The hippocampo-amygdala control of contextual fear expression is affected in a model of intellectual disability

Chun-Lei Zhang, Xander Houbaert, Marilyn Lepleux, Melissa Deshors, Elisabeth Normand, Frédéric Gambino, Etienne Herzog, Yann Humeau
Brain Struct Funct. 2014-08-27; 220(6): 3673-3682
DOI: 10.1007/s00429-014-0882-x

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1. Brain Struct Funct. 2015 Nov;220(6):3673-82. doi: 10.1007/s00429-014-0882-x. Epub
2014 Aug 27.

The hippocampo-amygdala control of contextual fear expression is affected in a model of intellectual disability.

Zhang CL(1), Houbaert X(1), Lepleux M(1), Deshors M(1)(2), Normand E(1)(2), Gambino F(1), Herzog E(1), Humeau Y(3)(4).

Author information:
(1)Team Synapse in Cognition, Institut Interdisciplinaire de NeuroScience, Centre National de la Recherche Scientifique CNRS UMR5297, Université de Bordeaux, Bordeaux, France.
(2)Pole In Vivo, Institut Interdisciplinaire de NeuroScience, Centre National de la Recherche Scientifique CNRS UMR5297, Université de Bordeaux, Bordeaux, France.
(3)Team Synapse in Cognition, Institut Interdisciplinaire de NeuroScience, Centre National de la Recherche Scientifique CNRS UMR5297, Université de Bordeaux, Bordeaux, France. .
(4)UMR5297 Institut Interdisciplinaire de NeuroScience, Centre de Génomique Fonctionnelle, 146 rue Léo Saignat, 33077, Bordeaux Cedex, France. .

The process of learning mainly depends on the ability to store new information,
while the ability to retrieve this information and express appropriate behaviors
are also crucial for the adaptation of individuals to environmental cues.
Thereby, all three components contribute to the cognitive fitness of an
individual. While a lack of behavioral adaptation is a recurrent trait of
intellectually disabled patients, discriminating between memory formation, memory
retrieval or behavioral expression deficits is not easy to establish. Here, we
report some deficits in contextual fear behavior in knockout mice for the
intellectual disability gene Il1rapl1. Functional in vivo experiments revealed
that the lack of conditioned response resulted from a local inhibitory to
excitatory (I/E) imbalance in basolateral amygdala (BLA) consecutive to a loss of
excitatory drive onto BLA principal cells by caudal hippocampus axonal
projections. A normalization of the fear behavior was obtained in adult mutant
mice following opsin-based in vivo synaptic priming of hippocampo-BLA synapses in
adult il1rapl1 knockout mice, indicating that synaptic efficacy at hippocampo-BLA
projections is crucial for contextual fear memory expression. Importantly,
because this restoration was obtained after the learning phase, our results
suggest that some of the genetically encoded cognitive deficits in humans may
originate from a lack of restitution of genuinely formed memories rather than an
exclusive inability to store new memories.

DOI: 10.1007/s00429-014-0882-x
PMID: 25158900 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus