THE ROLE OF NEUROINFLAMMATION IN NEUROREGENERATION AFTER NEUROTOXIC LESION IN ZEBRA FINCH BRAIN

Damage to the CNS and neurodegenerative disorders frequently trigger an inflammatory response. Neuroinflammation can either promote or suppress adult neurogenesis, depending on its severity and duration. In contrast to mammals, the adult songbird brain retains a remarkable capacity for regeneration even after neurotoxic injury. This study aims to characterize the dynamics of neuroinflammation by assessing temporal changes in the expression of cytokines and trophic factors and to quantify cell proliferation within the neurogenic niche following striatal lesion.
A total of 39 adult male zebra finches (Taeniopygia guttata) were assigned to three post-lesion survival groups: 2 days (2D), 2 weeks (2W), and 3 months (3M). Each group consisted of a control and a lesioned group. Lesions were induced bilaterally in the striatal area using ibotenic acid. Two hours before euthanasia, birds were administered the cell proliferation marker. Gene expression of pro-inflammatory cytokines and trophic factors was quantified in one hemisphere and proliferation was assessed in the other hemisphere.
Our results show that pro-inflammatory molecules IL-12 and TNF-α were elevated during the early (2D) and middle (2W) phases of inflammation, while IGF and BDNF increased in the middle to late phases (2W-3M), reflecting the transition from inflammation to regeneration. Moreover, lesioned animals exhibited enhanced cell proliferation during the early inflammatory phase (2D).
Our results suggest that the acute inflammation may promote cell proliferation, while the later stages of inflammation contribute to the regeneration of the lesioned striatal region in songbirds.
This study is supported by VEGA 2/0150/24.