Abstract
Mitochondrial uncoupling protein 2 (UCP2) is induced by cellular stress and is involved in regulation of fuel utilization, mitochondrial bioenergetics, cell proliferation, neuroprotection and synaptogenesis in the adult brain. Here we show that natural birth in mice triggers UCP2 expression in hippocampal neurons. Chemical inhibition or genetic ablation of UCP2 lead to diminished neuronal number and size, dendritic growth and synaptogenezis in vitro and impaired complex behaviors in the adult. These data reveal a critical role for Ucp2 expression in the development of hippocampal neurons and circuits and hippocampus-related adult behaviors.
Highlights
The perinatal environment represents a critical period in brain development that determines the adult architecture of the central nervous system and related functions
We sought to determine whether uncoupling protein 2 (Ucp2) induction occurs in the hippocampus perinatally, and if so, whether Ucp2-associated cellular mechanisms are involved in the development of neuronal circuits in vitro with implications for adult behavior
uncoupling protein 2 (UCP2) mRNA is induced by birth We analyzed Ucp2 expression in the hippocampus of mice delivered with Caesarian section (CS), vaginal birth (VB) and in various postnatal ages from animals born naturally
Summary
The perinatal environment represents a critical period in brain development that determines the adult architecture of the central nervous system and related functions. Ucp promotes free radical scavenging [3,4,5], which is critical for enabling fatty acid beta oxidation in neurons [2]. This mechanism is critical for adult synaptogenesis [6]. We sought to determine whether Ucp induction occurs in the hippocampus perinatally, and if so, whether Ucp2-associated cellular mechanisms are involved in the development of neuronal circuits in vitro with implications for adult behavior
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