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Neurones from the dorsal root ganglia of neonatal rat pups were grown in tissue culture and voltage clamped using patch electrodes for whole cell recording. The electrodes were filled with a KMeSO4 solution containing 1.1 mM-EGTA. 15-24 h prior to recording cultures were infected with one of three strains of herpes simplex virus type 1 previously characterized on the basis of a cell fusion assay in cultures of the MRC-5 and BHK-21 cell lines. Infection of sensory neurones with either of the two non-syncitial strains of virus caused a nearly complete loss of the hyperpolarization-activated inward rectifying conductance normally present in these neurones, but did not appear to affect depolarization-activated, calcium-dependent outward currents or voltage-dependent delayed outward rectification. The loss of inward rectification appeared to result from inactivation of the underlying conductance mechanism, rather than from a shift in the gating properties of the conductance mechanism to unphysiological values. In contrast to these results inward rectification was present in sensory neurones infected with another, syncitial, strain of herpes simplex virus. However, quantitative analysis suggested a reduced availability compared to that recorded in uninfected neurones.

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