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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #129423
Title: ELECTROPHYSIOLOGICAL PROPERTIES OF RAT RETINAL MULLER (GLIAL) CELLS IN POSTNATALLY DEVELOPING AND IN PATHOLOGICALLY ALTERED RETINAE

Author
item FELMY, F - TUBINGEN, GERMANY
item PANNICKE, T - TUBINGEN, GERMANY
item Richt, Juergen
item REICHENBACH, A - TUBINGEN, GERMANY
item GUENTHER, E - TUBINGEN, GERMANY

Submitted to: Glia
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/1/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary: Borna disease (BD) is a sporadically occurring, usually fatal polioencephalomyelitis that primarily affects horses and sheep. More rarely, a range of other domestic and zoo species and possibly humans are affected. The etiological agent of BD, the Borna Disease Virus (BDV), is an enveloped virus characterized by a non-segmented negative strand RNA genome ethat belongs to the new family Bornaviridae within the order Mononegavirales. As part of our ongoing electrophysiological studies on the retinal changes observed regularly after BDV-infection we found that the substantial neuroretinal degeneration did not result in a strong reduction of inward currents and of the zero current potential of the Muller cells. This work on the electrophysiological properties of retinal cells after BDV-infection will lead to a better understanding how neurotropic viruses interact with host cells and will therefore help us to define areas for prophylactic intervention and treatment.

Technical Abstract: Retinal glial Muller cells are characterized by dominant K(+) conductances. The cells may undergo changes of their membrane currents during ontogeny and gliosis as described in rabbit and man. Although the rat retina is often used in physiological experiments, the electrophysiology of rat Muller cells is less well studied. The aim of the present study was to characterize their membrane currents in postnatal development and in two models of retinal degeneration. Freshly isolated cells were subjected to whole-cell patch clamp recordings. During the first 4 weeks after birth of rats, their Muller cells displayed an increase in all membrane currents, particularly in the inward currents elicited at hyperpolarizing potentials. The decrease of the membrane resistance from more than 760 MOmega to less than 50 MOmega was accompanied by a shift of the zero current potential from about -20 mV to -80 mV, similar as earlier observed in developing rabbit Muller cells. These developmental changes were found in pigmented Brown Norway rats as well as in rats with inherited retinal dystrophy (RCS rats). Moreover, an infection of Lewis rats with the Borna disease virus caused substantial neuroretinal degeneration but did not result in a strong reduction of inward currents and of the zero current potential of the Muller cells. Thus, rat Muller cells fail to change their basic membrane properties in two different models of retinal pathology. This is in contrast to human and rabbit Muller cells, which have been shown to undergo dramatic changes of their membrane physiology in response to retinal diseases and injuries.