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Department of Neurobiology and Behavior, University of California, Irvine, CA 92697. *To whom correspondence should be addressed. E-mail: lukemcgowan1@yahoo.com.

and may generate abnormal patterns of cerebrospinal fluid flow; both abnormalities would generate disturbances in tectal lamination. Overall, our findings suggest that evolutionary expansion of sheet-like, laminated brain regions requires a concomitant expansion of the pia mater.

Evolutionary increases in brain region volumes are common (Striedter, 2005). For example, the neocortex is disproportionately enlarged in primates relative to other mammals, and the telencephalon is disproportionately enlarged in parrots and songbirds relative to other birds (Stephan et al., 1981; Boire and Baron, 1994; Iwaniuk and Hurd, 2005; Striedter, 2005). Recent work in evolutionary developmental neurobiology has shown that these evolutionary increases in brain region volumes are often caused by delays in cell cycle exit of neuronal precursors (Finlay et al., 2001; Charvet et al., 2011). Among birds, for example, parrots and songbirds exhibit delayed telencephalic neurogenesis relative to chicken-like birds (Charvet and Striedter, 2008, 2009; Striedter and Charvet, 2008). Among mammals, cell cycle exit in the neocortex is similarly delayed in primates, which have a disproportionately enlarged neocortex (Clancy et al., 2000, 2001, 2007; Finlay et al., 2001).

Unfortunately, the downstream effects of delayed cell cycle exit on subsequent developmental processes and adult morphology remain poorly understood. One way to fill this gap in our knowledge is to experimentally recreate the key species differences in the laboratory by means of carefully selected developmental manipulations. A good example of this phenocopy approach was the creation of transgenic mice with a constitutively active form of β-catenin that prolongs proliferation, increases neocortical volume, and generates cortical folds (Chenn and Walsh, 2002). In another example, it has been shown that intraventricular injections of FGF2 in rats delay neocortical cell cycle exit, leading to dramatic increases in neocortex volume and neuron number (Vaccarino et al., 1999). Based in part on these experiments, it is becoming increasingly common to explain human cortical evolution and expansion in terms of delayed and prolonged precursor proliferation (Rakic, 1995a; Kriegstein et al., 2006).

The present study began as an attempt to phenocopy natural variation in telencephalon size among birds. Specifically, we reasoned that FGF2 injections into ventricles of embryonic chicks should, by analogy to the work in mammals (Vaccarino et al., 1999), increase telencephalon volume, effectively creating chickens with a telencephalon as large as that of parrots and songbirds (Striedter and Charvet, 2008; Charvet and Striedter, 2009). However, our FGF2 injections did not significantly alter telencephalon development. Instead, they increased the size of the optic tectum, disrupted tectal lamination, and created tectal gyri and sulci.



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