We report here the
protein expression of
TRPV1 receptor in axotomized rat retinas and its possible participation in mechanisms involved in retinal ganglion cell (RGC) death. Adult rats were subjected to unilateral, intraorbital
axotomy of the optic nerve, and the
retinal tissue was removed for further processing. TRPV1 total
protein expression decreased progressively after
optic nerve transection, reaching 66.2% of control values 21 days after
axotomy. The number of cells labeled for TRPV1 in the remnant GCL decreased after 21 days post-lesion (to 63%).
Fluoro-Jade B staining demonstrated that the activation of TRPV1 in acutely-lesioned eyes elicited more intense neuronal degeneration in the GCL and in the inner nuclear layer than in
sham-operated retinas. A single
intraocular injection of
capsazepine (100 μM), a TRPV1 antagonist, 5 days after optic nerve lesion, decreased the number of GFAP-expressing Müller cells (72.5% of control values) and also decreased
protein nitration in the
retinal vitreal margin (75.7% of control values), but did not affect lipid peroxidation. Furthermore,
retinal explants were treated with
capsaicin (100 μM), and remarkable
protein nitration was then present, which was reduced by blockers of the constitutive and inducible
nitric oxide synthases (7-NI and
aminoguanidine, respectively). TRPV1 activation also increased GFAP expression, which was reverted by both TRPV1 antagonism with
capsazepine and by 7-NI and
aminoguanidine. Given that Müller cells do not express TRPV1, we suppose that the increased GFAP expression in these cells might be elicited by TRPV1 activation and by its indirect effect upon
nitric oxide overproduction and
peroxynitrite formation. We incubated
Fluorogold pre-labeled
retinal explants in the presence of
capsazepine (1 μM) during 48 h. The numbers of surviving RGCs stained with
fluorogold and the numbers of apoptotic cells in the GCL detected with TUNEL were similar in lesioned and control retinas. We conclude that
TRPV1 receptor expression decreased after
optic nerve injury due to death of TRPV1-containing cells. Furthermore, these data indicate that TRPV1 might be involved in intrinsic
protein nitration and Müller cell reaction observed after
optic nerve injury.