Inflammation in the brain, called neuroinflammation, is typically considered a negative response following neuronal injury and damage. However, neuroinflammation can also play a beneficial role in the healthy adult brain. For example, one type of inflammatory cell, microglia, become polarized from the “inactive” surveying (or ramified) state following neuronal loss and promote the classic “negative” inflammatory response. Alternatively, in the healthy brain microglia elicit positive effects through neuronal and synapse pruning to maintain proper neuronal number and connections. To identify the dynamics of microglial responses between healthy and natural degenerative states, we employed the seasonal neuronal regression of avian motor pathways for song production in Gambel’s white crowned sparrow (Zonotrichia leucophrys gambelii). Neuronal number in the song control nucleus HVC (proper name) changes seasonally such that as male sparrows transition from nonbreeding to breeding conditions, HVC neuronal number increases by about 68,000 neurons. Useful for our study, an equal number of HVC neurons die through programed cell death as sparrows transition from breeding to nonbreeding conditions. Using this unique model of natural and rapid neurodegeneration, we quantified the number of ramified and activated microglia in HVC of birds maintained in breeding and nonbreeding conditions using immunohistochemistry. To identify microglial promotion of local neuroinflammation within HVC, we examined the number of ramified and activated microglia in HVC of birds treated with pro- and anti-inflammatory agents. Additionally, we identified and quantified a putative downstream effect of this local inflammation: reactive neurogenesis, or the birth of new neurons following neuronal loss. Our results indicate that microglia promote reactive neurogenesis through local inflammation, and suggest that discrete microglial activity could have therapeutic consequences for various neurological diseases.