No abstract

No 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.

The influence of the hypothalamic paraventricular nucleus (PVN) on neurones in the dorsal medulla has been examined in 71 urethane/sagatal-anaesthetised rats. Of 536 neurones localised and tested for responses to electrical stimulation of both the vagus and/or the PVN, 378 were synaptically or antidromically activated following vagal stimulation 72 of which were synaptically activated by stimulation within PVN. The majority of those were located at the border between NTS and dorsal motor nucleus of the vagus in caudal NTS. None showed cardiac or ventilatory rhythm. Neurones showing such rhythms were not affected from PVN. Of 89 neurones in dorsal motor nucleus of the vagus, ten were synaptically activated and two synaptically depressed from PVN. PVN activated neurones in NTS tested for responses to stimulation of arterial baroreceptors and carotid body chemoreceptors were either unaffected or inhibited, but gastric inflation excited them. The results suggest a powerful PVN influence on the dorsal medulla, which is largely confined to the ventral and caudal NTS. There is little evidence for an effect on neurones with a cardiovascular function, but the abdominal vagal influence suggests a link with feeding.

The pathway for chemoreceptor input to hypothalamic supraoptic nuclei has been examined in anaesthetised lactating and non-lactating rats. In lactating rats, the increase in intramammary pressure following bilateral carotid occlusion, which is probably mainly due to vasopressin, was abolished by lesions in the septum, but not by lesions in more caudal regions of the hypothalamus. In non-lactating rats, electrophysiological experiments demonstrated that the input from carotid body chemoreceptors to phasically-discharging supraoptic neurones is ipsilateral only. The effects of chemoreceptor stimulation on the neurones can be mimicked by electrical stimulation within the medial preoptic area and anterior hypothalamus in a region medial and rostral to the supraoptic nuclei. Lesions within this region abolish the chemoreceptor input to the supraoptic nuclei, but leave the baroreceptor input intact. It is proposed that chemoreceptor afferents to the supraoptic nuclei pass in the lateral hypothalamus to the region of the septum where they turn medially and descent through the medial part of the rostral hypothalamus. The results are discussed in terms of the general role of the chemoreceptor reflex and, more specifically, with respect to the possible significance of vasopressin in the control of arterial blood pressure.