Presynaptic D 2 dopamine receptors control long-term depression expression and memory processes in the temporal hippocampus

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Background Dysfunctional mesocorticolimbic dopamine signaling has been linked to alterations in motor and reward-based functions associated with psychiatric disorders. Converging evidence from patients with psychiatric disorders and use of antipsychotics suggests that imbalance of dopamine signaling...

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Autor principal: Rocchetti, J.
Otros Autores: Isingrini, E., Dal Bo, G., Sagheby, S., Menegaux, A., Tronche, F., Levesque, D., Moquin, L., Gratton, A., Wong, T.P, Rubinstein, M., Giros, B.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Elsevier USA 2015
Acceso en línea:Registro en Scopus
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Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
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024 7 |2 cas  |a dopamine, 51-61-6, 62-31-7; Dopamine D2 Receptor Antagonists; DRD2 protein, mouse; Receptors, Dopamine D2; RNA, Messenger 
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030 |a BIPCB 
100 1 |a Rocchetti, J. 
245 1 0 |a Presynaptic D 2 dopamine receptors control long-term depression expression and memory processes in the temporal hippocampus 
260 |b Elsevier USA  |c 2015 
270 1 0 |m Giros, B.; Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche en Santé 1130France 
506 |2 openaire  |e Política editorial 
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520 3 |a Background Dysfunctional mesocorticolimbic dopamine signaling has been linked to alterations in motor and reward-based functions associated with psychiatric disorders. Converging evidence from patients with psychiatric disorders and use of antipsychotics suggests that imbalance of dopamine signaling deeply alters hippocampal functions. However, given the lack of full characterization of a functional mesohippocampal pathway, the precise role of dopamine transmission in memory deficits associated with these disorders and their dedicated therapies is unknown. In particular, the positive outcome of antipsychotic treatments, commonly antagonizing D 2 dopamine receptors (D2Rs), on cognitive deficits and memory impairments remains questionable. Methods Following pharmacologic and genetic manipulation of dopamine transmission, we performed anatomic, neurochemical, electrophysiologic, and behavioral investigations to uncover the role of D2Rs in hippocampal-dependent plasticity and learning. Naïve mice (n = 4-21) were used in the different procedures. Results Dopamine modulated both long-term potentiation and long-term depression in the temporal hippocampus as well as spatial and recognition learning and memory in mice through D2Rs. Although genetic deletion or pharmacologic blockade of D2Rs led to the loss of long-term potentiation expression, the specific genetic removal of presynaptic D2Rs impaired long-term depression and performances on spatial memory tasks. Conclusions Presynaptic D2Rs in dopamine fibers of the temporal hippocampus tightly modulate long-term depression expression and play a major role in the regulation of hippocampal learning and memory. This direct role of mesohippocampal dopamine input as uncovered here adds a new dimension to dopamine involvement in the physiology underlying deficits associated with neuropsychiatric disorders. © 2015 Society of Biological Psychiatry.  |l eng 
536 |a Detalles de la financiación: Canada Research Chairs 
536 |a Detalles de la financiación: This work was supported by the Canada Research Chairs program (BG is a Canadian Research Chair in the Neurobiology of Mental Disorders), the Canadian Foundation for Innovation, the Graham Boeckh Foundation for Schizophrenia Research (BG), and the Fond de Recherche du Québec-Santé (postdoctorate grants to GDB and EI). We thank Erika Vigneault and Marie-Eve Desaulnier for excellent care and maintenance of all mice colonies. The authors report no biomedical financial interests or potential conflicts of interest. Appendix A 
593 |a Department of Psychiatry, Douglas Mental Health University Institute, McGill University, 6875 Lasalle Boulevard, Montreal, QC H4H 1R3, Canada 
593 |a Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche en Santé 1130, France 
593 |a Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8246, Sorbonne University Université Pierre et Marie Curie, Paris, France 
593 |a Département de Pharmacie, Université de Montréal, Montreal, QC, Canada 
593 |a Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Instituto de Investigaciones en Ingenieria Genética y Biologia Molecular (CONICET), Universidad de Buenos Aires, Argentina 
593 |a Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina 
690 1 0 |a ANTIPSYCHOTICS 
690 1 0 |a D 2 DOPAMINE RECEPTORS 
690 1 0 |a LTD 
690 1 0 |a MEMORY 
690 1 0 |a NEURONAL PLASTICITY 
690 1 0 |a TEMPORAL HIPPOCAMPUS 
690 1 0 |a DOPAMINE 
690 1 0 |a DOPAMINE 2 RECEPTOR 
690 1 0 |a PRESYNAPTIC RECEPTOR 
690 1 0 |a DOPAMINE 2 RECEPTOR 
690 1 0 |a DOPAMINE 2 RECEPTOR BLOCKING AGENT 
690 1 0 |a DRD2 PROTEIN, MOUSE 
690 1 0 |a MESSENGER RNA 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a BRAIN ELECTROPHYSIOLOGY 
690 1 0 |a COGNITIVE DEFECT 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DOPAMINERGIC TRANSMISSION 
690 1 0 |a GENE EXPRESSION 
690 1 0 |a HIPPOCAMPAL CA1 REGION 
690 1 0 |a HIPPOCAMPUS 
690 1 0 |a LONG TERM DEPRESSION 
690 1 0 |a LONG TERM POTENTIATION 
690 1 0 |a MALE 
690 1 0 |a MEMORY DISORDER 
690 1 0 |a MOUSE 
690 1 0 |a NERVE CELL PLASTICITY 
690 1 0 |a NEUROANATOMY 
690 1 0 |a NEUROCHEMISTRY 
690 1 0 |a NEUROMODULATION 
690 1 0 |a NONHUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a REGULATORY MECHANISM 
690 1 0 |a SPATIAL LEARNING 
690 1 0 |a SPATIAL MEMORY 
690 1 0 |a TASK PERFORMANCE 
690 1 0 |a ANIMAL 
690 1 0 |a C57BL MOUSE 
690 1 0 |a DEPTH PERCEPTION 
690 1 0 |a DRUG EFFECTS 
690 1 0 |a EXCITATORY POSTSYNAPTIC POTENTIAL 
690 1 0 |a GENETICS 
690 1 0 |a HIPPOCAMPUS 
690 1 0 |a LEARNING 
690 1 0 |a LONG TERM DEPRESSION 
690 1 0 |a MEMORY 
690 1 0 |a METABOLISM 
690 1 0 |a NERVE TRACT 
690 1 0 |a PHYSIOLOGY 
690 1 0 |a TRANSGENIC MOUSE 
690 1 0 |a VENTRAL TEGMENTUM 
690 1 0 |a ANIMALS 
690 1 0 |a DOPAMINE D2 RECEPTOR ANTAGONISTS 
690 1 0 |a EXCITATORY POSTSYNAPTIC POTENTIALS 
690 1 0 |a HIPPOCAMPUS 
690 1 0 |a LEARNING 
690 1 0 |a LONG-TERM POTENTIATION 
690 1 0 |a LONG-TERM SYNAPTIC DEPRESSION 
690 1 0 |a MALE 
690 1 0 |a MEMORY 
690 1 0 |a MICE, INBRED C57BL 
690 1 0 |a MICE, TRANSGENIC 
690 1 0 |a NEURAL PATHWAYS 
690 1 0 |a RECEPTORS, DOPAMINE D2 
690 1 0 |a RNA, MESSENGER 
690 1 0 |a SPACE PERCEPTION 
690 1 0 |a VENTRAL TEGMENTAL AREA 
700 1 |a Isingrini, E. 
700 1 |a Dal Bo, G. 
700 1 |a Sagheby, S. 
700 1 |a Menegaux, A. 
700 1 |a Tronche, F. 
700 1 |a Levesque, D. 
700 1 |a Moquin, L. 
700 1 |a Gratton, A. 
700 1 |a Wong, T.P. 
700 1 |a Rubinstein, M. 
700 1 |a Giros, B. 
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856 4 0 |u https://doi.org/10.1016/j.biopsych.2014.03.013  |y DOI 
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