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PubMed1997

[Surgical metabolism].

Trauma, operative interventions, infection and other disturbances of homeostasis lead to a uniform reaction of the body, namely release and activation of hormones and cytokines. Profound alterations of substrate flow result, with mobilization of energy stores and degradation of structural and functional proteins of vital organs like the gut mucosa. Due to these reactions the energy demands of the organs are met and energy-consuming synthesis of substrates is indicated. Clinically, hypermetabolism, hyperglycemia, lipolysis and increased urea production with negative nitrogen balance can be observed. The metabolic reactivity is reached by an increased substrate cycling. To avoid negative consequences such as organ dysfunction, a rational situation-adapted substrate supply is warranted as well as reduction of catabolic stimuli and stimulation of anabolic factors. The metabolic care of the surgical patient is still a basic and important task.

Energy Metabolism↗
PubMed1990

Altered arachidonic acid metabolism during differentiation of the human monoblastoid cell line U937.

The human cell line U937 was used as a model for differentiation along the mononuclear phagocyte lineage. Following treatment with the phorbol ester TPA, PGE2 and TxB2 secretion was induced 50-100-fold, and both PGF2 alpha and PGI2 levels became detectable in the supernatant of TPA-differentiated U937 cells. The content of the prostaglandin precursor, arachidonic acid, remained unchanged in the cellular phospholipids of undifferentiated and TPA-differentiated U937 cells. Of the enzymes involved in the availability and metabolism of arachidonic acid, phospholipase A2 activity was increased 2-fold in the membranes of TPA-differentiated U937 cells, whereas lysophosphatide acyltransferase activity remained unaltered. Cyclooxygenase activity, however, was enhanced 5-10-fold, which was due to enhanced expression of the enzyme as demonstrated by dot-blot analysis. The data suggest that the capacity to secrete prostaglandins is acquired during differentiation with TPA and results mainly from an increased cyclooxygenase activity. Despite the capacity of TPA-differentiated U937 cells to synthesize prostaglandins, none of the known monocytic stimuli further stimulated prostaglandin secretion in TPA-differentiated U937 cells. Generation of leukotrienes appears to represent a later state in the differentiation along the monocyte-macrophage lineage, since neither LTB4 nor cysteinyl-leukotrienes were detectable in the supernatants of either undifferentiated or TPA-differentiated U937 cells.

Arachidonic Acid↗
PubMed1982

The effect of digital nerve stimulation on recruitment order of motor units in the first deep lumbrical muscle of the cat.

The normal recruitment order of EMG spikes of the first deep lumbrical muscle of the cat's hindpaw, usually seen during cortical stimulation, pad pinch and weak plantar nerve stimulation, was temporarily reversed after stimulation of the medial digital nerve of the foot at 50 Hz for 2 min, and normal order was recovered in 2 to 10 min. The longer the period of stimulation of the medial digital nerve was, the longer the time for recovery. Alteration of order is repeatable and reversible after an interval of more than 15 min. After prolonged medial digital nerve stimulation, EMG responses to pad pinch and plantar nerve stimulation were facilitated. Combination of some stimuli (e.g. cortical stimulation and plantar nerve stimulation, pad pinch and plantar nerve stimulation, plantar nerve and medial digital nerve stimulation) also produced reversal of recruitment order during the period of stimulation. A functionally single motor nerve fiber to the first deep lumbrical muscle was isolated from the motor nerve axons in L7 and S1 of the spinal cord of cats, and physiological properties of pairs of motor units whose recruitment order was temporarily altered by plantar nerve stimulation after prolonged stimulation of the medial digital nerve of a foot were examined. Motor units with large action potentials were more facilitated than motor units with small action potentials after prolonged stimulation of the medial digital nerve. The former motor units showed fast contraction time, large twitch tension, low resistance to fatigue and presence of sag-behavior. The latter motor units showed slow contraction time, small twitch tension and high resistance to fatigue. High threshold motor units with middle-sized surface EMG records were recruited after motor units with large potentials had been recruited; motor units with middle-size action potentials were beta motor axons branching to both intrafusal and extrafusal muscle fibers. The beta motor axons also showed fast conduction velocity and the presence of sag-behavior.

Animals↗
PubMed1991

Efferent projections of pulmonary rapidly adapting receptor relay neurons in the cat.

Axonal projections of second order neurons activated by vagal afferent fibers originating from pulmonary rapidly adapting receptors (RARs) were studied electrophysiologically in Nembutal-anesthetized, paralyzed and artificially ventilated cats. Extracellular recordings from these neurons (referred to as 'RAR-cells') were made in the commissural subnucleus (COM) of the nucleus of the solitary tract (NTS). They were identified by a combination of stimuli including stimulation of the vagus nerve(s), hyperinflation and deflation of the lungs, and a brief period of ammonia vapor inhalation. A total of 80 RAR-cells were tested for axonal projections to a respiration-related area in the brain-stem, either the dorsolateral rostral pons or the dorsal respiratory group (DRG) or the ventral respiratory group (VRG) or the Bötzinger complex (BOT) and/or the spinal cord. Twenty-two of the 47 (47%) RAR-cells tested for ipsilateral pontine projection could be antidromically activated, and in 8 cases evidence for axonal arborization was obtained. Only 1 of the 11 RAR-cells tested for DRG projection, and 1 of the 10 RAR-cells tested for VRG projection, were antidromically activated. No RAR-cells were activated from the BOT (n = 8) or from the C3-C4 segments of the spinal cord (n = 11). Bilateral lesions of the COM abolished the reflex responses induced by ammonia inhalation or hyperinflation of the lungs, but not the Hering-Breuer reflex. These results indicate that a pathway from the COM to the rostral pons forms part of the reflex arc originating from RARs.

Animals↗
PubMed1976

Electroencephalographic synchronization induced by stimulation of small intestine and splanchnic nerve in cats.

1. In freely moving cats, the cortical desynchronization elicited by painless rhythmic distension, or by low voltage electric stimulation, of the small intestine in drowsiness and slow wave sleep is extinguished following a few repetitions. After extinction of the arousal reaction, similar intestinal stimulation was systematically followed by the appearance of synchronized activity, or an increase of spontaneous synchronization, in the explored cortical areas (parieto-occipital). 2. Intestinal or splanchnic stimulation at an intensity below threshold for cortical desynchronization immediately induced synchronized activity without any need of previous repetitions of stimulation. 3. Stimuli which were followed by synchronization excited only the large (Abeta) splanchnic afferents. The authors conclude that intestinal receptors may be one of the sources of synchronizing influence which can contribute to the regulation of the sleep-wakefulness cycle and that the large splanchnic afferents may play a role in the induction of synchronization.

Afferent Pathways↗
PubMed1976

Eectroencephalogram in "locked-in" syndrome.

Twenty-three EEG studies in eight patients with "locked-in" syndrome were reviewed. The EEG was either normal or minimally slow in all except one patient. All showed reactivity to various stimuli. Photic stimulation elicited a photic driving response at one time or another in all the seven patients where it was attempted. Althouth the basic activity may be similar, it is the preservation of alertness and the presence of reactivity of the EEG which distinguishes the "locked-in" patients from those comatose due to an extensive brain stem lesion. In an unresponsive patient, an EEG resembling that of the waking state, although highly suggestive of an intrinsic brain stem insult, may also occur at times in association with diffuse cortical damage, secondary to prolonged cardio-pulmonary arrest.

Akinetic Mutism↗
PubMed1988

Neurogenic stimuli alter preoptic area and amygdala unit activity: central effects of olfactory projections on paraventricular nucleus units.

Unit responses were recorded in the preoptic area and amygdala of conscious male rats during exposure to stressful neurogenic stimuli. Olfactory stimulation elicited increases in preoptic area activity on all occasions and also increased activity in the intercalating, medial, and basomedial nuclei of the amygdala, but not in other regions. Acoustic stimulation had less specific effects, even inhibiting unit activity in the central amygdala. A separate series of experiments using urethane-anesthetized rats was carried out to examine the effects of electrical stimulation of the medial amygdala and olfactory tubercle on single-unit activity within the hypothalamic paraventricular nucleus. Inhibition was the predominant response following olfactory tubercle stimulation while excitatory responses predominated following stimulation of the medial amygdala. This was the case particularly for those paraventricular nucleus units identified as projecting to the median eminence (P less than 0.005 vs unidentified cells). The results obtained may be related to the neural regulation of adrenocortical activity as well as higher central nervous activity and have been discussed within these contexts.

Acoustic Stimulation↗
PubMed1991

The fate of human polymorphonuclear leukocyte aminopeptidases upon cell stimulation with phagocytic and chemical stimuli.

1. After being treated with nonopsonized zymosan A or phorbol-12-myristate-13-acetate, human polymorphonuclear leukocytes release aminopeptidases together with granules marker-enzymes and vitamin B12-binding protein. 2. Chemotactic peptide, fMet-Leu-Phe and its analogs, fMet-Phe, fMet-Ala and fMet-Leu-Phe-Lys have a similar effect. 3. By their isoelectric point determinations the released aminopeptidases correspond to the enzymes from granules. Among aminopeptidases released the highest activities were those toward methionine- and alanine-2-naphthylamide and the lowest one toward arginine-2-naphthylamide.

Aminopeptidases↗
PubMed1986

The calcium sensitive dehydrogenases of vertebrate mitochondria.

Three important dehydrogenases in vertebrate mitochondria are activated by Ca2+ ions with half-maximal effects at about 1 microM. These are pyruvate dehydrogenase, NAD+-isocitrate dehydrogenase and 2-oxoglutarate dehydrogenase. Activation of these enzymes can also be demonstrated within intact mitochondria when extramitochondrial Ca2+ is increased within the range of concentrations generally considered to occur in the cytoplasm of vertebrate cells. It is argued that the main role of the calcium transport system in the inner membrane of vertebrate mitochondria is to relay changes in the cytoplasmic concentration of Ca2+ into the mitochondrial matrix. In this way, hormones and other extracellular stimuli which stimulate ATP-requiring processes such as contraction and secretion through increases in the cytoplasmic concentration of Ca2+ may also increase intramitochondrial oxidative metabolism and hence the replenishment of ATP.

Adenosine Triphosphate↗
PubMed1987

Increases in plasma catecholamines during naturally elicited defensive behavior in the cat.

Defensive behavior was evoked in 12 adult cats by the presentation of both interspecific (barking dog) and intraspecific (hypothalamically stimulated cat) stimuli. Each stimulus was presented 3 times. Concomitant activation of the sympatho-adrenal (SA) system was evaluated by radioenzymatic assay of plasma norepinephrine (NE) and epinephrine (E). The somatic and autonomic displays which accompanied defensive behavior were similar between stimuli, consisting of mydriasis, piloerection, growling, hissing and paw strikes. However, the sympatho-adrenal responses associated with interspecific and intraspecific defensive behaviors were different. Interspecific defensive behavior was accompanied by adrenal medullary release of both NE and E, which decreased with successive trials. Intraspecific defensive behavior was initially associated with release of E from the adrenal medulla; the pattern of catecholamine release in successive trials suggested that in later trials NE was released primarily from the sympathetic nerves. Furthermore, increases in plasma NE and E, as well as increases in heart rate and mean arterial blood pressure during the first trial were significantly greater when the behavioral stimulus was a dog. Although aspects of the feline display to threatening stimuli are stereotyped, the data suggest that the sympatho-adrenal response is more specific, and indicates preparation for fighting or escape.

Animals↗
PubMed1992

Adenosine A2 receptor antagonist facilitates the reversal of long-term potentiation (depotentiation) of evoked postsynaptic potentials but inhibits that of population spikes in hippocampal CA1 neurons.

The effects of the adenosine A2 receptor antagonist CP-66713 on the reversal of long-term potentiation (LTP) were studied in CA1 neurons of guinea pig hippocampal slices. Reduction of LTP (depotentiation, DP) was effected by delivering a train of low-frequency afferent stimuli (depotentiation stimulation, DPS) which was given 20 min after tetanus (100 Hz, 100 pulses). DPS (1 Hz, 1000 pulses) was applied during perfusion of CP-66713 (10 microM). In the presence of CP-66713, DPS reduced the potentiated component of the slope of the field EPSP (S-EPSP) and the amplitude of the population spike (A-PS) by 101.7% and 19.1% of the potentiated amount, respectively (mean, n = 8). The reduction of LTP of the S-EPSP was significantly larger than the control (68.5% (mean, n = 6)) while that of the A-PS was significantly smaller than the control (80.1% (mean, n = 6)). Based on these results, we conclude that the inhibition of DP in the EPSP, the facilitation of DP in the PS, and the consequent attenuation in the EPSP-PS relationship follow from activation of adenosine A2 receptors.

Animals↗
PubMedDate not supplied

Potassium-depolarization induces motility in isolated outer hair cells by an osmotic mechanism.

Outer hair cells in vitro contract in response to various stimuli: electrical stimulation, K+-depolarization, elevation of intracellular calcium or osmotic changes of the extracellular medium. The characteristics of motile responses induced by K+-depolarization, osmotic changes, and calcium injection were compared in this study in order to delineate the underlying mechanisms. Slow shape changes in outer hair cells were induced by changes of the osmolality or the K+/Na+-ratio of the bathing medium, or by intracellular injections of calcium. K+- and osmotically induced contractions of isolated outer hair cells had identical morphological features and the same rate (50-200 nm/s) and amplitude (up to greater than 10% of original length) of shortening. The shortening of the cells was linearly related to an increase in volume in both cases. In contrast, the active contraction induced by Ca2+/ATP exhibited a somewhat faster rate and no increase in volume. Furthermore, the K+-induced contractions in outer hair cells, unlike those reported in smooth muscle cells, were unaffected by the removal of external Ca2+ (i.e. medium without Ca2+/Mg2+ and supplemented with 1 mM EGTA) or the presence of D600, an inhibitor of the Ca2+ inward current. The results strongly suggest that K+ induces shape changes of outer hair cells via osmotic forces and that intracellular calcium mediates contractions by a different mechanism.

Adenosine Triphosphate↗
PubMed1992

SRC-related proto-oncogenes and transcription factors in primary human T cells: modulation by cyclosporin A and FK506.

Activation of T lymphocytes induces transcription of genes encoding for lymphokines. Interleukin-2 (IL-2) gene expression is controlled transcriptionally by the cooperative activity of specific trans-activating factors that bind to the IL-2 enhancer. Cyclosporin A (CsA) and FK506 inhibit the production of IL-2 in T lymphocytes at the level of gene transcription. A member of the src gene family, the lymphocyte-specific protein tyrosine kinase, p56lck, has been implicated in IL-2 production. CsA was found not to inhibit lck gene expression, nor the activity of the lck gene product. However, CsA and FK506 inhibit the appearance of DNA binding activity of factors that bind to the NF-AT and AP-1 sites in the IL-2 enhancer. Since the induction of NF-AT and AP-1 is induced by the same stimuli that stimulate IL-2 production, these results indicate that the immunosuppressant action of CsA and FK506 is exerted at the level of these trans-activating factors.

Blotting, Northern↗
PubMed1992

Antidepressant treatment prevents chronic unpredictable mild stress-induced anhedonia as assessed by ventral tegmentum self-stimulation behavior in rats.

The effect of chronic unpredictable mild stress on sensitivity to reward was evaluated using the brain self-stimulation procedure. Rats were allowed to electrically self-stimulate the ventral tegmental area, one of the main cerebral structures subserving positive reinforcement. Stimulation thresholds (frequency of stimuli) for self-stimulation responses were determined prior to, during, and following a 19-day period of exposure to a variety of mild unpredictable stressors. Stimulation threshold was increased in stressed rats, suggesting a decrease in the rewarding properties of brain stimulation. This deficit became evident after about 1 week of mild stress, lasted throughout the stress period, and progressively diminished following termination of the stress regime. In stressed rats concomitantly treated with the tricyclic antidepressant desipramine (5 mg/kg b.i.d.), no stress-induced increase in self-stimulation threshold was observed. However, desipramine did not modify self-stimulation threshold in non-stressed animals. Thus, the increased threshold for brain self-stimulation produced by a period of chronic unpredictable mild stress can be completely prevented by concomitant antidepressant treatment and may provide an heuristic animal model of depression.

Animals↗
PubMed2006

Effects of medial amygdala inactivation on a panic-related behavior.

In the last years, the role played by the medial nucleus of the amygdala (MeA) in the modulation of fear- and anxiety-related behaviors has been increasingly investigated. This nucleus plays an important role in the processing of predator odor-induced defensive reactions, i.e. freezing and risk-assessment behaviors. Immunohistochemical evidence also indicates that the MeA may be involved in the regulation of escape, a defensive behavior related to panic attacks. In this study, we further addressed this question by investigating the effects of the reversible inactivation of the nucleus on escape behavior generated in male Wistar rats by two different aversive stimuli, electrical stimulation of the dorsal periaqueductal gray matter (dPAG) and exposure to one of the open arms of the elevated T-maze. Results showed that intra-MeA administration of either the reversible sodium channel blocker lidocaine (34 nmol/0.2 microl) or the GABA(A) receptor agonist muscimol (0.22 nmol/0.2 microl) raised the threshold of aversive electrical stimulation, increasing the amount of current that applied to the dPAG evokes escape, an antiaversive effect. Local microinjection of muscimol (0.22 nmol/0.2 microl) inhibited escape behavior in the elevated T-maze, also suggesting an antiaversive effect. In this latter test, muscimol did not affect inhibitory avoidance, a behavior associated with generalized anxiety disorder. Muscimol effect in the elevated T-maze was independent of changes in general exploratory activity as measured in an open-field. Taken together, our data corroborate previous evidences suggesting that the MeA is involved in the modulation of escape. Dysfunction of this regulatory mechanism may be of relevance in the genesis/maintenance of panic disorder.

Amygdala↗
PubMed2005

Seizures induce proliferation and dispersion of doublecortin-positive hippocampal progenitor cells.

One neuropathological hallmark of temporal lobe epilepsy is granule cell dispersion, a widening of the hippocampal granule cell layer (GCL) with abnormally positioned excitatory neurons. The finding that seizure activity also induces adult hippocampal neurogenesis was taken largely as indicative of a regenerative attempt, not as part of the pathology. The aim of our study was to characterize a potential relationship between granule cell dispersion and seizure-induced neurogenesis. Kainic acid (KA)-induced seizures in mice led to increased cell proliferation and new neurons persisted for months after the seizures. We show that the proliferative stimulus did not affect nestin-expressing early precursor cells that primarily respond to physiologic mitogenic stimuli, but stimulated the division of late type-3 progenitor cells, which express doublecortin (DCX), a protein associated with cell migration. This delayed proliferation presumably interfered with migration, leading to a significant dispersion of DCX-positive progenitors and early postmitotic neurons within the dentate gyrus granule cell layer. We propose that initial seizures induce ectopic precursor cell proliferation resulting in the dispersion of immature neurons within the adult granule cell layer. Thus, seizure-generated neurons might contribute to the disease process of epilepsy.

Analysis of Variance↗
PubMed2006

Hypoxia-induced fatty acid transporter translocation increases fatty acid transport and contributes to lipid accumulation in the heart.

Protein-mediated LCFA transport across plasma membranes is highly regulated by the fatty acid transporters FAT/CD36 and FABPpm. Physiologic stimuli (insulin stimulation, AMP kinase activation) induce the translocation of one or both transporters to the plasma membrane and increase the rate of LCFA transport. In the hypoxic/ischemic heart, intramyocardial lipid accumulation has been attributed to a reduced rate of fatty acid oxidation. However, since acute hypoxia (15 min) activates AMPK, we examined whether an increased accumulation of intramyocardial lipid during hypoxia was also attributable to an increased rate of LCFA uptake as a result AMPK-induced translocation of FAT/CD36 and FABPpm. In cardiac myocytes, hypoxia (15 min) induced the redistribution of FAT/CD36 from an intracellular pool (LDM) (-25%, P<0.05) to the plasma membranes (PM) (+54%, P<0.05). Hypoxia also induced an increase in FABPpm at the PM (+56%, P<0.05) and a concomitant FABPpm reduction in the LDM (-24%, P<0.05). Similarly, in intact, Langendorff perfused hearts, hypoxia induced the translocation of a both FAT/CD36 and FABPpm to the PM (+66% and +61%, respectively, P<0.05), with a concomitant decline in FAT/CD36 and FABPpm in the LDM (-24% and -23%, respectively, P<0.05). Importantly, the increased plasmalemmal content of these transporters was associated with increases in the initial rates of palmitate uptake into cardiac myocytes (+40%, P<0.05). Acute hypoxia also redirected palmitate into intracellular lipid pools, mainly to PL and TG (+48% and +28%, respectively, P<0.05), while fatty acid oxidation was reduced (-35%, P<0.05). Thus, our data indicate that the increased intracellular lipid accumulation in hypoxic hearts is attributable to both: (a) a reduced rate of fatty acid oxidation and (b) an increased rate of fatty acid transport into the heart, the latter being attributable to a hypoxia-induced translocation of fatty acid transporters.

AMP-Activated Protein Kinases↗