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    Aspartic and glutamic acids increase in the frontal cortex during prostaglandin E1 hyperthermia.

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    The aim of the present experiment was to evaluate the role played by aspartic acid and glutamic acid of frontal cerebral cortex during the hyperthermia induced by prostaglandin E1. Two groups of six Sprague Dawley male rats were anaesthetized with ethyl-urethane. The frontal cortical concentrations of aspartic and glutamic acids, the firing rate of the sympathetic nerves to the interscapular brown adipose tissue, the colonic and interscapular brown adipose tissue temperatures were monitored both before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Aspartic and glutamic acids were collected using a microdialysis probe placed in the frontal cortex. Concentrations of aspartic and glutamic acids were measured by high-pressure liquid chromatography with fluorescence detector. Prostaglandin E1 induced an increase in the concentrations of aspartic and glutamic acids, in the firing rate of sympathetic nerves and in the colonic and interscapular brown adipose tissue temperatures. The findings of the present experiment indicate that an intracerebroventricular injection of prostaglandin E1 causes release of aspartic and glutamic acids in the frontal cortex

    Nitric oxide reduces hypophagia induced by threonine free diet in the rat.

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    Food intake and concentrations of glutamic (GLU) and aspartic (ASP) acids in the nucleus accumbens were monitored in male Sprague-Dawley rats fed a threonine free diet. These variables were measured before and after an intracerebroventricular injection of 20 nmole nitroprusside (NP), a non-enzymatic nitric oxide donor. The same variables were also monitored in: (a) rats fed a threonine free diet and injected with saline; (b) animals fed a standard diet and injected with nitroprusside; (c) rats fed a standard diet and injected with saline. The results showed that the threonine-free diet reduced food intake and GLU and ASP concentrations in the accumbens. NP reduced the hypophagia, but it did not change GLU and ASP levels in rats fed the threonine-free diet. In animals fed the standard diet, NP increased GLU and ASP concentration, and food intake. No change was found in the animals with saline injection. These findings suggest that nitric oxide reduces the hypophagia in the rats fed a threonine-free diet. The lack of increase in GLU and ASP concentration in the nucleus accumbens of the hypophagic rats indicates that NP acts on hypophagia independently by GLU and ASP

    Procaine injection into the paraventricular nucleus reduces sympathetic and thermogenic activation induced by frontal cortex stimulation in the rat.

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    These experiments were designed to test the effect of procaine injection into the paraventricular nucleus on the sympathetic and thermogenic changes induced by frontal cortex stimulation. Oxygen consumption, firing rate of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (T(IBAT) and T(C)) were monitored in fasted male Sprague-Dawley rats before and 25 min after an electrical stimulation of the frontal cortex. The same variables were monitored in rats with administration of procaine into the paraventricular nucleus. The results show that cortical stimulation raises oxygen consumption, sympathetic neuron firing rates, T(IBAT), and T(C). This increase is reduced by procaine injection. These findings suggest that the paraventricular nucleus plays a key role in the sympathetic and thermogenic changes induced by cortical stimulation

    Ibotenate lesion of the ventromedial hypothalamus lowers hyperthermic effects of prostaglandin E1.

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    This experiment tested the effects of an intracerebroventricular injection of prostaglandin E1 on the sympathetic activation and the thermogenic changes in rats with ibotenate lesions of the ventromedial hypothalamus. Under pentobarbital anesthesia, twelve Sprague-Dawley male rats were lesioned bilaterally in the ventromedial hypothalamus with an injection of ibotenic acid (30 nmol into each side). Sham lesions were carried out in other twelve control rats. After 48 h, all animals were anesthetized with ethyl-urethane. The firing rate of the sympathetic nerves innervating the interscapular brown adipose tissue and the colonic and interscapular brown adipose tissue temperatures were monitored before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Prostaglandin E1 induced an increase in the firing rate of sympathetic nerves and the colonic and interscapular brown adipose tissue temperatures. These effects were reduced by the ventromedial hypothalamic lesion. Since ibotenic acid destroys cell bodies, the findings indicate that neurons of the ventromedial hypothalamus play a considerable role in the control of sympathetic activation and the thermogenic changes during prostaglandin E1 hyperthermia

    Sucrose rich diet modifies thermogenic response to injection of muscimol into the posterior hypothalamus in the rat.

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    The firing rate of the nerves innervating interscapular brown adipose tissue, temperatures of colon and interscapular brown adipose tissue, heart rate and oxygen consumption were monitored in urethane-anaesthetized male Sprague-Dawley rats fed with a sucrose rich diet. These variables were measured for 40 min before (baseline values) and 40 min after a 56 ng muscimol injection into the posterior hypothalamus. The same variables were monitored in other rats fed with a laboratory standard diet. Saline was injected into the posterior hypothalamus of control rats fed with sucrose or standard diet. Muscimol injection induced a decrease in firing rate, interscapular brown adipose tissue and colonic temperatures and oxygen consumption. This reduction was more evident in the rat fed with a sucrose rich diet than animals fed with standard diet. The kind of diet did not modify the decrease in heart rate induced by muscimol. These findings suggest that a sucrose rich diet modifies GABA-ergic responses to muscimol injection into the posterior hypothalamus

    Cortical spreading depression reduces paraventricular activation induced by hippocampal neostigmine injection.

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    The firing rate of the neurons of the hypothalamic paraventricular nucleus, the temperatures of the interscapular brown adipose tissue and of the colon (TIBAT and Tc) were monitored in 24 urethane-anesthetized male Sprague-Dawley rats divided into four groups. These variables were measured before and after hippocampal injection of neostigmine (5x10(-7) mol) in the 1st and 2nd groups or of saline in the 3rd and 4th groups. The hippocampal injection was preceded by cortical spreading depression in the 1st and 3rd groups, while the cortical depression was not induced in the 2nd and 4th groups. The results show an increase of firing rate, TIBAT and Tc after neostigmine injection in the rats without cortical depression. Cortical spreading depression significantly reduces these enhancements. These findings demonstrate that: (1) the paraventricular nucleus plays a significant role in the hyperthermia induced by neostigmine injection into the hippocampus; and (2) the cerebral cortex is involved in the control of the paraventricular activity

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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