Expression of trkA, trkB, and trkC in injured and regenerating retinal ganglion cells of adult rats.
OBJECTIVE
To investigate changes in percentage of tyrosine kinase (trk)A-, trkB-, and trkC-immunopositive ((+)) retinal ganglion cells (RGCs) at various times after optic nerve (ON) axotomy; the proportion of RGCs regenerating axons into peripheral nerve (PN) grafts that are trkA(+), trkB(+), and trkC(+); whether intravitreal PN-ON implants affect trk immunoreactivity; and the levels of trk mRNAs in ON-injured retinas.


METHODS
The ON was transected intraorbitally. Proportions of trkA(+), trkB(+), and trkC(+) RGCs and levels of trk mRNAs were studied by using immunocytochemistry and Northern blot methods, respectively, in injured and RGC-regenerating retinas.


RESULTS
In normal retinas, only small numbers of trkB(+) and trkC(+), but not trkA(+), RGCs were seen. The optic fiber layer was intensively immunolabeled with trkB. After ON injury, the proportions of trkA(+), trkB(+), and trkC(+) RGCs rapidly increased and reached their peaks by 3 to 5 days. During the next 3 weeks, the proportion of trkA(+) or trkB(+) RGCs gradually decreased, but the proportion of trkC(+) RGCs remained high. Intravitreal implants of PN+ON segments transiently but significantly suppressed injury-induced increases in all these trk(+) RGC proportions for approximately 5 days. In contrast, 3 days after ON injury, quantitative retinal expression of trkA mRNA, and to a lesser extent trkC mRNA, was downregulated, whereas trkB mRNA expression remained unaffected. Higher proportions of trkA(+) and trkB(+) RGCs and higher levels of all trk mRNAs were seen in regenerating RGCs and retinas, respectively.


CONCLUSIONS
This study provides a kinetic analysis of expression of trk in RGCs and retinas after ON injury and during regeneration.
Cui
Qi
Q
Department of Anatomy, Faculty of Medicine, The University of Hong Kong, China.
Tang
Louisa S
LS
Hu
Bing
B
So
Kwok-Fai
KF
Yip
Henry K
HK
D000818:Animals; D019771:Axotomy; D015152:Blotting, Northern; D002470:Cell Survival; D015342:DNA Probes; D015536:Down-Regulation; D019084:Fluorescent Antibody Technique, Indirect; D009416:Nerve Regeneration / Q000502:physiology*; D009900:Optic Nerve / Q000502:physiology*; D020221:Optic Nerve Injuries / Q000201:enzymology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000235:genetics* / Q000378:metabolism; D020813:Receptor, trkB / Q000235:genetics* / Q000378:metabolism; D020812:Receptor, trkC / Q000235:genetics* / Q000378:metabolism; D012160:Retina / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000201:enzymology*; D013997:Time Factors
D015342:DNA Probes; D012333:RNA, Messenger; D020917:Receptor, trkA; D020813:Receptor, trkB; D020812:Receptor, trkC