Miguel R. Covian

Alterations in sodium chloride and water intake after septal lesions in the rat

Abstract Alterations in sodium chloride and water intake induced by septal lesions employing the standard “two bottle” self-selection procedure were studied. An increase of NaCl and a decrease of water ingestion resulted after placement of the lesions. In rats with bilateral destruction of the septal area changes endured for 2–3 months (end of the experiments) while in those with unilateral lesions the changes subsided after about 45 days. Taking into account previous findings which indicate the role played by the hypothalamus and amygdala in the regulation of NaCl and water intake, it is suggested that impulses come down from the septal area and reach the hypothalamus either directly or indirectly through the amygdala and modulated the activity of hypothalamic regions involved in the regulation of NaCl and water consumption.

Influence of some limbic structures upon somatic and autonomic manifestations of pain

Abstract In guinea pigs under pentobarbital anesthesia a painful stimulation was applied through a monopolar electrode introduced in the dental pulp of one incisor and the effects on motor movements, respiration and vocalization were registered. It was observed that association of painful and septal stimuli resulted either in abolition or diminution of painful manifestations. Sometimes, according to the electrode position, septal stimulation elicited painful expression. Changes in frequency of stimulation without changing the electrode placement resulted either in analgesic-like effect or algesic-like effect. The stimulation of amygdala, stria terminalis and hippocampus elicited also both kinds of manifestations, sedative and painful. The results here reported support the existence of a limbic modulation of painful messages.

Natriuresis, kaliuresis and diuresis in the rat following microinjections of carbachol into the septal area

The effects of intraseptal injection of carbachol on natriuresis, kaliuresis and diuresis has been studied in conscious, unrestrained water-loaded male rats. Urinary sodium and potassium excretion increased following injections into the septal area. The intensity of the natriuresis and kaliuresis was dose-related. An antidiuretic effect was also observed. The Na+/K/ ratio increased with increasing doses of carbachol, indicating that the rise in urinary sodium exceeded that of potassium. Systematic mapping of the septal area yielded about the same results for all sites, excepting a zone located in the anterior-dorsal part of the medial nucleus which appeared more sensitive. The natriuretic effect of intraseptal carbachol in adrenalectomized rats demonstrated the secondary role played by the adrenals. Contrariwise the decrease of the natriuretic effect observed either in hypophysectomized rats or in rats bearing a median eminence lesion receiving intraseptal carbachol showed the important participation of these structures in urinary Na+ excretion. Adrenalectomy or median eminence lesions did not modify the kaliuretic response while hypophysectomy produced a transitory diminution. This fact favours the hypothesis of different mechanisms involved in Na+ and K+ excretion following intraseptal carbachol. These results leave open the question as to mechanism of action but suggest a possible role of the pituitary in mediating the responses. Also, the possibility of a role played by hemodynamic shifts is suggested.

Role of amygdaloid complex in sodium chloride and water intake in the rat.

Abstract Bilateral electrolytic lesions in the amygdaloid complex of the rat elicited either a decrease or increase in 1.5 per cent NaCl intake. The studies were made employing the standard “two bottle” self-selection procedure. Lesions placed in the corticomedial complex, especially the cortical nucleus, resulted in an increase of NaCl and also of the total fluid intake. Bilateral lesions placed principally in the lateral nucleus but also reaching the medial, basolateral and basomedial nuclei resulted in a decrease of NaCl and total fluid ingestion. Sodium balance studies showed that changes in Na consumption preceded changes in urinary output. These results together with those already reported from our laboratory support the assumption of the existence of an intricate circuit related to hydromineral metabolism which involves the septal area, amygdala and hypothalamus.

Adrenergic stimulation of the lateral hypothalamic area on sodium and potassium excretion

The effects of adrenergic stimulation of the lateral hypothalamic area on sodium and potassium excretion were studied in rats bearing implanted cannulae. When noradrenaline was injected into several points of the lateral hypothalamic area, a dose-related increase in natriuresis and kaliuresis was observed. Rats previously injected through the same cannulae with alpha (Regitine) or beta (Propranolol) blocking agents showed different natriuretic responses when injected with noradrenaline. It was observed that the normal noradrenaline-induced natriuresis was abolished by the alpha-adrenergic blockers, while beta-adrenergic blockers increased the response. Intrahypothalamic injection of Isoproterenol, and activator of the beta-adrenergic receptor, induced a decrease in natriuresis, kaliuresis and urinary volume. In contrast, injection of Metaraminol, an alpha-adrenergic agonist, caused an increase in sodium and potassium excretion and a reduction of urinary volume. Drugs blocking the destruction of noradrenaline or its reuptake by the presynaptic nerve endings potentiated 2-fold the action of 20 nmol of noradrenaline. These experiments provide good evidence for the existence of an adrenergic mechanism consisting of alpha and beta receptors which works antagonistically on the regulation of sodium and potassium excretion. The excretion on the two electrolytes is stimulated by the alpha-adrenergic system, and inhibited by the beta-adrenergic system.

Decreased blood pressure due to brain septal stimulation: Parameters of stimulation, bradycardia, baroreceptor reflex

Abstract Effects of varying the pulse length, frequency and duration of the electrical stimulus applied to the septal area of the chloralosed cat were studied. The degree of the blood pressure fall was taken as an index of the efficiency of the stimulation. Unidirectional pulses of 0.1,1,5,10, and 15 msec were tested. Pulse duration of 10 msec was generally the most effective. Frequencies of 15–50 and 80 cps were used, the frequency of 50 c/s was the most efficient. Stimulation time prolonged to 28.5 min showed that the septal area is very resistant to fatigue. Bradycardia was also studied and it was observed that eserine enhance the bradycardic effect of septal stimulation. Sometimes bradycardia was still present after vagotomy thus suggesting a diminution of cardiac sympathetic tone. The baroreceptor reflex was blocked by the hypotension due to septal stimulation; the possibility is advanced of a partial inhibition of the bulbar vasomotor center by impulses originating in the septal area.

Lever-pressing behavior caused by intraseptal angiotensin II in water satiated rats.

Abstract Intracerebral injection of angiotensin II induced drinking behavior in satiated rats. In the present experiments five rats, presenting a positve drinking response to the intraseptal injection of angiotensin II, were trained to press a lever for water in a standard chamber, used for operant behavior studies. The injection of 1 μg of angiotensin II into the septal area of the brain caused the animals, previously satiated in the experimental chamber, to resume lever pressing under a continuos reinforcement schedule of water presentation. The number of responses emitted after angiotensin was considerably higher than after a control injection of saline. This result supports the hypothesis that angiotensin has a dipsogenic action in the CNS that mimicks the effect of water deprivation.

Interaction between hypothalamus, amygdala and septal area in the control of sodium chloride intake ☆

Abstract The studies were made in rats employing the standard two-bottle self-selection procedure. Rats with increased salt intake due to lesions in the amygdaloid complex or in septal area diminished their intake following hypothalamic lesions which in the intact rat causes decreases. When the hypothalamic lesions were made first, amygdaloid or septal lesions did not induce any change. Rats with decreased salt intake because of amygdaloid lesions showed an augmented ingestion after septal lesions but if septal lesions were made first the increased intake elicited was not modified by amygdaloid lesions which in the intact rat causes decreases. It was concluded that the hypothalamus is the main structure controlling sodium intake and that the amygdala and septal area have modulating influences on the hypothalamus. In turn, septal area overcomes the action of the amygdala.

Water and sodium chloride intake following microinjections of angiotensin II into the septal area of the rat brain

Abstract The effects of 1 μg of angiotensin II on tap water and 1.5% NaCl intake when injected into the septal area of conscious and unrestrained rats were studied, employing the standard “two bottle” self-selection procedure. Angiotensin yielded a strong dipsogenic action preferentially of tap water. The effect was of short latency and drinking was obsessive. There was not any change in the consumption of food. The drug injected in the dorsal vein of the penis did not shift the intakes of fluids. It was observed in the same group of rats but under nembutal anesthesia that intraseptal angiotensin did not modify the sistemic blood pressure which raised when the drug was given intravenously. The action of angiotensin seems not to be mediated through cholinergic, adrenergic, nor-adrenergic or triptaminergic pathways because neither atropine, propranolol, phentolamine nor methylsergide blocked its dipsogenic effect. Based on some findings the possibility of a direct action of angiotensin on neurons is advanced.

Antagonism of the dipsogenic action of intraseptal angiotensin II in the rat

Abstract The injection of 0.01 to 2.0 μg of antiotensin II (A II) into the medial septal area of unanesthetized rats in normal water balance caused dose-dependent drinking, during the 60 min period following drug administration. A hyperbolic dose-response curve, rectified by a log dose scale was obtained. Pretreatment with 5 and 10 μg of locally injected haloperidol, 15 min prior to A II (0.3 μg), partially antagonized the dipsogenic effects of A II and a dose of 25 μg of haloperidol completely blocked this effect. A cataleptic-like state followed haloperidol administration. The injection of doses as high as 25 μg of dopamine in the same brain site caused no drinking. Pretreatment with 3 μg of intraseptal Sar 1 , Ala 3 , Ile 8 — angiotensin I, a competitive antagonist of A II at peripheral receptors, completely antagonized the dipsogenic effect of A II. The same dose (3 μg) of the A II analog alone caused only a mild but significant drinking response. These results suggest that A II acts of specific receptors in the CNS that may be similar to peripheral angiotensin receptors. On the other hand, the role of brain catecholamines in the mediation of A II-induced drinking remains uncertain.