Lesions of the locus coeruleus abolish baroreceptor‐induced depression of supraoptic neurones in the rat.

Urethane‐anaesthetized rats were used to investigate the influence of lesions within the locus coeruleus on the inhibition of phasically discharging supraoptic neurones that normally follows the activation of arterial baroreceptors. Carotid sinus baroreceptors were stimulated by the inflation of a blind sac of the carotid bifurcation. A general activation of arterial baroreceptors was evoked by increasing arterial blood pressure following the intravenous injection of the pure alpha‐adrenoreceptor agonist phenylephrine. The locus coeruleus of one side only was destroyed either by thermal (radio‐frequency) lesions, or by the injection of 6‐hydroxydopamine (1 microliter, 0.5 mg/ml). The extent of each lesion was assessed histologically in stained tissue and with fluorescence histochemistry. Lesions in locus coeruleus abolished all baroreceptor input to supraoptic neurones on the side ipsilateral to the lesion. The lesions had no effect on the cardiovascular responses to the stimulus, and did not abolish the excitation of supraoptic neurones after ipsilateral carotid body chemoreceptor activation. 6‐Hydroxydopamine lesions (1 microliter, mg/ml) in the rostral part of the ventrolateral A1 catecholamine neurones were less consistent in their abolition of baroreceptor input to the supraoptic nucleus. When the input from ipsilateral carotid sinus baroreceptors was abolished, there was an equivalent effect on the influence of the carotid body chemoreceptors. Input from other arterial baroreceptors, activated by phenylephrine injection, was not affected. From these results, it is proposed that the baroreceptor‐induced depression of‐phasically discharging supraoptic neurones is mediated via a direct noradrenergic input from the locus coeruleus.