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Glial responses after chorda tympani nerve injury.

The Journal of comparative neurology | 2012

The chorda tympani (CT) nerve innervates lingual taste buds and is susceptible to damage during dental and inner ear procedures. Interruption of the CT results in a disappearance of taste buds, which can be accompanied by taste disturbances. Because the CT usually regenerates to reinnervate taste buds successfully within a few weeks, a persistence of taste disturbances may indicate alterations in central nervous function. Peripheral injury to other sensory nerves leads to glial responses at central terminals, which actively contribute to abnormal sensations arising from nerve damage. Therefore, the current study examined microglial and astrocytic responses in the first central gustatory relay, the nucleus of the solitary tract (nTS), after transection of the CT. Damage to the CT resulted in significant microglial responses in terms of morphological reactivity and an increased density of microglial cells from 2 to 20 days after injury. This increased microglial population resulted primarily from microglial proliferation from 1.5 to 3 days, which was supplemented by microglial migration within subdivisions of the nTS between days 2 and 3. Unlike other nerve injuries, CT injury did not result in recruitment of bone marrow-derived precursors. Astrocytes also reacted in the nTS with increased levels of glial fibrillary acidic protein (GFAP) by 3 days, although none showed evidence of cell division. GFAP levels remained increased at 30 days, by which time microglial responses had resolved. These results show that nerve damage to the CT results in central glial responses, which may participate in long-lasting taste alterations following CT lesion.

Pubmed ID: 22315167 RIS Download

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Associated grants

  • Agency: NIDCD NIH HHS, United States
    Id: P30 DC004657
  • Agency: NHLBI NIH HHS, United States
    Id: HL68864
  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL081151
  • Agency: NIDCD NIH HHS, United States
    Id: DC009762-01 F31
  • Agency: NIDCD NIH HHS, United States
    Id: R01 DC00147
  • Agency: NIDCD NIH HHS, United States
    Id: P30 DC04657
  • Agency: NIDCD NIH HHS, United States
    Id: R56 DC00147
  • Agency: NHLBI NIH HHS, United States
    Id: HL81151
  • Agency: NIDCD NIH HHS, United States
    Id: F31 DC009762
  • Agency: NIDCD NIH HHS, United States
    Id: R01 DC000147
  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL068864
  • Agency: NIDCD NIH HHS, United States
    Id: R56 DC000147

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