Brain stem mechanisms and the inhibition of angiotensin-induced drinking

Abstract

The present studies examine the effect of lesions of the ventrolateral region of the lateral parabrachial nucleus (VLLPBN) and of the area postrema and medial region of the nucleus of the solitary tract (AP/mNTS) on water intake induced by intracerebroventricular administration of angiotensin II (ANG II) and of the cholinergic receptor agonist, carbachol. Water intake was measured in rats with bilateral electrolytic lesions of the VLLPBN or thermocautery ablation of the AP/mNTS after intracerebroventricular delivery of ANG II (50 and 100 ng/2 microliter), carbachol (100 and 250 ng/2 microliter), and isotonic saline (2 microliter). Rats with lesions of the VLLPBN drank significantly more water during a 30-min test period to both doses of ANG II, but not to carbachol, than did sham lesion rats. Similarly, AP/mNTS lesion rats drank significantly more than sham lesion animals in response to the high dose of ANG II but not to carbachol. These results suggest that the previously reported exaggerated drinking responses to systemically administered ANG II demonstrated by rats with either VLLPBN or AP/mNTS lesions is not the result of a direct peripheral action of the octapeptide. Furthermore, the similarity of the induced drinking responses produced by these two lesions suggests that the AP/mNTS and the VLLPBN may be linked in a common thirst-mediating pathway.

Role of the lateral parabrachial nucleus in the control of sodium appetite

“…Initial studies on the role of the LPBN in the control of fluid and electrolyte balance were directed at investigating hindbrain control of water intake. Results from these experiments showed that electrolytic or neurotoxic lesions of the LPBN increased thirst induced by manipulations that are related to the depletion of extracellular fluid but not to the reduction of intracellular volume (44,105,106). Also the inactivation of LPBN neurons with bilateral injections of lidocaine or by nonselective antagonism of serotonin receptors by injecting methysergide into the LPBN increased ANG II-induced water intake (94).…”

Differential projections to the intralaminar and gustatory thalamus from the parabrachial area: A PHA-L study in the rat

“…Dorsal to the bc, the pPB area centered in the central lateral (pPBcl) and the external lateral (pPBel) subnuclei are involved in numerous autonomic processes (Mraovitch et al, 1982;Cechetto and Calaresu, 1983;Darlington and Ward, 1985a,b;Lumb and Morrison, 1987;Ward, 1988Ward, , 1989Ohman and Johnson, 1989;Herbert et al, 1990;Chamberlin and Saper, 1992).…”

Further evidence for the involvement of the spinoparabrachial pathway in nociceptive processes: A c-Fos study in the rat

“…The lateral and external parts of this area respond to noxious stimuli (Bernard and Besson, 1990;Bernard et al, 1994;Bester et al, 1995c). This region is also involved in different autonomic regulatory processes (Bertrand and Hugelin, 1971;Mraovitch et al, 1982;Cechetto and Calaresu, 1983;Darlington and Ward, 1985a,b;Lumb and Morrison, 1987;Ward, 1988Ward, , 1989Ohman and Johnson, 1989;Herbert et al, 1990;Jhamandas et al, 1991;Chamberlin and Saper, 1992) and aversive behaviour (Berntson, 1973;Berntson et al, 1988;Depoortere et al, 1990a,b;Bucherelli and Tassoni, 1992;Agü ero et al, 1993;Bechara et al, 1993). The lateral and external parts of the PB area are also a major relay, transmitting nociceptive information from the lamina I neurones to either the centralis nucleus (Ce) of the amygdala or the ventromedial (VMH) nucleus of the hypothalamus (Wiberg and Blomqvist, 1984;Cechetto et al, 1985;Hylden et al, 1985Hylden et al, , 1986McMahon and Wall, 1985;Swett et al, 1985;Light et al, 1987Light et al, , 1993Tabata, 1989, 1990;Lima and Coimbra, 1989a,b;Bernard and Besson, 1990;Yamada and Kitamura, 1992;Kitamura et al, 1993;Bernard et al, 1994Bernard et al, , 1995Slugg and Light, 1994;Bester et a...…”