Adult neurogenesis, an essential mechanism of brain plasticity, enables brain development along postnatal life, constant addition of new neurons, neuronal turnover, and/or regeneration. It is amply distributed but negatively modulated during development and along evolution. Widespread cell proliferation, high neurogenic, and regenerative capacities are considered characteristics of teleost brains during adulthood. These anamniotes are promising models to depict factors that modulate cell proliferation, migration, and neurogenesis, and might be intervened to promote brain plasticity in mammals. Nevertheless, the migration path of derived cells to their final destination was not studied in various teleosts, including most weakly electric fish. In this group adult brain morphology is attributed to sensory specialization, involving the concerted evolution of peripheral electroreceptors and electric organs, encompassed by the evolution of neural networks involved in electrosensory information processing. In wave type gymnotids adult brain morphology is proposed to result from lifelong region specific cell proliferation and neurogenesis. Consistently, pulse type weakly electric gymnotids and mormyrids show widespread distribution of proliferation zones that persists in adulthood, but their neurogenic potential is still unknown. Here we studied the migration process and differentiation of newborn cells into the neuronal phenotype in the pulse type gymnotid Gymnotus omarorum. Pulse labeling of S-phase cells with 5-Chloro-2′-deoxyuridine thymidine followed by 1 to 180 day survivals evidenced long distance migration of newborn cells from the rostralmost telencephalic ventricle to the olfactory bulb, and between layers of all cerebellar divisions. Shorter migration appeared in the tectum opticum and torus semicircularis. In many brain regions, derived cells expressed early neuronal markers doublecortin (chase: 1–30 days) and HuC/HuD (chase: 7–180 days). Some newborn cells expressed the mature neuronal marker tyrosine hydroxylase in the subpallium (chase: 90 days) and olfactory bulb (chase: 180 days), indicating the acquisition of a mature neuronal phenotype. Long term CldU labeled newborn cells of the granular layer of the corpus cerebelli were also retrogradely labeled “in vivo,” suggesting their insertion into the neural networks. These findings evidence the neurogenic capacity of telencephalic, mesencephalic, and rhombencephalic brain proliferation zones in G. omarorum, supporting the phylogenetic conserved feature of adult neurogenesis and its functional significance.
The dorsolateral bed nucleus of the stria terminalis (BNST DL ) has high expression of oxytocin (OT) receptors (OTR), which were shown to facilitate cued fear. The BNST DL contains GABAergic neurons classified based on intrinsic membrane properties into three major types. Using in vitro patch-clamp recordings in male rats, we demonstrate that OT selectively excites Type I neurons in an OTR-dependent manner as revealed by a significantly increased resting membrane potential, increased input resistance, reduced rheobase, reduced fast and medium spike afterhyperpolarization, reduced threshold and latency to a first spike, as well as a left shift in the spike frequency/current relationship. As Type I neurons are putative BNST DL interneurons, we next recorded inhibitory synaptic transmission in all three types of neurons and we demonstrate that OT increases the frequency, but not amplitude, of spontaneous inhibitory post-synaptic currents (sIPSCs), selectively in Type II neurons. This effect was abolished by the presence of an OTR antagonist or tetrodotoxin, the latter suggesting an indirect effect via an OT-induced increase in firing of Type I interneurons. As Type II neurons were shown to project to the central amygdala (CeA), we also recorded from retrogradely labeled BNSTèCeA neurons, which we identified as Type II. These results present a model of fine-tuned modulation of intrinsic BNST DL neurocircuitry by OT, which selectively excites Type I neurons, leading to increased GABA-ergic inhibition in Type II projection neurons. Lastly, we demonstrate that fearconditioning increases sIPSCs frequency in Type II neurons, mimicking the effect of OT. Based on the findings, we propose that OTR in the BNST DL facilitate cued fear by inhibiting BNSTèCeA neurons.
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