Trigeminal ganglion

Acute infection is typically initiated in the mucosal epithelium, and then HSV-1 establishes latency in sensory neurons located in trigeminal ganglia (TG) or sacral dorsal root ganglia. Despite a vigorous immune response during acute infection, latency is established. As many as 20-30% of sensory neurons are latently infected (reviewed in Tones, 1998, 2003). As a consequence of primary infection, HSV-1 genomic DNA is also present in the central nervous system (CNS) of a significant proportion of the adult human population (Fraser et al., 1981). 

Davies, A. and Lumsden, A. (1983) Influence of NGF on developing dorso-medial and ventro-lateral neurons of chick and mouse trigeminal ganglia. Int. J. Dev. Neurosci. 1 171-177. 

Thut, P. D., Wrlgley, D., Gold, M. S. 2003. Cold transduction in rat trigeminal ganglia neurons in vitro. 

Rebeck, G.W., Maynard, K.I., Hyman, B.T. and Moskowitz, M.A. (1994) Selective 5-HTiDa serotonin receptor gene expression in trigeminal ganglia implications for antimigraine drug development. Proc. Natl. Acad. Set. USA, 91, 3666-3669. 

Matsuka Y, Neubert JK, Maidment NT, Spigelman I. Concurrent release of ATP and substance P within Guinea pig trigeminal ganglia in vivo. Brain Res 2001 915 248-255. Alcayaga J, Varas R, Arroyo J, Iturriaga R, Zapata P. Dopamine modulates carotid nerve responses induced by acetylcholine on the cat petrosal ganglion in vitro. Brain Res 1999 831 97-103. 

---