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Cerebral Cortex Advance Access originally published online on March 29, 2007
Cerebral Cortex 2008 18(1):1-12; doi:10.1093/cercor/bhm026
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© 2007 The Authors
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

D1 but not D5 Dopamine Receptors Are Critical for LTP, Spatial Learning, and LTP-Induced arc and zif268 Expression in the Hippocampus

Noelia Granado1, Oskar Ortiz1, Luz M. Suárez2, Eduardo D. Martín3, Valentín Ceña3, José M. Solís2 and Rosario Moratalla1

1 Instituto Cajal, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain, 2 Hospital Ramón y Cajal, 28034 Madrid, Spain, 3 Departamento de Ciencias Médicas, Universidad de Castilla-La Mancha, 02006 Albacete, Spain

Address correspondence to Rosario Moratalla, Instituto Cajal, Consejo Superior de Investigaciones Científicas, Avda Dr Arce 37, 28002 Madrid, Spain. Email: moratalla{at}cajal.csic.es.

Recent evidence suggests that glutamatergic and dopaminergic afferents must be activated to induce persistent long-term potentiation (LTP) in the hippocampus. Whereas extensive evidence supports the role of glutamate receptors in long-lasting synaptic plasticity and spatial learning and memory, there is less evidence regarding the role of dopamine receptors in these processes. Here, we used dopamine D1 receptor knockout (D1R–/–) mice to explore the role of D1R in hippocampal LTP and its associated gene expression. We show that the magnitude of early and late phases of LTP (E-LTP and L-LTP) was markedly reduced in hippocampal slices from D1R–/– mice compared with wild-type mice. SCH23390, a D1/D5R antagonist, did not further reduce L-LTP in D1R–/– mice, suggesting that D5Rs are not involved. D1R–/– mice also showed a significant reduction of D1R-induced potentiation of N-Methyl-D-aspartic acid-mediated currents, via protein kinase activated by cyclic adenosine 3',5'-monophosphate activation. Finally, LTP-induced expression of the immediate early genes zif268 and arc in the hippocampal CA1 area was abolished in D1R–/– mice, and these mice showed impaired learning. These results indicate that D1R but not D5R are critical for hippocampal LTP and for the induction of Zif268 and Arc, proteins required for the transition from E-LTP to L-LTP and for memory consolidation in mammals.

Key Words: behavior • cognition • dopamine • knockout • LTP • memory • water maze

Noelia Granado, Oskar Ortiz, and Luz M. Suárez contributed equally in this work


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