Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland; Neuroscience Center, University of Helsinki, Helsinki, Finland
Jonas Englund
Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland; Neuroscience Center, University of Helsinki, Helsinki, Finland
Alexandra Shintyapina
Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland; Neuroscience Center, University of Helsinki, Helsinki, Finland
Johanna Huupponen
Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland; Neuroscience Center, University of Helsinki, Helsinki, Finland
Vasilii Shteinikov
Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland
Asla Pitkänen
A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland
Juha M Partanen
Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland
Molecular and Integrative Biosciences Research Program, University of Helsinki, Helsinki, Finland; Neuroscience Center, University of Helsinki, Helsinki, Finland
Perturbed information processing in the amygdala has been implicated in developmentally originating neuropsychiatric disorders. However, little is known on the mechanisms that guide formation and refinement of intrinsic connections between amygdaloid nuclei. We demonstrate that in rodents the glutamatergic connection from basolateral to central amygdala (BLA-CeA) develops rapidly during the first 10 postnatal days, before external inputs underlying amygdala-dependent behaviors emerge. During this restricted period of synaptic development, kainate-type of ionotropic glutamate receptors (KARs) are highly expressed in the BLA and tonically activated to regulate glutamate release via a G-protein-dependent mechanism. Genetic manipulation of this endogenous KAR activity locally in the newborn LA perturbed development of glutamatergic input to CeA, identifying KARs as a physiological mechanism regulating formation of the glutamatergic circuitry in the amygdala.
