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The thyroid function was studied by means of a comparison between rats that drank daily less than 2 mEq of a NaCl solution (control) and rats that spontaneously drank daily above 4 mEq of this solution (0.25 M), which is considered aversive to rats. It was found that, in these rats, the protein-bound iodine (PBI-127) and the radioactive iodine uptake (I-131) were less than in the control rats, in spite of similar thyroid weight. It seems, therefore, that the rats that drank high levels of the aversive salt solution have hypothyroidism. This finding shows another link between the thyroid gland and NaCl intake. These data have implications in the design and interpretation of experiments in which NaCl intake is studied.

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1. The present study was undertaken to investigate the influence of the septal area on neural mechanisms involved in feeding behavior elicited by electrical stimulation of the lateral hypothalamic area of the rat. 2. Electrolytic damage to medial and lateral septal nuclei induced a significant increase (18.29 +/- 1.69 to 25.05 +/- 2.31 g, P less than 0.05, N = 14) in food intake elicited by hypothalamic stimulation. The threshold current for stimulus-induced eating decreased by 20% after septal lesion. 3. A significant decrease in food ingestion was observed after electrical stimulation of the septal nuclei, either preceding (27.47 +/- 1.57 to 19.30 +/- 2.06 g, P less than 0.05, N = 13) or simultaneous (26.20 +/- 1.60 to 12.10 +/- 2.40 g, P less than 0.05, N = 11) with hypothalamic stimulation. 4. The results indicate an inhibitory effect of the septum on the lateral hypothalamic area and also suggest that the functional state of the lateral hypothalamus, which is responsible for the feeding behavior, depends on the activity pattern of the septal area.

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The present study was undertaken to investigate the influence of the septal area on neural mechanisms involved in feeding behavior elicited by electrical stimulation of the lateral hypothalamic area of the rat. Electrolytic damage to medial and lateral septal nuclei induced a significant increase (18.29 + or - 1.69 to 25.05 + or - 2.31 g, P<0.05, N = 14) in food intake elicited by hypothalamic stimulation. The threshold current for stimulus-induced eating decreased by 20% after septal lesion. A significant decrease in food ingestion was observed after electrical stimulation of the septal nuclei, either preceding (27.47 + or - 1.57 to 19.30 + or - 2.06 g P <0.05, N = 13) or simultaneous (26.20 + or - 1.60 to 12.10 + or - 2.40 g, P<0.05, N = 11) with hypothalamic stimulation. The results indicate an inhibitory effect of the septum on the lateral hypothalamic area and also suggest that the functional state of the lateral hypothalamus, which is responsible for the feeding behavior, depends on the activity pattern of the septal area

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By using the two-bottle, self-selection method it was found that an excess of thyroid hormone administration to rats increased water and sodium intake. Thyroidectomy changed the initial preference from water to sodium chloride. Oral treatment of the thyroidectomized rats with thyroid hormones brought salt ingestion back to normal levels and greatly augmented the water intake. Two-week treatment was followed by an increase in salt intake, which was characterized by large oscillations resembling the corresponding effects of adrenalectomy and treatment with deoxycorticosterone.

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Since lesion of subcortical structures may affect the barbiturate sleeping time (bST), we decided with the present study to elucidate the role of the caudate nucleus in the determination of central sensitivity to barbiturates. Rats implanted with a cannula in the caudate nucleus of one or both sides, as well as with a jugular cannula, were utilized. Intravenous injections of sodium pentobarbital (40 mg/kg), intracerebral injections of Xylocaine (0.04 microgram), carbachol (0.2 micrograms) or artificial cerebrospinal fluid (ACF) into the caudate nucleus were performed. Both Xylocaine and carbachol, but not ACF, increased the bST regardless of the preparation used, the only exception being Xylocaine which did not alter the bST, if injected into the left caudate nucleus. The results suggest that the caudate nucleus may act as a modulator of the central sensitivity to barbiturates.

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The present study examined the effects of carbachol and angiotensin II injected into the medial and lateral septal areas (MSA and LSA) on the ingestion of primary taste solutions in a free-choice situation. The injection of carbachol or angiotensin II into MSA and LSA of water sated rats evoked a preference for the sweet tasting saccharin solution and water. The lateral septal rats also preferred acetic acid solution. Only the total fluid intake differed significantly among the four groups. In the water deprived rats injection of chemical to the respective groups induced the ingestion of NaCl solution. The MSA rats on injection of carbachol also preferred saccharin apart from NaCl. There was a significant difference in the NaCl intake among the four groups. The quinine solution was not consumed by all the groups. These results indicate that both the carbachol and angiotensin II induce the ingestion of saccharin, NaCl and water. The MSA might be more sensitive in inducing NaCl intake as compared with LSA during deprivation schedule and cholinergic stimulation. The LSA also evokes a preference for the sour tasting acetic acid. Furthermore, the data also suggest that the neurons sensitive to angiotensin are more potent than cholinergic neurons of LSA in producing salt preference.

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In the present study, electrical stimulation of medical or laternal septal areas and total or restricted lesions of these were conducted to observe the effect on ingestion of primary taste solutions in a free-choice situation. Stimulation induced a specific decrease in the intake of NaCl solution and had no effect on saccharin, acetic acid and quinine solutions and water. Total septal lesion or restricted lesions of medial or lateral septal areas induced hyperdipsia in rats. The lesioned rats, in a free-choice situation preferred NaCl, saccharin, as well as acetic acid solutions. This increase in acetic acid intake after lesion suggests that sour taste is also affected. Furthermore, there was no consumption of quinine solution before and after the lesion. This might be due to the presence of sweet tasting saccharin solution in this free-choice situation. These results indicate that the septal area causes aversion to NaCl intake, probably by inhibiting lateral hypothalamic neurons responsible for NaCl ingestion. The consumption of large quantities of saccharin, NaCl and acetic acid after the septal lesion suggests that the rats become overresponsive to taste factors in a free-choice situation.

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To study the role played by neurotransmitters and their receptor mechanisms in the control of feeding behavior elicited by electrical stimulation, drugs that affect neurotransmission were injected via cannula electrodes into the lateral hypothalamic area. Pretreatment with noradrenaline (0.5 and 1.0 nmol) significantly increased the effect of hypothalamic stimulation on feeding, whereas injection of 1.0, 2.0 and 4.0 nmol of adrenaline or dopamine was ineffective. Phentolamine (40.0, 80.0 and 100.0 nmol) and propranolol (40.0, 80.0 and 120.0 nmol) induced a decrease in food intake, suggesting the involvement of both alpha and beta receptors in this mechanism. However, isoprenaline (20.0 nmol) also reduced food intake. Reduction of food intake by propranolol was probably related to the action of the local anesthetic. Alphamethyl-p-tyrosine (203.0 nmol), reserpine (32.8 nmol) and 6-hydroxydopamine (200.0 nmol) inhibited the feeding behavior elicited by electrical stimulation of the lateral hypothalamic area. These results suggest that electrical stimulation of the lateral hypothalamic area elicits feeding behavior by releasing noradrenaline. Alpha-adrenergic receptors seem to play a facilitatory role in feeding behavior.

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Bipolar stainless steel electrodes or stainless steel cannulas were implanted stereotaxically into the lateral hypothalamus of rats. Drinking was elicited by electrical or chemical (carbachol or angiotensin II) stimulation of animals, which were offered water and solutions of sodium chloride, saccharin, acetic acid and quinine. During electrical stimulation, ingestion of water and of all the solutions increased significantly. The same rats ingested significantly more sodium chloride and saccharin solution after 23 h water deprivation and electrical stimulation of the lateral hypothalamus. Carbachol administered into the lateral hypothalamus induced ingestion of saccharin solution and water but not of sodium chloride. Angiotensin II injected into the lateral hypothalamus did not induce drinking in most of the rats and those which drank preferred sodium chloride, saccharin and water. Several of the rats which did not respond to angiotensin II injection into the lateral hypothalamus, 72 h after angiotensin II responded to injection of carbachol by drinking the saccharin solution. The results of electrical stimulation suggest that the lateral hypothalamus consists of neurons involved in the ingestion of primary taste solutions. Depending on the functional state of the organism, lateral hypothalamic stimulation modifies ingestion of other taste substances but not of salt, as indicated by water deprivation. Chemical stimulation indicates that the neurotransmitter responsible for salt intake is not cholinergic and that the cholinergic neurons evoke preference for sweet taste and water. It appears that angiotensin II is involved in salt intake, as well as in producing preference for sweet taste and water.

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Cholinergic and adrenergic agonists and antagonists were injected directly into the subfornical organ (SFO), via implanted cannulae, and the volume of water ingested was recorded over a period of 1 hour after injection. Application of 2 nmol carbachol caused intense water intake in 100% of the animals (8.78 +/- 0.61 ml), with a very short intake latency. When the 2 nmol carbachol dose was preceded by increased doses of atropine, a progressive reduction in water intake was observed, with complete blockage of the thirst-inducing response to carbachol at the 20 nmol dose level with atropine. Followed by several doses of hexamethonium, the water intake caused by application of 2 nmol carbachol was reduced, although the response was not totally blocked. Injection of 80 nmol of nicotine had a significant thirst-inducing effect in 50% of the animals studied (1.06 +/- 0.18 ml) and increase in water intake was further reduced by application of increased doses of hexamethonium. Raising the dose levels of noradrenaline into the SFO caused an increase in water intake although to a lesser degree than was observed after carbachol injection. When the 40 nmol dose of noradrenaline was preceded by increased doses of propranolol (5 to 40 nmol), there was a gradual reduction in water intake, with total blockage at the 40 nmol dose. Application of phentolamine in doses of 10 to 80 nmol caused no reduction in water intake after 40 nmol of noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

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Sodium chloride intake was studied in rats submitted to different neurosurgical procedures. Intake decreased in animals submitted to bilateral destruction of the basolateral amygdaloid complex, and increased after the same animals were submitted to destruction of the anterior lateral hypothalamus, a procedure which is known to cause increased intake in intact rats. In the reverse experiment, where the anterior lateral hypothalamus was destroyed before the basolateral amygdaloid complex, the effect of increased sodium chloride intake induced by destruction of the hypothalamus overcame the decreased expected upon destruction of the amygdaloid complex. These results permit us to conclude that the hypothalamic areas which inhibit sodium chloride intake predominate over the stimulating areas of the amygdaloid complex in the control of sodium chloride intake.

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Rats bearing lesions in the septal area (SA), or in the subfornical organ (SFO) or simultaneously in both regions were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesion of the SA drank more water than either normal rats or SFO-lesioned animals under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by SA lesions was blocked after SFO lesions. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in SFO-lesioned animals even after destruction of the SA. Animals with SFO lesions did not show increase of the water intake after cellular dehydration. The results obtained suggest that the SFO acts as the main structure in the regulation of water intake elicited by angiotensin with two opposite effects: one direct, facilitating water intake and the other indirect inhibiting the SA. The SA has an inhibitory effect on the SFO and on water intake.

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Rats bearing lesions in the septal area (SA), or in the subfornical organ (SFO) or simultaneously in both regions were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesion of the SA drank more water than either normal rats or SFO-lesioned animals under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by SA lesions was blocked after SFO lesions. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in SFO-lesioned animals even after destruction of the SA. Animals with SFO lesions did not show increase of the water intake after cellular dehydration. The results obtained suggest that the SFO acts as the main structure in the regulation of water intake elicited by angiotensin with two opposite effects: one direct, facilitating water intake and the other indirect inhibiting the SA. The SA has an inhibitory effect on the SFO and on water intake.

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Rats bearing lesions in the septal area (SA), or in the subfornical organ (SFO) or simultaneously in both regions were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesion of the SA drank more water than either normal rats or SFO-lesioned animals under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by SA lesions was blocked after SFO lesions. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in SFO-lesioned animals even after destruction of the SA. Animals with SFO lesions did not show increase of the water intake after cellular dehydration. The results obtained suggest that the SFO acts as the main structure in the regulation of water intake elicited by angiotensin with two opposite effects: one direct, facilitating water intake and the other indirect inhibiting the SA. The SA has an inhibitory effect on the SFO and on water intake.

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Luteinizing hormone (LH) secretion by the anterior pituitary gland was investigated in hemidecorticate (HD) rats under several conditions. Higher plasma and lower pituitary LH levels were observed in HD rats in the afternoon of proestrus, after unilateral ovariectomy, and at the 7th and 14th days after bilateral castration. The ovarian hypertrophy observed in HD rats did not differ from control. When hormonal substitutive therapy was started 3 days after bilateral ovariectomy, larger doses of estradiol benzoate (EB) were required to reduce plasma LH levels in control than in HD animals. The increase in pituitary weight was, however, significantly higher in the HD castrated group. When substitutive therapy started at the 7th and 14th days after castration no significant differences between the 2 experimental groups were observed. The results of substitutive therapy suggest that hemidecortication induces an increase in the sensitivity of hypothalamic-pituitary axis to estrogen negative feedback. This change in sensitivity is clearly seen in HD rats during the first few days after castration. These results suggest that hemidecortication may release the hypothalamus from inhibitory influences coming from rhinencephalic or cortical structures, thus rendering the preoptic-suprachiasmatic complex (POA-SCH) more sensitive to LH-releasing mechanisms.

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