NR AXPW
AU Kincaid,A.E.; Bartz,J.C.
TI Neuroinvasion following Nasal Cavity Infection in Hamsters
QU International Conference - Prion 2007 (26.-28.9.2007) Edinburgh International Conference Centre, Edinburgh, Scotland, UK - Book of Abstracts: Pathology and Pathogenesis P03.136
IA http://www.prion2007.com/pdf/Prion Book of Abstracts.pdf
PT Konferenz-Poster
AB
Background: Some animal species that acquire prion diseases are olfactory-driven and use their sense of smell for a variety of basic behaviors. Therefore their nasal cavity could be an initial site of contact for any material in the environment that harbors the infectious agent. Recently it has been demonstrated that the nasal cavity is a more efficient route of infection than per os inoculation in hamsters. The disease-associated form of the prion protein (PrPd) was detected in nasal associated lymphoid tissue and submandibular lymph nodes as early as 4 weeks after placement of infected brain homogenate inferior to the nostrils. Surprisingly, there was no evidence of PrPd in the olfactory epithelium or olfactory nerve fibers at any time after inoculation.
Objectives: The aim of this study was to determine the route by which PrPd was transported into the central nervous system (CNS) following extranasal prion infection in hamsters.
Methods: The brain, spinal cord, trigeminal ganglia and superior cervical ganglia were collected at 2 week intervals following extranasal inoculation of infected brain homogenate and processed for immunohistochemical (IHC) detection of PrPd.
Results: PrPd was initially identified in the brainstem and the intermediolateral cell column of the spinal cord at 12 and 14 weeks post inoculation, respectively. In the brainstem PrPd was restricted to the sensory root of the trigeminal nerve (V), the spinal tract of V, the principal nucleus of V and the spinal nucleus of V at the earliest time points after inoculation. However, PrPd was not identified in the Vth ganglia or the superior cervical ganglia until 22 weeks post inoculation.
Conclusions: The results of this study suggest that neuroinvasion following prion exposure to the nasal cavity occurs via the Vth and sympathetic nerves. The lack of PrPd in the Vth and superior cervical ganglia prior to spread into the CNS suggests that the agent does not accumulate to any degree within these structures prior to neuroinvasion, remaining undetectabld with IHC until just prior to the onset of clinical symptoms.
AD A.E. Kincaid, J.C. Bartz, Creighton University, USA
SP englisch
PO Schottland