DISTRIBUTION OF TUMOR-NECROSIS-FACTOR RECEPTOR MESSENGER-RNA IN NORMAL AND HERPES-SIMPLEX VIRUS-INFECTED TRIGEMINAL GANGLIA IN THE MOUSE

Purpose: to investigate the distribution of p55 and p75 tumor necrosis factor (TNF) receptor mRNA in normal murine trigeminal ganglia, and i n murine trigeminal ganglia acutely infected with McKrae strain herpes simplex virus (HSV). Methods: in situ hybridization with antisense S- 35-labeled riboprobes for mRNA encoding both the p55 and p75 TNF recep tor (TNFR) subtypes was used in normal and HSV-infected murine trigemi nal ganglia. Sense riboprobes were used as controls. Results: in situ hybridization with both p55 and p75 riboprobes produced a strong autor adiographic 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 inf ection was accompanied by an intense leukocytic infiltrate into the op hthalmic portion of the trigeminal ganglia, and, in this setting, incr eased 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 subtype s did not appear to change following infection. Signal over control se ctions hybridized with sense p55 and p75 TNFR cRNA probes was comparab le to background. Conclusions: the observed distribution of p55 and p7 5 TNFR mRNA over trigeminal sensory neurons and over the arachnoid lay ers 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 re gulation. Increased signal for TNFR mRNA in acutely infected trigemina l ganglia appears to reflect infiltration by receptor-bearing white bl ood cells.