Influence of the subfornical organ on meal-associated drinking in rats

2001 ◽  
Vol 280 (3) ◽  
pp. R669-R677 ◽  
Author(s):  
Elizabeth M. Starbuck ◽  
Douglas A. Fitts

A lesion of the subfornical organ (SFO) may disrupt drinking after a meal of dry chow as it does drinking after intragastric administration of hypertonic saline. Food and water intakes of SFO-lesioned (SFOX) and sham-lesioned rats were measured during 90-min tests following various lengths of food deprivation. During the tests, all rats began eating before they began drinking. After 20–24 h of food deprivation, latency to begin drinking after eating had started was longer for SFOX than for sham-lesioned rats. Plasma osmolality was elevated by 2–3% in both lesion groups at 12 min, the latency for sham-lesioned rats to drink, but SFOX rats nevertheless continued eating and delayed drinking. Eating after shorter 4-h food deprivations and ad libitum feeding produced more variable drinking latencies and less consistent effects of SFO lesion. During 24 h of water deprivation, SFO lesion had no effect on the suppression of food intake and did not affect food or water intakes during the first 2 h of subsequent rehydration. These findings indicate that the SFO is involved in initiating water intake during eating and in determining drinking patterns and the amount of water ingested during a meal.

1972 ◽  
Vol 24 (2) ◽  
pp. 215-224 ◽  
Author(s):  
F. M. Toates ◽  
Keith Oatley

Inhibition of ad libitum feeding in rats was induced by hypertonic NaCl injections. Though osmotic loads of sufficient size were capable of abolishing feeding completely for a time, the effect was not as large as had been predicted from a hypothesis of strictly linear subtractive inhibition. Feeding at a low level of hunger seems to be somewhat less affected by osmotic inhibition than feeding on a deprivation schedule. Inhibition of feeding was also produced by deprivation of water, and both the inhibition of food intake during deprivation, and the disinhibition by subsequent drinking indicated that the amount of inhibition of food intake is a non-linear (accelerating) function of water deficit. A model of the process indicating that the thirst signal undergoes a non-linear transformation before being subtracted from the signal corresponding to food demand is proposed.


1983 ◽  
Vol 245 (3) ◽  
pp. R339-R344 ◽  
Author(s):  
K. I. Honma ◽  
S. Honma ◽  
T. Hiroshige

The effects of food on plasma corticosterone levels were examined in rats under restricted daily feeding or prolonged food deprivation. High hormone levels before feeding were observed when the daily meal was restricted to 2 h at a fixed time of day, but it was not detected when food availability was extended to 6 h. The amount of food intake under the latter condition was comparable to that in 24 h of ad libitum feeding. After the termination of restricted feeding, the prefeeding hormone peak was maintained in rats fasted subsequently but disappeared when rats were returned to ad libitum feeding. Food deprivation for 10 days increased plasma corticosterone levels in the light period, resulting in abolition of the circadian rhythm. A subsequent meal decreased the hormone level such that the 24-h mean hormone level after food ingestion was inversely related to the amount of food intake. When rats were allowed to feed for 6 h after prolonged food deprivation, the prefeeding hormone peak observed at the second meal disappeared at the fourth meal. The amount of food consumption in these rats increased and reached a level comparable to that with ad libitum feeding at the third meal. It is concluded that the amount of food intake is critical for the development and maintenance of the prefeeding hormone peak under restricted feeding; prolonged fasting.


1996 ◽  
Vol 271 (2) ◽  
pp. E239-E245 ◽  
Author(s):  
T. Yoshihara ◽  
S. Honma ◽  
Y. Katsuno ◽  
K. Honma

Extracellular neuropeptide Y (NPY) in the vicinity of the paraventricular nucleus (PVN) as well as NPY concentrations in the PVN were measured in rats under ad libitum feeding and 2-day and 10-day food deprivation. Plasma corticosterone levels were not changed by 2-day food deprivation but were increased by subsequent refeeding. In contrast, the extracellular NPY levels were increased by 2-day food deprivation and were decreased rapidly by refeeding. The NPY concentrations were also increased and increased further by refeeding. On the other hand, plasma corticosterone levels were elevated by 10-day food deprivation and were decreased by subsequent refeeding. The extracellular NPY levels were also increased by food deprivation and decreased gradually after refeeding. However, the postprandial levels were still elevated when plasma corticosterone levels were returned to the basal levels. The NPY concentrations were also increased and increased further by refeeding. The amount of food intake after refeeding was positively correlated with the extracellular NPY levels. It is concluded that extracellular NPY levels in the PVN do not necessarily covariate with plasma corticosterone levels in rats under food deprivation.


1999 ◽  
Vol 277 (6) ◽  
pp. R1749-R1759 ◽  
Author(s):  
Elena Timofeeva ◽  
Yves Deshaies ◽  
Frédéric Picard ◽  
Denis Richard

The present study was conducted to verify whether experimental conditions such as obesity and food deprivation, which promote food intake and reduce thermogenesis, could modify the expression of the corticotropin-releasing hormone (CRH)-binding protein (BP) in the rat brain. In situ hybridization, histochemistry, and immunohistochemistry were used to assess the expression of CRH-BP in lean ( Fa/?) and obese ( fa/fa) Zucker rats that were fed ad libitum, food deprived for 24 h, or food deprived for 24 h and refed for 6 h. In both lean and obese rats, food deprivation led to a reduction in body weight that was accompanied by a reversible increase in plasma corticosterone levels. Food deprivation and, to a lesser degree, obesity induced the expression of CRH-BP mRNA in the dorsal part of the medial preoptic area (MPOA). This induction of the CRH-BP gene led to by food deprivation was confirmed by the appearance in the dorsal part of the MPOA of neurons immunoreactive to CRH-BP. Food deprivation (in particular) and obesity also increased the levels of CRH-BP mRNA in the basolateral amygdala (BLA). The enhanced CRH-BP expression in the MPOA and BLA in response to food deprivation was reversed by refeeding. In lean Fa/? rats, the CRH-BP mRNA level in the pituitary cells was significantly decreased after food deprivation and restored after refeeding. When food was provided ad libitum, the number of cells expressing CRH-BP in the anterior pituitary was significantly higher in lean rats than in obese animals. Food deprivation for 24 h decreased dramatically the number of pituitary cells expressing CRH-BP in lean rats. Altogether, the present results demonstrate that food deprivation and, to a lesser extent, obesity can selectively affect the expression of CRH-BP. Given both the inactivating effect of CRH-BP on the CRH system and the potential roles played by the MPOA and BLA in the thermogenic and anorectic effects of CRH, it can be argued that the induction of the CRH-BP gene in obesity and after food deprivation occurs as a mechanism to reduce energy expenditure and to stimulate food intake.


1986 ◽  
Vol 250 (6) ◽  
pp. R1052-R1059 ◽  
Author(s):  
M. J. McKinley ◽  
D. A. Denton ◽  
R. G. Park ◽  
R. S. Weisinger

The subfornical organ (SFO) and surrounding periventricular tissue were ablated in sheep. Such a lesion did not significantly reduce water drinking in response to intracarotid, intravenous, or intracerebroventricular infusions of [Val5]angiotensin II amide (ANG II) but caused reduced intake of water in response to intracarotid infusion of hypertonic saline. The dipsogenic response of these sheep to water deprivation for 3 days was similar to that of normal sheep subjected to water deprivation. Although the results are not conclusive in excluding the SFO from having a role in ANG II-induced drinking, they show that there are receptors outside the SFO sensitive to blood-borne ANG II that are involved in water drinking in sheep. The results also show that tissue in the SFO or its surroundings may be involved in drinking caused by acute hypertonicity.


1984 ◽  
Vol 24 (124) ◽  
pp. 77 ◽  
Author(s):  
BA McGregor

Kids six months old and of mean liveweight 22 kg were offered a basal ration of barley and lupins (crude protein 15 .4%) supplemented with three levels of chopped hay (0, 13% of total intake and ad libitum). Supplementation of the basal ration with 13% hay increased total dry matter intake from 479 to 753 g/d (P< 0.001) and liveweight gain from 10 to 54 g/d (P<0 .01). Non-significant increases in total food intake and liveweight gains were achieved by supplementing with ad libitum hay; kids fed ad libitum hay actually consumed 26.9% of their diet as hay. They were then offered various mixtures of barley, oats and lupins with 13% chopped hay at near ad libitum feeding. Differences in intake or growth were not significant at P= 0.05 with kids growing at 74, 65 and 101 g/d for those fed barley, oats and lupins respectively. Results indicate that highest food intake was obtained when 13% chopped hay was added to whole barley grain rations.


1995 ◽  
Vol 198 (5) ◽  
pp. 1137-1149 ◽  
Author(s):  
A Butt ◽  
H Taylor

The roles of coxal and anal excretion in the regulation of haemolymph osmolality, [Na+] and [K+] were studied in the mygalomorph spider Porrhothele antipodiana (mass 0.7&shy;1.0 g) under differing conditions of feeding and hydration state. Dehydration of starved spiders by removal of drinking water caused progressive mass loss at a rate of about 2.5 % of initial body mass per day and was associated with increases in the whole-body [Na+] and [K+] and in the osmolality, [Na+] and [K+] of the haemolymph. On provision of prey, feeding partially restored this mass loss but further elevated body and haemolymph ion concentrations. Dehydration reduced fluid excretion by the anal excretory system and the four coxal organs in both starved and feeding spiders. Starved hydrated spiders initially produced anal urine at 5 &micro;l day-1 and this was progressively reduced to zero after 4 days of water deprivation. Spiders dehydrated to less than 12 % mass loss would nevertheless feed and this initiated a small post-prandial anal diuresis (&lt;5 &micro;l day-1 compared with &gt;30 &micro;l day-1 in fed hydrated spiders). Coxal fluid was produced by dehydrated spiders only during feeding and was delivered into the prey, the rate of production by single organs decreasing from about 19 &micro;l h-1 g-1 body mass in hydrated spiders to about 4 &micro;l h-1 g-1 body mass in spiders dehydrated to 11 % mass loss. There was an increase in urine [K+] and in the rate of anal K+ excretion associated with ad libitum feeding in dehydrated spiders. However, urine [Na+] and the rate of anal excretion of Na+ were not increased by feeding. This was associated with an increase in [K+] of the stercoral fluid above that observed in either fed or starved hydrated spiders, but no significant change in [Na+]. Conversely, [Na+] of the coxal fluid produced during feeding was increased by dehydration whereas [K+] was not. These observations are consistent with the previously postulated roles of the coxal organs (Na+) and anal system (K+) in the excretion of ions ingested with the prey. Full elimination of the prey ions was accomplished only after drinking water was resupplied, which initiated further anal and coxal diureses. Smaller anal and coxal diureses also occurred on rehydration of unfed spiders. The production of coxal fluid in the absence of prey is further evidence that the coxal organs have a true excretory function besides, presumably, assisting ingestion. During dehydration and feeding, P. antipodiana, unlike many insects, is unable simultaneously to conserve water and to eliminate ions by production of a highly concentrated excretory fluid. Both coxal fluid and anal urine were approximately iso-osmotic to the haemolymph and the urine was markedly hypo-ionic.


1987 ◽  
Vol 54 (2) ◽  
pp. 153-163 ◽  
Author(s):  
Kristina Dahlborn

SummaryWhen four goats were subjected to total water deprivation for 48 h once in early lactation and once in mid lactation and their voluntary food intake and effects on milk secretion were observed, milk volume decreased and lactose and fat concentration increased during both periods. However, when the goats were then fed the mean of their own food intake at the two previous water deprivation experiments, and were left free access to water, it was found that decreased food consumption had only a minor influence on milk secretion. When six goats were subjected to 48 h of food deprivation and six to 48 h of water deprivation, milk secretion decreased, but the reduction was delayed and of smaller magnitude during water deprivation. During food deprivation lactose concentration decreased and the milk protein and fat increased; the fatty acid composition changed from a greater proportion of short-chain to more long-chain fatty acids. During water deprivation milk fat and lactose concentrations increased, and only after 44 h did a change from short-chain to a larger proportion of long-chain fatty acids become evident. These experiments indicate that not only food intake, but also water intake are concerned with milk production.


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