controversial'.There is a bit of controversy brewing here and there in this issue, with several pieces containing strong personal opinions.Our hope, as ever, is that these
Early and chronic loss of taste input from the chorda tympani is associated with abnormal taste behaviors. We found that compared to when the chorda tympani is sectioned acutely, chronic nerve loss leads to amplification of spared inputs in the gustatory pons, with higher response to salty and sour stimuli. Findings point to plasticity that may compensate for sensory loss, but permanent deficits in taste signaling also occur following early denervation.
While contributions of microglia and astrocytes are regularly studied in various injury models, how these contributions differ across development remains less clear. We previously demonstrated developmental differences in microglial profiles across development in an injury model of the gustatory system. Nerves of the rat gustatory system have limited capacity to regenerate if injured during neonatal ages but show robust recovery if the injury occurs in adulthood. Using this developmentally disparate model of regenerative capacity, we quantified microglia and astrocytes in the rostral nucleus of the solitary tract (rNTS) following transection of the gustatory chorda tympani nerve (CTX) of neonatal and adult rats. We found that neonatal CTX induced an attenuated microglia response but a larger astrocyte response compared to adult CTX. To elucidate the interplay between the microglia and astrocyte responses in the CTX model, we used our novel intraperitoneal injection protocol for the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia in the neonatal and adult rat brain prior to and after CTX. PLX5622 depleted microglia by 80–90% within 3 days of treatment, which increased to > 90% by 7 days. After 14 days of PLX5622 treatment, microglia were depleted by > 96% in both neonates and adults while preserving baseline astrocyte quantity. Microglia depletion eliminated the adult astrocyte response to CTX, while the neonatal astrocyte response after injury remained robust. Our results show injecting PLX5622 is a viable means to deplete microglia in neonatal and adult rats and suggest developmentally distinct mechanisms for astrogliosis following neural injury.
The peripheral taste system of the adult rodent is highly resilient against damage, with morphological, behavioral, and functional recovery evident after regeneration of a transected nerve. If chorda tympani transection (CTX) occurs at early postnatal ages however, the nerve fails to regenerate and effects on tongue morphology and behavior are more severe and longer-lasting compared to adult denervation. To examine whether neonatal CTX induces functional changes in intact nerves, whole-nerve electrophysiology was performed on the glossopharyngeal (GL) and chorda tympani (CT) nerves of adult rats that received CTX at P10. Attenuation of NaCl-elicited GL responses were observed in CTX rats 2 months after surgery, with bilateral denervation causing the largest decreases in responses. When assessed 1 year after neonatal CTX, amiloride-sensitive responses to NaCl in the contralateral CT increased while amiloride-insensitive responses decreased. Responses to other tastants were consistent with control animals. This is the first evidence of long-term functional changes to the peripheral taste system after injury in rats fed a normal diet. This study further characterizes the developing peripheral taste system as highly susceptible to change following neural injury.
