The neuroscientific community accepted the existence of adult neurogenesis in the 1980s -- and labcoaters worldwide have been tripping over themselves with excitement ever since. Adult neurogenesis! The cure to all neurodegenerative disorders! Its effects on behaviors must be drastic! And memory! Sleep! Learning! TBI! Much of this hoopla is in fact only hoopla. But for songbirds, adult neurogenesis (and the parallel pruning of adult born neurons) is key in their breeding behaviors. Adult neurogenesis contributes neurons to brain nuclei in certain avian species -- here we focus on Gambel's White Crowned Sparrows (GWS) -- allowing them to sing songs for attraction and territorial claiming purposes. This is a highly energy intensive process. The field postulates that in order to preserve resources in nonbreeding conditions, these same species show modulations in adult neurogenesis to keep their song nuclei smaller. What we know with complete clarity is that in breeding season, increased natural light levels trigger increased levels of testosterone in GWS, certain song-associated brain nuclei (HVC, for one) increase in size due to the addition of new neurons in breeding season ( spring ) and male birds sing their songs. In nonbreeding conditions, decreased light levels are associated with lower circulating testosterone levels, the number of neurons in song nuclei decrease and birds stop singing (and the fading light of winter reminds us that life has no reason). The ongoing work of Tracy Larson and others digs into the nitty gritty of these known processes.
Here I examine the minutiae of how adult neurogenesis is modulated in breeding and nonbreeding conditions in GWS. This is primarily a visualization and hyopthesis-simulating tool. A series of time-step differential equations are used to model/visualize four different cell populations (VZ progenitors, migrators ie the daughters of the progenitors that migrate out of VZ, new neurons in HVC, total neurons in HVC) over time. Variables that affect these populations are breeding season (binary, either 0 or 1), stable or plastic states of circuit (probably receptor sensitivity to T?), proliferation in VZ, success of migrators' migration to HVC and apoptosis in HVC.
I'm a neuroscientist and budding bioinformatician.
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