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Biomedical subjects

A Puerto

Publications and source records attributed to A Puerto.

At least 37 records · Page 2Linked to original sources

Mammillary polydipsia and diabetes insipidus: a study of the rhythmicity of water intake.

Rats with polydipsia induced by electrolytic mammillary lesions show a normal daily rhythmicity of water intake compared with sham lesioned animals, when kept in a 12:12 hours light-dark cycle of illumination. Water is mainly consumed during the dark phase (approximately 80-90% of the total amount). On the other hand, rats with centrally induced diabetes insipidus by means of electrolytic lesions in the median eminence show a clear-cut alteration in this rhythmicity, drinking only 67% of the total amount during the dark phase. This effect could be due to the continuous necessity of these animals to drink water in order to maintain fluid homeostasis, and is not related to food rhythmicity alterations. Taken together, and on the basis of the daily rhythmicity of water intake, these results suggest that mammillary polydipsia may be different from that observed when diabetes insipidus is present.

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Peripheral pathways mediating salivary secretion after nucleus parvocellularis activation in the rat.

The present study demonstrates that activation of the nucleus parvocellularis in the pontine reticular formation of the rat evokes salivary hypersecretion. The secretory effect observed was found to be mediated by parasympathetic mechanisms, as transection of the preganglionic parasympathetic salivatory fibers at the level of the middle ear blocked the flow of saliva evoked by activation of the nucleus parvocellularis (Experiment 1). Furthermore, transection of these salivatory fibers was followed several days later by the development of a prandial model of drinking. These behavioral data suggest that the transection procedure employed in the present study indeed affected those parasympathetic fibers which control the secretory activity of all three pairs of major salivary glands (Experiment 2).

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Effects of atropine injection on food-associated drinking in rats with superior salivatory nucleus lesions.

The neuropharmacological mechanisms involved in the prandial drinking pattern seen in rats with superior salivatory nucleus lesions + parotidectomy were investigated with behavioral methods. Results showed that the administration of low doses (0.1 mg/kg body wt) of atropine in lesioned rats potentiated previously established prandial drinking. Higher doses of atropine (1.0 mg/kg), however, were required to induce a similar degree of prandiality in control rats (parotidectomy alone). These findings suggest that the salivatory nucleus lesions affected a cholinergic brainstem-salivary gland system involved in the neural control of food-associated drinking.

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[Primary/secondary characteristics of polydipsia induced by electrolytic lesion of the mammillary bodies].

Rats with mammillary electrolytic lesions show a strong polydipsia and polyuria. This over-consumption may be primary or secondary to the polyuric effect. In this regard, mammillary lesioned rats excrete a greater amount of urine compared with control animals when matched in daily water consumption (partial water deprivation). Moreover, this abnormal water intake is significantly reversed by treatment with Pitressin, a vasopressin analogue. These results suggest that the polydipsia may be determined by the urinary water loss. However, when subjected to the bilateral ureter ligation, the experimental animals still outdrink the control ones, thus also suggesting a primary component of the polydipsia under study. The possible explanation of these components in relation to the mammillary polydipsia is discussed.

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A study of the response to several dipsogenic treatments in rats with mammillary polydipsia and with centrally induced diabetes insipidus.

Several brain areas have been implicated in the regulation of water intake and body fluid homeostasis. Electrolytic lesions located in the mammillary area have proved to induce a strong polydipsia. The cause of this overconsumption is not understood, although other studies have indicated a possible relationship with the mechanisms involved in sodium control. In this paper, we consider whether mammillary polydipsia is related to diabetes insipidus. In this regard, animals with mammillary lesions were submitted to several dipsogenic treatments, both osmotic and volemic. These subjects showed a differential response to hypertonic NaCl compared with controls. No effect could be seen in relation to the other treatments employed, that is, sucrose and polyethylene glycol. On the other hand, this differential response to NaCl was not observed in those animals with diabetes insipidus centrally induced by means of lesions in the median eminence. Thus, mammillary polydipsia and diabetes insipidus-related water intake seem to be different phenomena. The possible relationship between mammillary polydipsia and sodium control is discussed.

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Submandibular and parotid salivary secretion after electrolytic lesioning of the brainstem nucleus parvocellularis in the rat.

The present study, in consonance with recent anatomical investigations, demonstrates that activation of the nucleus parvocellularis in the rat evokes a potent hypersecretory effect in the submandibular and sublingual (S-S) salivary glands. Furthermore, electrolytic lesioning of this region in conjunction with peripheral removal of the parotid glands is followed by an increase in the number of drinking responses in the presence of dry food. Such prandial drinking behavior is only observed after total impairment of salivation (i.e., removal of the S-S + parotid glands), thus suggesting that the parvocellularis lesion led to a marked deficit in S-S salivary secretion. On the other hand, the activation of the nucleus parvocellularis was seen to have only a slight effect on parotid salivary secretion. Electrolytic lesions to this zone, when associated with peripheral removal of the S-S glands, failed to induce prandiality, suggesting that the parvocellularis nucleus exerted a low level of control over parotid salivary secretion. These results are interpreted as functional proof of the relationship between the parvocellularis reticular formation and the superior salivatory nucleus in the secretion of S-S saliva.

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The nucleus parvocellularis reticularis regulates submandibular-sublingual salivary secretion in the rat: a pharmacological study.

This experiment shows that activation of the nucleus parvocellularis reticularis in the rat brainstem provokes salivary hypersecretion by the submandibular-sublingual glands. The secretory effect is mediated by cholinergic mechanisms, as the administration of atropine blocked the flow of saliva evoked by stimulation of the nucleus parvocellularis. In contrast, injection of dihydroergotamine (an alpha-blocker) and/or propranolol (a beta-blocker) failed to significantly reduce submandibular and sublingual salivary secretion when compared to a control group injected with distilled water. The cholinergic nature of the salivary response suggests that the nucleus parvocellularis reticularis exerts its secretory effect on the salivary glands parasympathetically rather than through mechanisms associated with sympathetic pathways. The area of the brainstem activated in the present study closely overlaps the region in which cell bodies of superior salivatory neurons have recently been identified with retrograde transport of peroxidase. The data presented herein represent functional proof in support of the location of the superior salivatory nucleus within the parvocellularis reticular formation.

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Electrical intracerebral stimulation of the area postrema on taste aversion learning.

The structural characteristics of the area postrema, its anatomical connections, participation in the detection of emesis-provoking substances and the effects of area postrema lesions on taste aversion learning acquisition, are all factors which speak in favor of a role as a chemoreceptor zone involved in the detection of aversive agents which act as effective inducers of taste aversion learning. The feasibility of substituting electrical intracerebral stimulation of the area postrema for the aversive stimulus was investigated in a taste aversion learning paradigm. In Expt. 1, 0.1-ms rectangular pulses of 50 Hz, delivered intermittently or continuously for 4 h after a 15-min delay following ingestion of the gustatory stimulus, produced reliable learning. Expt. 2 showed the learning thus induced to reflect all the characteristics features attributed to taste aversion learning: one-trial learning, long interstimulus delay and cue-consequence specificity. These results suggest that the area postrema could participate in the detection of the aversive consequences of particular taste aversion learning-inducing agents.

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Salivatory neurons in the brainstem nucleus parvocellularis of the rat: effects of electrolytic lesions.

This study was based on several recent anatomical studies suggesting that the superior salivatory nucleus is located within the area parvocellularis of the brainstem reticular formation. The aforementioned zone was lesioned in order to observe the alterations produced in salivary secretion. Electrolytic lesion of the area parvocellularis was followed by salivary hypersecretion as an immediate and transitory effect of the stimulatory capacity of the electrolytic lesioning method. Some days later the animals presented a markedly impaired salivary secretion as shown by the appearance of inefficient feeding behavior and the development of a prandial drinking pattern. The prandial behavior, which was characterized by numerous drinking episodes during dry food intake, was reversed when wet food was offered, suggesting a true deficit in salivary secretion caused by the parvocellularis lesion. Following the administration of pilocarpine, the submandibular and sublingual salivary glands of experimental animals showed an increased capacity for response (postsynaptic supersensitivity) in comparison to the control group.

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Refractory periods of neurons mediating stimulation-elicited eating and brain stimulation reward: interval scale measurement and tests of a model of neural integration.

Paired-pulse stimulation methods have been used in many studies to measure the excitability properties of the directly stimulated neurons mediating stimulation-elicited behaviors. In this article those methods are evaluated quantitatively. The most frequently used method, in which rate of behavior is measured as a function of conditioning-test (C-T) interval, is shown to be inadequate since the results obtained depend on the frequency of stimulation. In order to account for this dependence, a physical model of brain stimulation which implies that the effects of frequency and C-T interval should be multiplicative is proposed. In separate experiments, conjoint and functional measurement methods were used to test this model and to measure the refractory periods of neurons mediating stimulation-elicited eating and brain stimulation reward. The results of both experiments strongly supported the multiplicative model for C-T intervals in the refractory period range (.4-2.0 msec) and indicated that the frequency threshold method (Yeomans, 1975, and the present Experiment 2) provides interval scale measurement of refractory period effects. The refractory period curves obtained for neurons mediating stimulation-elicited eating and brain stimulation reward were very similar, rising steeply at C-T intervals from .4 to 1.2 msec and more gradually at intervals from 1.2 msec to 2.0 msec. These curves were also similar to one previously obtained for bar-pressing self-stimulation (Yeomans, 1975). The implications of these similarities are discussed.

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Comparison between some digestive processes after eating and gastric loading in rats.

Physiological and biochemical differences were found between normal and intragastric feeding in the rat. Milk ingested orally remained in the stomach significantly longer than milk ingested via a chronic intragastric fistula. Milk samples were removed from the stomach at intervals of 5, 20 and 45 min after ingestion and it was found that milk which had been ingested via intragastric fistula underwent substantially less lipolysis than did milk which had been ingested orally. These results are discussed in relation to the aversive and rewarding effects obtained by injections of edible nutrients into the stomachs of rats.

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Rapid discrimination of rewarding nutrient by the upper gastrointestinal tract.

When certain nutrients are injected into the stomachs of rats that are drinking one of two samples of nonnutrient, flavored water, the rats will (within a 10-minute session) choose the flavor paired with the nutrient. Such rewarding effects have obtained with predigested milk but not with similarly treated glucose or fresh milk. The results suggest the presence of rapidly acting, specialized, nutrient receptors in the upper gastrointestinal tract.

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Histologic and enzymatic studies of the mesolimbic and mesostriatal serotonergic pathways.

Selective lesions of the dorsal (B7), median (B8), or lateral (B9) raphe nuclei were made stereotaxically in male rats 4 weeks before sacrifice. The extent of damage to each raphe nucleus was quantified histologically by means of a simplified formaldehyde histochemical method for visualization of serotonin in cryostat sections. A detailed mapping of the distribution of the yellow-fluorescent raphe perikarya provided the basis for quantification. Tryptophan hydroxylase activity was measured in 6 forebrain regions from each animal, and the results were correlated with the per cent damage to each raphe nucleus. Tyrosine hydroxylase was also assayed in 5 of these regions; it was not significantly affected by any of the raphe lesions. Dorsal raphe lesions reduced tryptophan hydroxylase activity in the striatum, thalamus, cortex, and hypothalamus, but not in the septal nuclei or hippocampus. Damage to B8 resulted in decrements in this serotonergic enzyme in the septal nuclei, hippocampus, cortex, and hypothalamus, but not in the striatum or thalamus. Lesions of the scattered B9 cells had no significant effect on enzyme activity in any region examined. These data suggest that the dorsal and median raphe nuclei provide two distinct though perhaps overlapping serotonergic systems innervating different parts of the forebrain: a mesostriatal pathway originating in B7 and a mesolimbic system derived from B8. Behavioral studies on the animals, which are presented in a companion paper, indicated that damage to the median nucleus is responsible for many of the behavioral effects previously reported after combined lesions of both major raphe nuclei.

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Behavioral studies following lesions of the mesolimbic and mesostriatal serotonergic pathways.

The behavior of rats with selective lesions of either the dorsal (B7), median (B8), or lateral (B9) raphe nuclei was compared to that of sham-lesioned controls in a variety of experimental situations. As described previously, the extent of damage to the midbrain raphe nuclei was determined by fluorescence histochemistry, and the tryptophan hydroxylase and tyrosine hydroxylase activities of 6 forebrain regions were measured for each rat. None of the lesions affected tyrosine hydroxylase activity. Lesions of B7, which reduced tryptophan hydroxylase in the striatum, thalamus, cortex, and hypothalamus, had no significant effect on any of the behavioral measures. Lesions of B9, although twice as large, neither reduced forebrain tryptophan hydroxylase significantly nor affected any of the behavioral variables. However, B8 lesions, which reduced hippocampal, septal, cortical, and hypothalamic tryptophan hydroxylase, had behavioral effects similar to those reported after combined raphe lesions parachlorophenylalanine. Median raphe-lesioned rats were hyperactive when placed in a novel environment and throughout the dark phase of the light/dark cycle. With respect to locomotor activity, B8-lesioned rats were also hyper-responsive to amphetamine. When placed in a stabilimeter and subjected to repeated air puff stimuli, rats with B8 lesions exhibited larger startle responses. Furthermore, only B8-lesioned animals perseverated when given two unreinforced trials in a Y-maze. All these histologic, biochemical, and behavioral variables were assessed individually for all 39 animals, and a multivariate correlational analysis incorporating the data of this and the preceding paper is presented here. These experiments suggest that the mesolimbic serotonergic pathway originating in B8 subserves some of the inhibition necessary to dampen behavioral responsivity.

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