Purpose: to investigate the distribution of p55 and p75 tumor necrosis factor (TNF) receptor mRNA in normal murine trigeminal ganglia, and in murine trigeminal ganglia acutely infected with McKrae strain herpes simplex virus (HSV). Methods: in situ hybridization with antisense 35S-labeled riboprobes for mRNA encoding both the p55 and p75 TNF receptor (TNFR) subtypes was used in normal and HSV-infected murine trigeminal ganglia. Sense riboprobes were used as controls. Results: in situ hybridization with both p55 and p75 riboprobes produced a strong autoradiographic signal over many, but not all, trigeminal sensory neurons. Signal for mRNA encoding both TNFR subtypes was also present over the arachnoid layers surrounding trigeminal ganglia. Acute ocular HSV infection was accompanied by an intense leukocytic infiltrate into the ophthalmic portion of the trigeminal ganglia, and, in this setting, increased p55 and p75 mRNA signal was closely related to the location and number of infiltrating white blood cells. The distribution and number of trigeminal sensory neurons expressing mRNA for the two TNFR subtypes did not appear to change following infection. Signal over control sections hybridized with sense p55 and p75 TNFR cRNA probes was comparable to background. Conclusions: the observed distribution of p55 and p75 TNFR mRNA over trigeminal sensory neurons and over the arachnoid layers surrounding trigeminal ganglia supports suggestions that TNF has a direct effect on neurons, either as a neuromodulator or neurotrophic factor, and that TNF may play a central role in blood-brain barrier regulation. Increased signal for TNFR mRNA in acutely infected trigeminal ganglia appears to reflect infiltration by receptor-bearing white blood cells.
- Trigeminal ganglion
- Tumor necrosis factor (TNF)