Lesions were placed in the paramedian pontine reticular formation ( PPRF ) of monkeys and the resulting gaze palsies studied. Brainstem regions were identified by single cell recordings before kainic acid was injected to selectively destroy neuronal cell bodies in the vicinity. Unilateral PPRF lesions led to a loss of all rapid eye movements towards the ipsilateral side. Deficits were identical to those after experimental electrolytic lesions in monkeys, or structural lesions in humans. Bilateral PPRF lesions produced two different syndromes. Rostral PPRF lesions led to a selective loss of horizontal rapid eye movements leaving vertical movements intact. Caudal PPRF lesions led in addition to a severe disruption of vertical rapid eye movements.

The dopamine (DA) content of the canine renal cortex is greater than can be attributed to its presence in noradrenergic axons only. Most of the excess DA is in the outer part of the cortex. By fluorescence histochemistry numerous catecholamine-containing axons are seen to be associated with renal cortical arteries and arterioles. The fluorescence is abolished following treatment of animals with 6hydroxydopamine or with reserpine, but is restored to some axons if reserpine is followed by systemic administration of I-DOPA. This procedure does not restore fluorescence to atrial noradrenergic axons after reserpine-induced depletion. Pre-treatment of animals with guanethidine abolishes axonal fluorescence and depletes tissue NA and DA from atrium, but in renal cortex the tissue DA level is little affected and some fluorescent axons remain. These results are discussed in the light of previous functional evidence for dopaminergic autonomic axons in the canine kidney.

No abstract

No abstract

No abstract