J.‐M. Billard

Université Paris Cité

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P. Dutar

Laboratoire Lumière, Matière et Interfaces

Anne Jouvenceau

Université Paris Cité

Y. Lamour

Inserm

Brigitte Potier

Laboratoire Lumière, Matière et Interfaces

Jacques Epelbaum

Mécanismes Adaptatifs et Evolution

Jean‐Pierre Mothet

CentraleSupélec

Emilie Rouaud

Institut de Psychiatrie et Neurosciences de Paris

Pierre‐Marie Sinet

Institut de Psychiatrie et Neurosciences de Paris

M. Le Moal

Inserm

Guillaume Junjaud

Inserm

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Inserm

Université Paris Cité

Centre National de la Recherche Scientifique

Délégation Paris 5

Institut de Psychiatrie et Neurosciences de Paris

Institut National de la Recherche Agronomique

Physiologie de la Nutrition et du Comportement Alimentaire

Université Paris-Saclay

Sorbonne Université

Université de Bordeaux

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HAL (Le Centre pour la Communication Scientifique Directe) (2013)

Isabelle Denis Brigitte Potier Alizée Latour Gaëlle Champeil‐Potokar Marie Hennebelle

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Journal of Neurochemistry (2006)

Guillaume Junjaud Emilie Rouaud Fabrice Turpin Jean‐Pierre Mothet J.‐M. Billard

Abstract The effects of the co‐agonist of the N ‐methyl‐ d ‐aspartate receptor (NMDAr) d ‐serine on glutamatergic neurotransmission and synaptic potentiation were studied in the CA1 hippocampal field of young (3–5 months old) and aged (25–27 months old) Sprague–Dawley rats using ex vivo extracellular electrophysiological recording techniques. Exogenous d ‐serine depressed fast neurotransmission mediated by the α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid/kainate subtype of glutamate receptors in young but not in aged rats by acting on inhibitory glycinergic interneurons. In contrast, d ‐serine dose‐dependently enhanced NMDAr‐mediated synaptic responses in both groups of animals, but with a larger magnitude in aged rats, thus preventing the age‐related decrease in NMDAr activation. d ‐serine also increased the magnitude of long‐term potentiation in aged but not in young rats. Finally, d ‐serine levels were dramatically reduced in hippocampal tissues of aged rats. Taken together, these results indicate a weaker activation of the NMDAr glycine modulatory site by endogenous d ‐serine in aged animals, which accounts for a reduced NMDAr contribution to synaptic plasticity in ageing.

Kainate receptor

10.1111/j.1471-4159.2006.03944.x

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Alteration of NMDA receptor-mediated synaptic responses in CA1 area of the aged rat hippocampus: Contribution of GABAergic and cholinergic deficits

Hippocampus (1998)

Anne Jouvenceau P. Dutar J.‐M. Billard

Synaptic responses mediated by the N-methyl-D-aspartate receptor (NMDAr) and non-NMDAr activation were compared in CA1 hippocampal region of young (3-4 months old) and aged (25-33 months old) Sprague-Dawley rats with the use of ex vivo extracellular recordings techniques. In aged rats, the amplitude of the NMDAr-mediated field excitatory postsynaptic potentials (fEPSPs) was not altered, whereas their duration was significantly increased. In contrast, the magnitude of non-NMDAr-mediated fEPSPs was significantly smaller. The presynaptic fiber volley was not affected by age. Considering that the depression of non-NMDAr-mediated responses was previously attributed to fewer synaptic contacts between glutamatergic afferent fibers and pyramidal cells in aged animals (see Barnes et al., Hippocampus 1992;2:457-468), the absence of age-related changes in the amplitude of NMDAr-mediated fEPSPs suggests that compensatory mechanisms may occur. The contribution of gamma-aminobutyric acid (GABA) and acetylcholine to these mechanisms was addressed. The NMDAr-mediated fEPSPs were then recorded (1) in young and aged rats before and after blockade of the GABA(B) receptor-mediated inhibition by the specific antagonist CGP 55845 and (2) in young rats after a selective cholinergic denervation of the hippocampus by the immunotoxin 192 IgG-saporin. The results did not indicate statistically relevant age-related effects of CGP 55845. In contrast, the loss of the cholinergic innervation by the immunotoxin induced a significant increase in both the amplitude and duration of the NMDAr-mediated fEPSPs. Our results indicate that the functional properties of the ionotropic glutamate receptor subtypes located on CA1 pyramidal cells are differentially affected by aging and suggest that the cholinergic deficit that occurs during aging may be involved in the maintenance of robust NMDAr-mediated synaptic responses.

10.1002/(sici)1098-1063(1998)8:6<627::aid-hipo5>3.0.co;2-x

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Motherhood‐induced memory improvement persists across lifespan in rats but is abolished by a gestational stress

European Journal of Neuroscience (2006)

Valérie Lemaire J.‐M. Billard P. Dutar Olivier George Pier Vincenzo Piazza

Motherhood modifies the biology and behavior of the female, a process which prepares the mother's cognitive systems that are needed for nurturance. It has recently been shown that motherhood enhances hippocampal-mediated spatial learning and synaptic plasticity. Deleterious and long-term effects of a stress experienced during gestation have been demonstrated on progeny. Surprisingly little is known about the effect of such stress on mothers. Here, we investigated the effect of gestational stress on the adaptive changes due to motherhood. Female rats were mated and stressed during the last week of gestation. Two weeks after weaning, they were submitted to behavioral tests or electrophysiological study. A group of females were then kept for 16 months after motherhood experience to study the long-term effect of gestational stress and motherhood on memory when they were 22 months old. We confirm that a single motherhood experience selectively increases hippocampal-mediated spatial memory during the entire lifespan of female rats and protects them from age-associated memory impairments. However, we demonstrate that a stressful experience during gestation totally abolishes the positive effects of motherhood both on spatial memory and on hippocampal synaptic plasticity (long-term potentiation). Environmental factors that induce biological vulnerability have negative effects even for fundamental biological behaviors.

Vulnerability

10.1111/j.1460-9568.2006.04870.x

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Citations (86)