00)81797-3
DO - 10.1016/S0092-8674(00)81797-3
M3 - Article
C2 - 8978607
AN - SCOPUS:0030582674
VL - 87
SP - 1025
EP - 1035
JO - Cell
JF - Cell
SN - 0092-8674
IS - 6
ER -