Abstract
Beyond its role in parturition and lactation, oxytocin influences higher brain processes that control social behavior of mammals, and perturbed oxytocin signaling has been linked to the pathogenesis of several psychiatric disorders. However, it is still largely unknown how oxytocin exactly regulates neuronal function. We show that early, transient oxytocin exposure in vitro inhibits the development of hippocampal glutamatergic neurons, leading to reduced dendrite complexity, synapse density, and excitatory transmission, while sparing GABAergic neurons. Conversely, genetic elimination of oxytocin receptors increases the expression of protein components of excitatory synapses and excitatory synaptic transmission in vitro. In vivo, oxytocin-receptor-deficient hippocampal pyramidal neurons develop more complex dendrites, which leads to increased spine number and reduced γ-oscillations. These results indicate that oxytocin controls the development of hippocampal excitatory neurons and contributes to the maintenance of a physiological excitation/inhibition balance, whose disruption can cause neurobehavioral disturbances.
Highlights
Oxytocin (Oxt) is produced by magnocellular neurons of the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the bloodstream from posterior pituitary nerve terminals
Oxt exposure did not affect neuronal survival (Figure 1—figure supplement 1a,b) but reduced the dendritic arborization of neurons at 14 days in vitro (DIV), as assessed by Sholl analysis (Sholl, 1953) of cells stained with an antibody to the dendrite marker Map2 (Figure 1a–c)
Oxt exposure reduced the number of juxtaposed glutamatergic pre- and post-synaptic sites, but no changes were detected in the spatial coincidence of pre- and postsynaptic labeling (Mander’s overlapping coefficient) (Figure 1e–g), indicating that the integrity of the remaining glutamatergic synapses is maintained
Summary
Oxytocin (Oxt) is produced by magnocellular neurons of the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the bloodstream from posterior pituitary nerve terminals. Oxt is released in the brain by synaptic release from projections of parvocellular PVN neurons and by hormone-like release from the somata and dendrites of magnocellular neurons (Ludwig and Leng, 2006). Based on these processes and its long half-life, Oxt can act in diverse Oxtr-expressing brain areas even when direct innervation by Oxt-containing fibers is absent (Stoop, 2012). Key regulatory effects of Oxt on animal and human behavior include promotion of facial recognition and maternal nurturing (Ferguson et al, 2001, 2000), control of anxiety (Bale et al, 2001; Yoshida et al, 2009), and regulation of spatial memory (Tomizawa et al, 2003).
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