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

Abstract

SUMMARY1. 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.2. 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 oc-adrenoreceptor agonist phenylephrine.3. The locus coeruleus of one side only was destroyed either by thermal (radiofrequency) lesions, or by the injection of 6-hydroxydopamine (1 PI, 05 mg/ml). The extent ofeach lesion was assessed histologically in stained tissue and with fluorescence histochemistry. 4. 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.5. 6-Hydroxydopamine lesions (1 ,u, 2 mg/ml) in the rostral part of the ventrolateral Al 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.6. 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.

Spatially and temporally differentiated patterns ofc‐fosexpression in brainstem catecholamilriergic cell groups induced by cardiovascular challenges in the rat

“…This may be construed as being consistent with data from lesion studies implicating the locus coeruleus as a major relay through which the baroreceptor-mediated inhibition of AVP secretion is effected (Banks and Harris, 1984). In view of its limited afferent supply, phenylephrine-induced activation of the locus coeruleus is presumably mediated via the C1 region (Kachidian et al, 1990;Pieribone and AstonJones, 1991).…”

Lateral hypothalamic lesions alter baroreceptor‐evoked inhibition of rat supraoptic vasopressin neurones.

“…Brainstem pathways conveying baroreceptor information to the hypothalamus have been a focus of recent investigation. Within the lower brainstem, electrophysiological data obtained after chemical or electrolytic lesions support involvement of the locus coeruleus (Banks & Harris, 1984) but not the caudal ventrolateral medulla , although the latter may contribute to the sensitivity of the reflex (Day & Sibbald, 1990).…”

A gamma‐aminobutyric‐acid‐mediated baroreceptor input to supraoptic vasopressin neurones in the rat.

“…Although lesions of the locus coeruleus interfere with baroreflex-induced depressions of s.o.n. neurones (Banks & Harris, 1984), it would appear that this noradrenergic cell group does not constitute the final pathway whereby peripheral baroreceptor information reaches VP neurones. Depletion of the terminal catecholamine plexus in s.o.n.…”