Attenuated Astrogliosis In The Olfactory Bulb Of Adult Zebrafish After Repeated Peripheral Damage
Traumatic brain injuries (TBIs), particularly if repetitive, causes massive disruptions in brain structure and function. The brain requires a degree of neuroplasticity to rewire and repair damaged neurons, and glia are crucial mediators of this process. When the brain is damaged, astrocytes, a type of glia, undergo astrogliosis characterized by hypertrophy and proliferation. Humans have evolved to have a limited degree of neuroplasticity, which inhibits the ability to recover from TBIs. Zebrafish, however, are renowned for their neuroplasticity, and their olfactory system is an excellent model for this. Therefore, we use the adult zebrafish olfactory system to explore neuroplasticity in response to repeated mechanical damage.
In our study we inserted a wax plug into the nasal cavity to damage the olfactory organ repeatedly over one week. This resulted in a decrease in sensory neurons projecting into the olfactory bulb. Our hypothesis was that mechanical damage to the olfactory organ will cause astrogliosis in the olfactory bulb. We found that in the olfactory bulb astrocyte processes that were associated with glomeruli hypertrophy after one day. However, astrocyte processes appeared to return to typical morphology at later time points. Since zebrafish astrocytes did not remain hypertrophied they likely returned to their typical function. This is in contrast to what would be expected of mammalian astrocytes, which would remain hypertrophied in the presence of persisting damaging stimuli. Exploring these glial cells in non-mammalian systems like the zebrafish may lead to novel medical treatments.