Neurogenesis in an adult avian song nucleus is reduced by decreasing caspase-mediated apoptosis - PubMed (original) (raw)

Comparative Study

Neurogenesis in an adult avian song nucleus is reduced by decreasing caspase-mediated apoptosis

Christopher K Thompson et al. J Neurosci. 2009.

Abstract

Neuron death and replacement are fundamental components of brain plasticity. Much remains unknown, however, about the mechanistic interaction between neuron death and neurogenesis in adult vertebrates. In seasonally breeding adult male white-crowned sparrows, the song system nucleus HVC loses approximately 26% of its neurons via caspase-dependent apoptosis within 4 d after a transition to nonbreeding physiological conditions. To determine whether neuronal death is necessary for the recruitment of new neurons, we infused caspase inhibitors into HVC in vivo and suppressed neurodegeneration for at least 20 d after the transition to nonbreeding conditions. The blockade of HVC neuron death reduced the number and density of new neurons recruited to the ipsilateral HVC by 48 and 29%, respectively, compared with contralateral HVC. Our results are the first to show that reducing neuronal death in the adult brain decreases the recruitment of new neurons.

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Figures

Figure 1.

Figure 1.

The avian song control system and timeline for experimental procedures. A, Schematic sagittal diagram of the song control system showing projections of major nuclei. The green arrows indicate the descending motor pathway. The red arrows indicate the anterior forebrain pathway. X, Area X; IMAN, lateral magnocellular nucleus of the anterior nidopallium; DLM, medial part of the dorsolateral thalamic nucleus; nXIIts, tracheosyringeal portion of the hypoglossal nucleus. B, Schematic timeline of the experimental procedures. Birds received daily injections of BrdU for 5 d.

Figure 2.

Figure 2.

In vivo infusion of caspase inhibitors preserved ipsilateral HVC 20 d after the transition from breeding to nonbreeding conditions. Each animal within each group is represented by a distinct color across all figures. Asterisks indicate significant differences across hemispheres (pairwise t test; *p < 0.01, **p < 0.005). A, Caspase inhibitors significantly protected ipsilateral HVC volume 20 d after transition to nonbreeding conditions. Infusion of negative control had no effect. B, Caspase inhibitors significantly protected ipsilateral HVC neuron number 20 d after transition to nonbreeding conditions. Infusion of negative control had no effect. C, D, Infusion of neither caspase inhibitors nor negative control significantly preserved ipsilateral HVC soma area and neuron density 20 d after the transition to nonbreeding conditions.

Figure 3.

Figure 3.

In vivo infusion of caspase inhibitors near HVC significantly reduced the rate of incorporation of new neurons into the ipsilateral HVC 20 d after the transition from breeding to nonbreeding conditions. A, B, Micrographs illustrating immunohistochemistry for Hu, a neuron-specific marker in a section containing HVC on the ipsilateral (A) and contralateral (B) hemisphere, show that caspase inhibitor infusion prevented the regression of the ipsilateral HVC, while the contralateral HVC regressed normally. Dashed lines indicate the ventral border of HVC. Scale bar, 200 μm. C–H, High-magnification micrographs of cells positive for BrdU (C, F) and Hu (D, G), and merge for both labels (E, H) depict fewer BrdU+/Hu+ neurons (arrowheads) in the ipsilateral HVC (E) than in the contralateral HVC (H). Brd+/Hu− cells are indicated with an arrow. Scale bar, 20 μm. I, J, Caspase inhibitor infusion significantly reduced the density (I) and number (J) of new neurons incorporated into the ipsilateral HVC. Infusion of a negative control had no effect. Asterisk indicates significant differences across hemispheres (pairwise t test; *p < 0.05, **p < 0.01).

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