[Inadvertent left endobronchial intubation during surgical removal of 4 molars].
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Adult↗
Biomedical subjects
L Aguado
Publications and source records attributed to L Aguado.
Tests for inhibition after extinction of a conditioned stimulus in the flavour aversion procedure.
In four experiments, rats received flavour aversion conditioning followed by extinction. The flavour was then subjected to retardation and summation tests. Experiment 1 showed that reacquisition of an extinguished flavour aversion was retarded with respect to the performance shown by rats for whom the flavour was novel. No retardation was found, however, with respect to a control group that had been given non-reinforced pre-exposure to the flavour. Experiment 2 demonstrated that extinction showed the same sensitivity to the effects of a retention interval as did latent inhibition, consistent with the view that the retardation effect was a consequence of the occurrence of latent inhibition during extinction. An extinguished stimulus was also found to alleviate the response governed by a separately trained excitor in a summation test (Experiments 3 and 4), but the size of this effect did not exceed that produced by a control stimulus when the procedure used ensured an equivalent aversion to the test excitor in the two cases. These results challenge the proposal that extinction can turn a stimulus into a net inhibitor.
Animals↗
Secretion from neuropeptide-treated splenocytes modifies ovarian steroidogenesis.
There are evidences for modulation of immune function by the sympathetic nervous system and its principal neurotransmitter norepinephrine (NE) through superior ovarian nerve (SON)-coeliac ganglion-noradrenergic postganglionic innervation of the spleen. Seven days after SON transection at 53 days of age, the rat splenocytes were isolated and then cultured for 48 h. These culture media, used to stimulate ovaries from 60-day-old intact rats (neither SON-transected nor sham-operated) at diestrus 2 stage, in in vitro incubations, showed a decrease in progesterone release, an increase in estradiol release and no change in androstenedione release in relation to splenocyte culture media from control (sham-operated) rats. When splenocytes from SON transected (SON-t) rats were treated with vasoactive intestinal peptide (VIP) or neuropeptide Y (NPY), both at 10(-6) M for 24 h, their secretions increased the progesterone release while decreasing the estradiol release from the intact ovaries, compared with the secretions of untreated splenocytes from SON-t rats. Although the secretions of splenocytes treated with VIP decrease the androstenedione release from the ovaries, the treatment with NPY produced no change in hormone release. In the present paper the ovarian steroidogenic response, which was modified by the effects of an in vivo SON transection on spleen cells, was reverted by an in vitro system in which the splenocytes were treated with VIP or NPY. This could indicate that the spleen of SON-t rats does not receive those neuropeptides by neural route however, when they are added to splenocyte culture in vitro, the cell secretions revert the profile of steroid hormones released from the intact ovary. We also present functional evidence for modulation of the immune function by sympathetic nervous system and neurotransmitters other than NE.
Animals↗
Adrenergic influences on coeliac ganglion affect the release of progesterone from cycling ovaries: characterisation of an in vitro system.
The superior ovarian nerve (SON) arrives at the ovary through the suspensory ligament and innervates mainly the ovarian stroma. Most neurones from which the SON fibres originate are located in the complex coeliac and mesenteric ganglia. Taking into account that other ganglia have been shown to have alpha- and beta-adrenergic receptors, and that the coeliac ganglion receives adrenergic fibres from other sympathetic paravertebral and preaortic ganglia, we utilised adrenergic agonists and antagonists specific to the ganglion, to analyse the role of the alpha and beta receptors in ovarian physiology. To that end, it was necessary to develop and standardise an in vitro coeliac ganglion-SON-ovary (coeliac ganglion-SON-O) experimental system that would enable study of the release of steroids in the ovary in the absence of humoral factors. We investigated the effect of adrenergic agents on the liberation of progesterone in the different stages of the oestrous cycle. To this end we placed the coeliac ganglion and the ovary in different compartments, connected through the SON, to produce a system being studied as a whole. Combined neural and hormonal (luteinising hormone (LH)) effects were also examined. Non-specific stimulation with KCl in the ganglion compartment evoked different responses in terms of release of progesterone, depending on the physiological conditions of the cycle; this demonstrated the sensitivity and viability of the system. During pro-oestrus, stimulation of the ganglion compartment with adrenergic agents such as the agonist noradrenaline or the beta-adrenergic antagonist propranolol, did not modify the release of progesterone. In contrast, the alpha-adrenergic antagonist, phentolamine, induced a strong inhibitory response. During the oestrous stage, noradrenaline was inactive, but phentolamine and propranolol exerted a strong stimulus throughout the experiment. On dioestrus day 1 (D1), both noradrenaline and propranolol increased the release of ovarian progesterone, whereas phentolamine had the opposite effect. Finally, on dioestrus day 2 (D2), what was noteworthy was the pronounced inhibitory effect of noradrenaline, whereas phentolamine was inactive and propranolol showed its greatest stimulatory effect. In order to compare the combined neural and endocrine effects on the ovarian release of progesterone, the experiment was carried out during stages D1 and D2, when the corpora lutea are at their peak of activity. Adrenergic agents were added to the ganglion and LH in a final concentration of 50 ng/ml was added to the ovarian comparment. Different effects were observed indicating a differential response to these agents in stimulated and basal conditions. We conclude that the in vitro coeliac ganglion-SON-ovary system is a functional entity because it possesses its own autonomic tone. This is verified because different basal values of progesterone appear in the different stages of the oestrous cycle. In similar fashion, variations of progesterone induced via the neural pathway were observed under different experimental conditions. In contrast, on D2, noradrenaline added to the ganglion compartment had an inhibitory effect on the liberation of ovarian progesterone. This would indicate that, during this phase, noradrenaline may not be the neurotransmitter released in the ovarian compartment, but that other inhibitory molecules might participate in the observed effects. Finally, during D2, the neural input would condition the ovarian response to LH, facilitating the decrease in progesterone necessary to start a new cycle. The experimental scheme is, in our opinion, a valuable tool for the study of peripheral neural participation in ovarian physiology.
Adrenergic Agents↗
Cold urticaria associated with intraoperative hypotension and facial edema.
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Adult↗
Illness-induced context aversion learning in rats with lesions of the dorsal hippocampus.
In 2 experiments, rats with electrolytic lesions of the dorsal hippocampus and sham-operated control subjects were given injections of lithium chloride after exposure to a distinctive context. This procedure establishes a context-illness association in intact subjects. In Experiment 1, the strength of the context aversion was assessed by measuring the subjects' willingness to consume a novel flavor in the context. It was found that lesioned subjects showed less suppression of consumption than controls. Experiment 2 tested the ability of the context to block subsequent flavor-aversion learning and revealed less effective blocking in lesioned rats. These results are consistent with the view that hippocampal lesions retard context conditioning; unlike previous work that has made use of conditioned freezing as the measure of context conditioning, the present results are not explicable in terms of lesion-induced changes in general activity.
Analysis of Variance↗
[Effect of adenohypophyseal pars tuberalis secretions on pars distalis prolactin liberation].
Evidences presented indicating that factors produced by the pars tuberalis (PT) affect the prolactin liberation by the pars distalis (PD). The effect of the secretion products of bovine PT cells in culture medium was checked on dispersed PD cells of rats. PD cells were assayed in incubations of 30 minutes and superfusion experiments. When medium was obtained from total PT cells, the addition of 9 micrograms of protein was needed to reach the major stimulation of prolactin liberation. However, when the medium from 50-60% Percoll gradient fractions was used, only 4 micrograms of total protein were required. The partial purification of such medium by Sephadex G50 produced the same effect on the liberation of prolactin by PD cells with 80 ng of total protein. The active factor/s should have a molecular weight higher than 30 kDal. The results obtained suggest, at least for the prolactotrophic cells, that PD could be the effector organ for some of the secretory product(s) of PT.
Animals↗
The NMDA-receptor antagonist ketamine as an unconditioned stimulus in taste aversion learning.
Three experiments studied the effectiveness of ketamine acting as an aversive unconditioned stimulus (UCS) in a conditioned flavor aversion procedure. In Experiment 1a, three conditioning trials where sucrose was paired with ketamine produced a weak but significant aversion to sucrose; Experiment 1b showed that this effect was not due to a reduced consumption of sucrose caused by ketamine-induced neophobia. In Experiment 2, acquisition of an aversion to sucrose paired with lithium chloride (LiCl) injections was retarded by prior repeated exposure to LiCl but not to ketamine. These results are not consistent with an interpretation of previous results, showing that ketamine impairs the acquisition of flavor aversions based on LiCl-induced illness, as an example of the UCS preexposure effect.
Animals↗
Effects of the NMDA receptor antagonist ketamine on flavor memory: conditioned aversion, latent inhibition, and habituation of neophobia.
In four experiments with rats, the effects of the NMDA antagonist ketamine on several forms of gustatory learning were studied. Replicating previous findings, in Experiment 1 ketamine was shown to impair one-trial acquisition of a flavor aversion at the dose of 25 mg/kg, but also produced a significant state-dependency effect. In Experiment 2 ketamine did not alter the process of habituation of neophobia to a new flavor. Abolition of latent inhibition by ketamine injected before preexposure in Experiment 3a was not replicated in Experiment 3b when ketamine was injected before all phases of the experiment. Finally, in Experiment 4 rats injected with ketamine showed slower acquisition of a flavor aversion with a multiple-trial procedure but finally reached a level similar to that shown by saline controls. The implications of these results for an interpretation of the effects of ketamine on flavor aversion learning in terms of interference with flavor memory storage are discussed.
Animals↗
Angiotensin II and glucocorticoid release: direct effect at the adrenal level and modulation of the adrenocorticotropin-induced glucocorticoid release.
Angiotensin II (A II) stimulates adrenal glomerulosa cells releasing mineralocorticoids; however, little is known about the A II effect on glucocorticoids output. The present study has been designed in order to see if A II could modify in vitro spontaneous and ACTH-induced corticosterone (B) release from both fasciculata-reticularis enriched and total adrenal cells. The results indicate that A II at 10(-12), 10(-11), 10(-10) and 10(-6) M concentrations did not modify basal B production and A II 10(-9), 10(-8) and 10(-7) M decreased basal B production from total adrenal cells. Whereas A II (10(-10)-10(-6) M) stimulated B release from fasciculata-reticularis enriched cells. On the one hand, 10(-8) M A II significantly decreased ACTH-elicited B release from total adrenal cells; effect completely abolished by saralasin (SAR, 10(-8) M), a specific A II receptor blocker. On the other hand, 10(-8) M A II did not modify ACTH-induced B release from fasciculata-reticularis enriched cells. Finally, 10(-10) to 10(-6) M A II and 22 pM ACTH stimulated aldosterone output from total adrenal cells; while, fasciculata-reticularis enriched cells did not secrete any measurable amount of aldosterone under basal condition and after incubation with A II. These data further suggest a regulatory role of A II in the release of glucocorticoids from the adrenal gland.
Adrenal Glands↗
Luteinizing hormone content of the pars tuberalis of the hypophysis of neonatally androgenized female rats.
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Animals↗
Effect of secretion of splenocytes after superior ovarian nerve section on the ovarian steroidogenesis.
It is known that ovary and spleen are innervated extensively by afferent and efferent noradrenergic sympathetic nerve fibers from the celiac ganglion. Furthermore, immune cells located in the ovary influence the ovarian physiology. However, the peripheral interaction between the immune and neuroendocrine system is poorly understood. This work was undertaken to study the effect of superior ovarian nerve (SON) transection, in adult rats, on the number of splenocyte beta-adrenergic receptors and their possible relation to ovarian steroidogenesis, measuring the effect of secretions of those splenocytes on progesterone and estradiol release from the ovary. Seven days after SON transection, the splenocytes were isolated and then cultured for 48 h. Their number of beta-adrenergic receptors, measured using [125I]-cyanopindolol as ligand, increased, and their culture media, used to stimulate ovaries from 60-day-old intact (neither SON-transected nor sham-operated) rats in vitro on diestrous day 2 showed a decrease in progesterone release and an increase in estradiol release in relation to splenocyte culture media of control rats (sham-operated; p < 0.001, respectively). The effects of in vivo SON transection were simulated by an in vitro system modulating the splenocyte beta-adrenergic receptor number. The splenocytes from SON-transectioned rats were preincubated with and without norepinephrine (NE) 10(-6) M for 48 h, a low and high number of beta-adrenergic receptors respectively, and then were stimulated with NE 10(-6) M for 24 h. After that, the culture medium from splenocytes with a low number of beta-adrenergic receptors induced progesterone release from the ovaries of intact rats (p < 0. 001), but produced no change in estradiol release. The data suggest that splenocyte secretions, which participate in the ovarian steroidogenic response, particularly in progesterone release, might be controlled by adrenergic influences since the number of splenocyte beta-adrenergic receptors changes through SON-celiac ganglion-noradrenergic postganglionic innervation of the spleen. In estradiol release, probably other neurotransmitters than norepinephrine (NE) are involved when the SON is sectioned. In this paper we also show functional evidence for modulation of immune function by the sympathetic nervous system and its principal neurotransmitter, NE.
Animals↗
[Cognitive processes and emotional brain systems].
AIMS: In this review we analyse the role of learning and memory processes in normal and pathological emotional phenomena from an integrating perspective that combines the behavioural, cognitive and neurobiological levels. We examine the most recent trends in research into the emotional systems of the brain, which provide important keys to understanding the nature of emotional phenomena. DEVELOPMENT: First, we discuss the existing evidence about the non conscious generation of affective responses, which come mainly from studies into Pavlovian fear conditioning. We then go on to analyse the relevance of the distinction between implicit and explicit memory in order to get a better understanding of the relations between cognition and emotion. The role played by the amygdala in the automatic evaluation of danger is considered a basic model for eliciting emotional responses. Finally, we describe how the interaction of the brain systems that the implicit and explicit aspects of emotional memory depend on provides an explanation for several characteristics of pathological anxiety, and we examine the positive or negative influences emotional activation can have on the consolidation of memory.
Amygdala↗