Oncotarget

Research Papers:

Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice

Raffaella Barbieri, Andrea Contestabile, Maria Grazia Ciardo, Nicola Forte, Antonella Marte, Pietro Baldelli, Fabio Benfenati and Franco Onofri _

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Oncotarget. 2018; 9:18760-18774. https://doi.org/10.18632/oncotarget.24655

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Abstract

Raffaella Barbieri1, Andrea Contestabile2, Maria Grazia Ciardo1, Nicola Forte3, Antonella Marte1, Pietro Baldelli1,3, Fabio Benfenati1,3,* and Franco Onofri1,*

1Department of Experimental Medicine, University of Genova, 16132, Genova, Italy

2Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, 16163, Genova, Italy

3Center for Synaptic Neuroscience and Technology, Istituto Italiano di Tecnologia, 16132, Genova, Italy

*These authors have contributed equally to this work

Correspondence to:

Franco Onofri, email: franco.onofri@unige.it

Keywords: adult neurogenesis, dentate gyrus, synapsins, brain-derived neurotrophic factor, epilepsy

Received: December 23, 2017     Accepted: February 25, 2018     Published: April 10, 2018

ABSTRACT

Adult neurogenesis is emerging as an important player in brain functions and homeostasis, while impaired or altered adult neurogenesis has been associated with a number of neuropsychiatric diseases, such as depression and epilepsy. Here we investigated the possibility that synapsins (Syns) I and II, beyond their known functions in developing and mature neurons, also play a role in adult neurogenesis. We performed a systematic evaluation of the distinct stages of neurogenesis in the hippocampal dentate gyrus of Syn I and Syn II knockout (KO) mice, before (2-months-old) and after (6-months-old) the appearance of the epileptic phenotype. We found that Syns I and II play an important role in the regulation of adult neurogenesis. In juvenile mice, Syn II deletion was associated with a specific decrease in the proliferation of neuronal progenitors, whereas Syn I deletion impaired the survival of newborn neurons. These defects were reverted after the appearance of the epileptic phenotype, with Syn I KO and Syn II KO mice exhibiting significant increases in survival and proliferation, respectively. Interestingly, long-term potentiation dependent on newborn neurons was present in both juvenile Syn mutants while, at later ages, it was only preserved in Syn II KO mice that also displayed an increased expression of brain-derived neurotrophic factor. This study suggests that Syns I and II play a role in adult neurogenesis and the defects in neurogenesis associated with Syn deletion may contribute to the alterations of cognitive functions observed in Syn-deficient mice.


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