Abstract

The intraventricular administration of 6-hydroxydopamine was used to destroy 80–90% of the noradrenergic terminals in the forebrain of male rats with little apparent damage to the cells of origin in locus coeruleus. Both 36 h and 21 days later the basal firing rate of these cells was elevated 4-fold above control levels. Moreover, microiotophoretic application of norepinephrine was significantly less effective in inhibiting the spontaneous activity of locus coeruleus cells in these rats relative to control animals. The increased firing may represent a compensatory response to the injury, leading to increased transmitter release from terminals spared by the lesion.

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