The first demonstration of how biochemical changes in neurons in specific parts of the brain direct a complete mammalian behavior derived from the effects of estrogens in hypothalamic neurons that facilitate lordosis behavior, the primary reproductive behavior of female quadrupeds (Pfaff. Estrogens and Brain Function. 1980; Pfaff. Drive: Neurobiological and Molecular Mechanisms of Sexual Motivation. 1999). Sex behaviors depend on sexual arousal that in turn depends on a primitive function: generalized CNS arousal (Pfaff. Brain Arousal and Information Theory. 2006). Here we summarize one of the ways in which a generalized arousal transmitter, norepinephrine, can influence the electrical excitability of ventromedial hypothalamic cells in a way that will foster female sex behavior.

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Femur bone densities and tibialis anterior muscle properties of type II collagen-induced arthritic mice were determined. Furthermore, voluntary running activities of arthritic mice were compared with those of controls. Arthritis was induced by an intradermal injection of type II collagen in the adjuvant. Body and muscle weights were lower in arthritic mice than in controls. Cortical and trabecular bone densities and muscle fiber cross-sectional areas were decreased by arthritis. After classifying the arthritic severity into slight, intermediate, and severe levels based on the degree of knuckle swelling, cortical and trabecular bone densities, fiber cross-sectional areas, and fiber succinate dehydrogenase activities were lowest when arthritis was most severe. Furthermore, arthritic mice, especially those with intermediate and severe levels, showed lower voluntary running activities. These findings indicate that lower bone density and muscle atrophy of type II collagen-induced arthritic mice are related to arthritic severity and decreased motor activity.

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We investigated the effects of NT-702, a selective phosphodiesterase (PDE) 3 inhibitor, on arterioles isolated from rabbit lumbar spinal cords. NT-702 caused a dose-dependent dilation of the isolated spinal arterioles. The disruption of endothelium produced a significant reduction of higher concentrations (10^–7 and 10^–6 M), but not lower concentrations (less than 10^–8 M), of NT-702–induced vasodilation. The NT-702–induced vasodilation of the arterioles with endothelium was not affected by pretreatment with an inhibitor of nitric oxide, cyclooxygenase, or cytochrome P-450 monooxygenase. In contrast, catalase reduced significantly the higher concentrations of NT-702–induced vasodilation only. Tetraethylammonium (TEA) completely reduced the lower concentrations of NT-702–induced vasodilation, but decreased only partially the higher concentrations of NT-702–induced vasodilation of the arterioles with endothelium. Hydrogen peroxide dilated significantly the isolated arterioles with endothelium, the response of which was reduced significantly by TEA. KT5720 (a selective protein kinase inhibitor) significantly decreased both the lower and higher concentrations of NT-702–induced vasodilation of the arterioles with endothelium. The findings suggest that NT-702 dose-dependently dilated the isolated spinal arterioles of rabbits via endothelium-dependent and endothelium-independent mechanisms. Protein kinase A (PKA)- and TEA-sensitive K⁺ channels may be involved in the NT-702–induced vasodilation. Moreover, hydrogen peroxide may contribute in part to the endothelium-dependent higher concentrations of NT-702–induced vasodilation.

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The embedding dimensions of normal and epileptic electroencephalogram (EEG) time series are analyzed by two different methods, Cao’s method and differential entropy method. The results of the two methods indicate consistently that the embedding dimensions of EEG signals during seizure will change and become different from that of normal EEG signals, and the embedding dimensions will vary intensively during seizure, whereas the embedding dimensions of normal EEG signals basically maintains stability. The embedding dimension results also reflect the variation of freedom degree of the human brain nonlinear dynamic system (NDS) during seizure. And based on the results of Cao’s method, it is also found that normal EEG signals are of some degree of randomness, whereas epileptic EEG signals have determinism.

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We investigated the pivotal roles of glucose and its transporter in the regulation of mechanical activity of isolated rat thoracic ducts and then examined whether mitochondrial ATP-sensitive K⁺ channels (mitoK_ATP) are involved in those responses. In the absence of extracellular glucose, the thoracic ducts showed pump activity during 120 min. Extracellular glucose caused a dose-dependent increase in the frequency of pump activity and a constriction in the thoracic ducts. Pump activity of the thoracic ducts in 0 mM glucose was completely inhibited in the presence of chlorogenic acid (an inhibitor of glucose-6-phosphatase). Cytochalasin B, an inhibitor of facilitative glucose transporter (GLUT), or phlorizin, an inhibitor of sodium-dependent glucose cotransporter (SGLT), significantly reduced the frequency of pump activity and dilated the thoracic ducts. A decrease in the frequency of pump activity induced by 5-hydroxydecanoate (5-HD, a selective blocker of mitoK_ATP) was completely reversed by ruthenium red (an inhibitor of Ca²⁺ uniporter in mitochondria). Diazoxide (a selective opener of mitoK_ATP) significantly increased the frequency of pump activity. Carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP, a protonophore of mitochondrial proton pump action) significantly reduced the frequency of pump activity and dilated the thoracic ducts. Collectively, these findings suggest that glucose derived from intracellular glycogen and/or through GLUT/SGLT in lymphatic smooth muscles contributes to the regulation of the pump activity of isolated rat thoracic ducts, and that mitoK_ATP in the cells may partially serve as a modulator of the mechanical functions associated with mitochondrial Ca²⁺ uptake.

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In urethane-anesthetized, artificially ventilated rats, alterations in dorsal spinal cord blood flow (SCBF) at the L4–6 level were measured with laser Doppler flowmetry in response to noxious mechanical cutaneous stimulation (pinching) of either a forepaw or a hindpaw. The stimulation was delivered ipsilaterally or contralaterally to the site of blood flow measurement. Pinching of the forepaw or the hindpaw on either side increased mean arterial pressure (MAP) to the same degree. However, the SCBF response to pinching of the ipsilateral hindpaw was significantly greater than that to other stimulations. These responses were not influenced by denervation of the baroreceptors. The responses of SCBF to pinching of the ipsilateral hindpaw persisted both after treatment with phenoxybenzamine and after spinalization at the C1–2 level, whereas the responses to pinching at other sites disappeared. The responses of MAP to stimulation at all four sites became negligible after treatment with phenoxybenzamine and after spinalization at the C1–2 level. These results indicate that noxious mechanical stimulation of the skin produces increases in SCBF via two mechanisms: one is via an elevation of systemic arterial pressure; the other is via a localized spinal mechanism evoked by ipsilateral, segmental inputs.

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Daily rhythmicity of physiological processes has been described for numerous variables in numerous species. A major source of this rhythmicity is a circadian pacemaker located in the mammalian hypothalamus, but very little is known about how the pacemaker generates the multiplicity of bodily rhythms. Research on rats has shown that the rhythm of blood glucose concentration is not a mere consequence of the rhythm of food ingestion, but is rather generated directly by the pacemaker. In this study, we investigated the rhythm of blood glucose concentration in four different species of domestic animals under four different feeding regimes. Our results suggest that, as in rats, the rhythm of blood glucose concentration is not a mere consequence of the rhythm of food ingestion in sheep and cattle. In dogs and horses, however, the rhythmicity of blood glucose concentration seems to be contingent on the presence of a feeding regime.

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We recently demonstrated that rat cerebellar Type-1 astrocytes express a very active Na⁺/Ca²⁺ exchanger highly colocalized with ryanodine receptors (RyRs), which in turn play a key role in glutamate-induced Ca²⁺ signaling through a calcium-induced calcium release (CICR) mechanism. In this work we have explored whether the Na⁺/Ca²⁺ exchanger has any role in the Ca²⁺ _i signal induced by hypo-osmotic stress in these cells, using microspectrofluorometric measurements with Fura-2, pharmacological tools, and confocal microscopy image analysis. We present evidence for the first time that the increase in [Ca²⁺]_i in rat cerebellar Type-1 astrocytes, resulting from moderate hypotonic shock, is mediated by Ca²⁺ release from ryanodine-operated Ca²⁺ _i stores, and that the magnitude of the intracellular Ca²⁺ signal induced by hypotonicity in the short term (up to 240 s) is small and controlled by the activity of the Na⁺/Ca²⁺ exchanger operating in its extrusion mode. With longer times in the hypotonic medium, intracellular Ca²⁺ store depletion leads to Ca²⁺ entry through store-operated Ca²⁺ channels. We found it interesting that the activity of the Na⁺/Ca²⁺ exchanger measured during this reverse mode operation (Ca²⁺ entry in exchange for internal Na⁺) was found to be greatly increased in hypotonic solutions and decreased in hypertonic ones. The buffering of the [Ca²⁺] _i rise induced by hypo-osmotic stress may prevent excessive increases in [Ca²⁺]_i, which otherwise might impair the normal function of this glial cell.

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Incremental exercise testing to a symptom-limited maximum has been used to measure the ratio of the increase in ventilation (VE) to the increase in CO₂ output (VCO₂) during exercise (VE/VCO₂ slope), a valuable index reflecting the severity of the ventilation-perfusion mismatch in heart failure. Here we studied whether this same value for the slope of VE/VCO₂ could be determined from a short constant work-rate exercise test of moderate intensity. Twenty-three patients with a previous myocardial infarction underwent moderate-intensity (69 ± 15 W) constant work-rate exercise for 6 min and an incremental work-rate exercise test to the max. The VE/VCO₂ slope was calculated from the incremental exercise test from the start of increasing the work-rate to the ventilatory compensation point. The VE/VCO₂ slope was similarly calculated from the start of constant work-rate exercise until the 4th minute, when VE and VCO₂ changed minimally. The VE/VCO₂ slope determined from incremental exercise was 33.8 ± 5.9, ranging from 20.9 to 42.8. The slope obtained from constant work-rate exercise was 32.9 ± 5.7. The VE/VCO₂ slopes obtained from the two exercise tests did not differ significantly. The slope obtained from constant work-rate exercise was significantly positively correlated with the slope obtained from the incremental exercise (r = 0.84, p < 0.0001). The VE/VCO₂ slope can be determined from constant work-rate exercise at a moderate intensity. This indicates that the relationship between ventilation and CO₂ output is consistent and independent of the mode of exercise testing.

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