Entry of Rabies Virus in the Olfactory Bulb of Mice and Effect of Infection on Cell Markers of Neurons and Astrocytes

• Published in: International journal of morphology Vol. 36; no. 2; pp. 670 - 676
• Main Authors: Torres-Fernández, Orlando, Daza, Natalia Andrea, Santamaría-Romero, Gerardo, Hurtado, Andrea P., Monroy-Gómez, Jeison
• Format: Journal Article
• Language: English
• Published: Sociedad Chilena de Anatomía 01.06.2018
• Subjects: ANATOMY & MORPHOLOGY; calbindina; Calbindin; Rabies; inmunohistoquímica; Olfactory bulb; GFAP, Immunohistochemistry; Rabia; Bulbo olfatorio; Parvalbumin; Parvoalbúmina; GFAP
• DOI: 10.4067/S0717-95022018000200670
• ISSN: 0717-9502

There are few studies of infection by rabies virus in the olfactory bulb (OB). This work was carried out with the purpose of establishing the time required to detect rabies antigens in the OB of mouse, after the intramuscular inoculation of the virus and to evaluate the effect of the infection on the expression of three proteins: calbindin (CB), parvalbumin (PV) and the glial fibrillary acidic protein (GFAP). Mice were inoculated with rabies virus intramuscularly in the hind limbs. Every 8 hours, after 72 hours postinoculation (p.i.), animals were sacrificed by perfusion with paraformaldehyde and coronal sections of OB were obtained for immunohistochemical study. These cuts were used to reveal the entry and spread of viral antigens. Tissue sections obtained in the terminal phase of the disease (144 hours p.i.), and controls of the same age were also processed for immunohistochemistry of CB, PV and GFAP. Rabies virus antigens were initially detected at 80 hours p.i. in a few mitral cells. At 88 hours p.i. the antigens had spread through most of these neurons but until the terminal phase of the disease there was little dispersion of the virus towards other cellular layers of the OB. The CB protein was expressed in cells of the glomerular stratum, the PV in cells of the outer plexiform layer and the GFAP was expressed in all the layers of the OB. Viral infection generated loss of CB expression and increase of PV expression. Immunoreactivity to GFAP was increased in the outer plexiform layer of the OB as a response to infection.