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    A Low Cost Amplifier And Acquisition System For Cortical-Electroncephalography In Non-Human Applications

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    A simple circuit is described to make an AC-amplifier and an analog-to-digital converter in a single, compact solution, for use in basic research, but not on humans. The circuit sends data to and is powered from a common USB port of modern computers; using proper firmware and driver the communication with the device is an emulated RS232 serial port

    Functional decortication lowers ventromedial hypothalamic activation induced by hippocampal neostigmine injection.

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    This experiment tested the effects of cortical spreading depression (CSD) on the ventromedial hypothalamic activity and on the related thermogenesis, both stimulated by an injection of neostigmine in the hippocampus. The firing rate of the neurons of the ventromedial hypothalamus, and the temperature of the interscapular brown adipose tissue and of the colon (T:(IBAT) and T:(C)) 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 (5 x 10(-7) mol) in the first and second groups or of saline in the third and fourth groups. The hippocampal injection was preceded by CSD in the first and third groups, while CSD was not induced in the second and fourth groups. The same procedure was carried out in the other four groups of six rats each and oxygen consumption was monitored. The results show an increase in the firing rate, T:(IBAT), T:(C) and oxygen consumption after the neostigmine injection. CSD significantly reduces these enhancements. The findings demonstrate that: (i) the activation of ventromedial hypothalamic neurons are involved in the thermogenic changes due to the effects of a neostigmine injection into the hippocampus; and (ii) integrity of cerebral cortex is required for this activation of thermogenesis

    Paradoxical [correction of parodoxical] effect of orexin A: hypophagia induced by hyperthermia.

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    This experiment tested the effect of the sympathetic and thermogenic activation induced by orexin A on eating behavior. The food intake, firing rate (FR) of the sympathetic nerves to interscapular brown adipose tissue (IBAT), IBAT and abdominal temperatures (T(IBAT) and T(ab)), and heart rate (HR) were monitored in 24 h-fasting male Sprague-Dawley rats for 15 h after food presentation. Orexin A (1.5 nmol) was injected into the lateral cerebral ventricle 6 h before food presentation while FR, T(IBAT) and T(ab), and HR were also monitored. The same variables were controlled in rats receiving orexin A contemporaneously to food presentation. Two other groups of control animals were tested with the same procedure, however orexin A was substituted by saline. The results showed that food intake was significantly lower in the group receiving orexin A 6 h before food presentation in comparison to all the other groups. FR, T(IBAT) and T(ab), and HR were significantly higher in the rats receiving orexin A with respect to rats receiving saline. These findings demonstrate that orexin A, so-called for its orexigen action, can also induce hypophagia. On the other hand, orexin A always induces an activation of the thermogenesis. These results suggest a revision of the role played by orexin A in the control of food intake, assigning to this peptide a primary role in the thermoregulation. The possibility that orexin A can induce hypophagia is well demonstrated by this experiment, so that the scientific community should use a different name for this peptide. An appropriate name could be 'hyperthermine' A

    Haloperidol reduces the sympathetic and thermogenic activation induced by orexin A.

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    This experiment tested the effect of haloperidol on the sympathetic and thermogenic effects induced by orexin A. The firing rates of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures and heart rate were monitored in urethane-anesthetized male Sprague-Dawley rats before and 5 h after an injection of orexin A (1.5 nmol) into the lateral cerebral ventricle. The same variables were monitored in rats with an intraperitoneal administration of haloperidol (1 mg/kg bw), a D(2) receptor antagonist. The results show that orexin A increases the sympathetic firing rate, IBAT and colonic temperatures and heart rate. This increase is reduced by the haloperidol. These findings suggest that dopaminergic system is activated during the orexin A-induced hyperthermia

    An aversive diet as thiamine-free food blocks food-induced release of excitatory amino acids in the accumbens.

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    As the nucleus accumbens shell plays an important role in the control of eating behaviour, the aim of this study was to evaluate the changes in: (a) the level of aspartic and glutamic acids in the accumbens shell of conditioned rats after the presentation of an aversive diet containing thiamine-free food; (b) the temperature of interscapular brown adipose tissue, effector of thermogenesis related to food intake.The concentration of aspartic and glutamic acids in the accumbens shell, and brown adipose tissue temperature were monitored in conditioned male Sprague-Dawley rats before and after the presentation of thiamine-free food or standard laboratory food. The aspartic and glutamic acids were collected using a microdialysis probe and quantified by HPLC. Food intake was also measured.The results indicated that an intake of standard laboratory food induced an increase in the level of aspartic and glutamic acids, and an elevation in temperature of brown adipose tissue; whereas an intake of thiamine-free food blocks these increases in the conditioned animals.The thiamine-free diet modifies the release of excitatory amino acids in the nucleus accumbens of conditioned animals. This diet also affects thermogenesis

    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
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