Gulacsi Alexandra, Lillien Laura
Department of Neurobiology and Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA.
J Neurosci. 2003 Oct 29;23(30):9862-72. doi: 10.1523/JNEUROSCI.23-30-09862.2003.
Cortical progenitors are competent to produce interneurons, but do not generate large numbers of interneurons in vivo under normal circumstances. This could reflect the absence of an inductive signal in the environment of the dorsal telencephalon and/or the presence of an inhibitory signal. To determine whether either or both mechanisms regulate interneuron generation, progenitors in dorsomedial and dorsolateral wall explants of mouse telencephalon were marked with a retrovirus and cultured under several conditions. When cultured separately, progenitors in dorsomedial wall explants produced fewer GABAergic interneurons than progenitors in dorsolateral wall explants. When cocultured with ventral telencephalic cells, however, dorsomedial wall progenitors produced more GABAergic interneurons than in dorsomedial wall explants alone. The inductive effect of ventral telencephalon depended on sonic hedgehog (Shh) and could be mimicked by exogenous Shh. In contrast, exogenous bone morphogenetic protein 4 (BMP4) reduced the production of interneurons in dorsolateral wall explants and inhibited the induction by exogenous Shh. Moreover, inhibiting BMP signaling in dorsomedial wall progenitors with a dominant-negative BMP receptor Ib (dnBMPIb) virus increased their production of interneurons, even if Shh was blocked. Shh and dnBMPRIb increased proliferation and the generation of interneurons, but FGF2 did not induce interneurons, although it increased proliferation. This suggests that proliferation per se does not control the production of interneurons. Our findings suggest that the generation of interneurons by dorsal telencephalic progenitors is normally limited by excess levels of BMPs. Shh may promote the generation of interneurons by antagonizing BMP, but may not be required directly for the generation of interneurons.
皮质祖细胞有能力产生中间神经元,但在正常情况下,其在体内不会产生大量中间神经元。这可能反映了背侧端脑环境中缺乏诱导信号和/或存在抑制信号。为了确定这两种机制是否单独或共同调节中间神经元的产生,用逆转录病毒标记小鼠端脑背内侧和背外侧壁外植体中的祖细胞,并在几种条件下进行培养。单独培养时,背内侧壁外植体中的祖细胞产生的γ-氨基丁酸能中间神经元比背外侧壁外植体中的祖细胞少。然而,当与腹侧端脑细胞共培养时,背内侧壁祖细胞产生的γ-氨基丁酸能中间神经元比单独的背内侧壁外植体中更多。腹侧端脑的诱导作用依赖于音猬因子(Shh),并且可以被外源性Shh模拟。相反,外源性骨形态发生蛋白4(BMP4)减少了背外侧壁外植体中中间神经元的产生,并抑制了外源性Shh的诱导作用。此外,用显性负性BMP受体Ib(dnBMPIb)病毒抑制背内侧壁祖细胞中的BMP信号,即使Shh被阻断,也会增加它们中间神经元的产生。Shh和dnBMPRIb增加了增殖和中间神经元的产生,但FGF2虽然增加了增殖,但并未诱导中间神经元的产生。这表明增殖本身并不控制中间神经元的产生。我们的研究结果表明,背侧端脑祖细胞产生中间神经元通常受到BMPs过量水平的限制。Shh可能通过拮抗BMP来促进中间神经元的产生,但中间神经元的产生可能并不直接需要Shh。