Effects of lesions of the ventral ventral median preoptic nucleus or subfornical organ on drinking and salt appetite after deoxycorticosterone acetate or yohimbine.

Abstract

Lesions of the ventral ventral median preoptic nucleus (VVMnPO) enhanced daily salt appetite induced by subcutaneous (sc) injections of deoxycorticosterone acetate (DOCA) but did not affect acute salt appetite or water intake after sc injections of 5 mg/kg of the alpha-2-adrenoreceptor blocker yohimbine. Lesions of the subfornical organ (SFO) or its rostral fiber pathways had no effect on fluid intakes during DOCA treatments but significantly reduced water intake after yohimbine. These findings extend those of a previous report (Fitts, Tjepkes, & Bright, 1990) of enhanced DOCA-induced saline intake in VVMnPO-lesioned rats and demonstrate that the effect is specific to lesions of the VVMnPO. The mechanism of the thirst and salt intake elicited by yohimbine is still unclear, but the SFO and its fiber pathways appear to be important for the expression of the water drinking component. Neither lesion reliably affected yohimbine-induced salt appetite.

Inhibition of sodium appetite by lipopolysaccharide: involvement of α2-adrenoceptors

“…The exact mechanism activated by YOH injected systemically to induce fluid intake is not known, although it depends at least on the integrity of the amygdala and subfornical organ (18,45). The present results suggest that the dipsogenic effect of YOH is independent from hypotension.…”

“…The unloading of cardiopulmonary receptors by hypotension may facilitate water and sodium intake (24); therefore, it is not possible to exclude some influence of the hypotension facilitating 0.3 M NaCl intake after the combination of YOH and LPS. Moreover, YOH injected systemically may induce water and sodium intake in satiated rats (18). However, we tested sodium appetite when arterial pressure had returned to preinjection baseline levels and the behavioral responses were, presumably, no longer directly influenced by hypotension.…”

The entorhinal cortex, but not the dorsal hippocampus, is necessary for single‐cue latent learning

“…The brain structures necessary for processing information about the taste of salt include the gustatory thalamus (Reilly, 1998), parabrachial nuclei (Spector, 1995), and the bed nucleus of the stria terminalis (Reilly et al, 1994). The brain structures necessary for processing information about salt appetite include the subfornical organ (Thunhorst et al, 1990(Thunhorst et al, , 1999Ruhf et al, 2001), the ventral ventral median preoptic nucleus (Fitts et al, 1990;Fitts, 1991), and the central nucleus of the amygdala (Seeley et al, 1993;Zardetto-Smith et al, 1994). Therefore, it does not appear that the requirement of the DH in the previous version of the LCP task was due to the use of salt as the irrelevant-incentive stimulus, but rather because of the use of contextual compartmental cues rather than a single compartmental cue in the latent learning task.…”

Effects of forebrain circumventricular organ ablation on drinking or salt appetite after sodium depletion or hypernatremia

“…Single lesions of either the SFO or OVLT have indeed been reported to reduce or abolish thirst or salt appetite in response to a variety of stimuli related to sodium depletion or cell dehydration (1, 8, 18, 20 -23, 27, 29 -36, 39, 40, 42, 45, 47). In some cases, one lesion has proved more effective than the other (4,5), and in other cases the same lesion has produced different results in different laboratories or different species (8,29,39,40,45).…”

“…By comparison, a lesion of the SFO produces only brief postsurgical adipsia, no chronic hypernatremia, and specific rather than general deficits in drinking behaviors (31,32,40,42,45,47). A lesion confined to the OVLT and only a small piece of the ventral MnPO produces variable adipsia but no hypernatremia and specific rather than general deficits in drinking behaviors (1,4,8,27). Thus we attempted to produce lesions that were confined as much as possible to these CVOs rather than lesions that damaged much of the surrounding tissue of the lamina terminalis and preoptic area.…”