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PubMed1995

Perinatal thermogenesis.

The rapid initiation of thermogenesis is crucial for the survival of newborn infants. At birth the fetus must adapt to cooling, increased oxygenation and separation from the placenta. An experimental approach in the chronically instrumental fetal sheep of 'simulated birth in utero' allowed the evaluation of each of these stimuli sequentially. Cooling stimulated shivering, cardiovascular and endocrine responses but not nonshivering thermogenesis (NST). Ventilation of the cooled fetus with oxygen caused only modest NST which was not altered by an infusion of triiodothyronine. Occluding the umbilical cord was followed by a rapid substantial rise in NST which was maintained until the placental circulation was re-established. Thus the placenta is secreting factors into the fetal circulation which inhibit the ability of the brown adipose tissue to respond to either hormonal or neural stimuli. Placental prostaglandin E2 and probably adenosine are tonic inhibitors of thermogenesis in utero. Effective thermogenesis after birth requires the combination of separation from the placental inhibitors of lipolysis, increased oxygenation from breathing and the stimulation of cutaneous cold receptors.

Adenosine↗

PubMed1982

Functional distinction of perigeniculate and thalamic reticular neurons in the cat.

Two types of neurons can be recognized in the region above the lateral geniculate nucleus. One cell type is found in the caudal part of the reticular nucleus of thalamus; these cells are accordingly called reticular neurons. The other cell type is located in the perigeniculate nucleus immediately above lamina A of the lateral geniculate nucleus and in the intermediate zone between the perigeniculate nucleus and the reticular nucleus. These cells are referred to as perigeniculate neurons. Electrical stimulation of the optic tract and the visual cortex typically evokes a short burst of spikes in the perigeniculate neurons, and the excitation has a shorter latency from the cortex (range 1.2-2.5 ms) than from the optic tract (range 1.5-3.1 ms). The perigeniculate neurons are also activated by adequate visual stimuli. In contrast, the reticular neurons are unresponsive to visual stimuli and electrical stimulation of the optic tract but they may respond with a burst of spikes to cortex stimulation with rather long latency (range 2.7-5.5 ms). It is concluded that only perigeniculate neurons qualify as interneurons in the recurrent inhibitory pathway to principal cells in the lateral geniculate nucleus.

Animals↗

PubMed1982

[Results of electromyographical and mechanographical investigations in myotonia congenita (author's transl)].

Electrical and mechanical investigations in myotonia were investigated in 20 patients with myotonia congenita. At first the parameters of the myotonic muscle fiber discharges were determined, than the EMG-activity was estimated during slight and maximal force of voluntary muscle contraction and finally the electromyogram and the mechanogram were simultaneously registered after indirect stimulation of the muscle. The results show, that there is a correlation between the myotonic muscle fiber discharges and the EMG- and mechanical findings depending on the frequency of stimulation and the force of contraction. The parameters of muscles did not differ between the patients and the health persons after single stimulation. Repetitive supramaximal stimuli (15 Hz) showed a rapid decline of EMG-amplitude in the patients with myotonia congenita. The fall of amplitude was observed, as soon as myotonia fiber discharges occured. The duration of contraction was longer both in the phase of contraction and in the phase of relaxation. When the frequency of stimulation was increased (30 Hz), the fall of EMG-amplitude was more increased whereas the contraction and relaxation time decreased. The findings are interpreted by means of the author's own experimental results and are discussed in connection with the chloride-hypothesis.

Adolescent↗

PubMed1993

Attenuation of hippocampal long-term potentiation by ethanol: a patch-clamp analysis of glutamatergic and GABAergic mechanisms.

Long-term potentiation of synpatic transmission (LTP) of the perforant path--dentate gyrus synapse is induced by 5 Hz, theta-like stimulation patterns. Such stimuli induce plasticity that is most likely driven by a decrease in synaptic inhibition (disinhibition) mediated by GABAB autoreceptors. In the present study, we demonstrate that LTP induced in this manner is completely antagonized by ethanol. In order to determine the site of ethanol inhibition of LTP induced by theta-like stimulation, we combined slice patch recordings with pharmacologic isolation of the individual glutamatergic and GABAergic synaptic currents. The present experiments revealed that ethanol inhibited NMDA receptor-mediated synaptic currents without potentiation of GABAA currents or attenuation of GABAB-mediated fading of GABAA synaptic currents. These observations with ethanol contrasted with the actions of the water-soluble benzodiazepine midazolam, which strongly potentiated GABAA synaptic currents, reversed the effect of GABAB-mediated fading of GABAA synaptic currents, and therefore blocked the resulting NMDA synaptic currents. These data indicate that the effects of ethanol on long-term changes in synaptic strength in the rat hippocampal formation are due primarily to an action at the NMDA receptor-channel complex.

Animals↗

PubMedDate not supplied

[Plasma growth hormone in obese patients. Comparison of response to arginine and L-dopa (author's transl)].

The present study aimed at testing the hypothesis that l-dopa could obtain a better growth hormone (G.H.) stimulation than metabolic stimuli in obese patients. Arginine (30 g i-v) and l-dopa (1 g per os) were used in 12 obese, non diabetic, female in patients. No significant difference of plasma G.H. peak level (arginine : 11,3 ng/ml +/- 8.6. L-dopa : 9.2 +/- 5.6) appeared between these two types of stimulation

Arginine↗

PubMed2002

Respiratory response to mechanical stimulation of the gallbladder.

Since stimuli from abdominal or pelvic viscera can affect respiratory muscle function, we hypothesized that mechanical stimulation of the gallbladder would result in inhibition of motor activity to the diaphragm and to upper airway muscles. We studied 12 decerebrate, vagotomized, paralyzed, artificially ventilated cats and recorded hypoglossal (HG) and phrenic (PHR) nerve activities while applying 600-1000 g of traction on the gallbladder during four respiratory cycles. Traction resulted in an initial reduction of PHR activity to 87.6+/-15.0% (mean+/-S.D.% of its baseline value), a reduction of HG activity to 74.2+/-27.5% and a lengthening of expiratory time to 178.8+/-81.0%. Subsequently, PHR activity and expiratory time returned toward control values, while HG remained diminished, at 66.4+/-19.1%. Our results show that mechanical stimulation of the gallbladder results in a respiratory inhibition with a disproportionate reduction in HG activity relative to PHR discharge. We speculate that gallbladder stimulation by contractions or surgery may compromise breathing by inhibition of phrenic discharge and upper airway obstruction.

Animals↗

PubMed2001

The endothelium in sepsis: source of and a target for inflammation.

OBJECTIVE: To discuss a possible role of the endothelium in sepsis. DATA SOURCES: Studies published in biomedical journals and our own experimental results. STUDY SELECTION: Studies on endothelial mechanisms in the context of sepsis. DATA EXTRACTION AND SYNTHESIS: Changes in endothelial cells on activation by inflammatory stimuli are reviewed briefly; potential mechanisms that lead to endothelial damage during sepsis are discussed. CONCLUSIONS: The endothelium is a key organ involved in the pathogenesis of sepsis. Dysfunction of or injury to the endothelium may be involved in the pathogenesis of multiple organ failure and should be discriminated from activation resulting from stimulation with inflammatory stimuli. Identification of the molecular mechanisms that contribute to endothelial dysfunction or damage is likely to provide novel targets for the treatment of sepsis.

Animals↗

PubMed2004

Fibrin stimulates platelets to increase factor VIIIa binding site expression.

Factor (F)VIII functions as an enzymatic cofactor on the membranes of stimulated platelets. However, thrombin stimulates platelets to express only a small number of binding sites for FVIII. We wished to determine whether molecules that are likely to be present in a developing thrombus stimulate platelets to up-regulate FVIII binding site expression. Flow cytometry was utilized to measure binding of fluorescein-labeled FVIIIa to activated platelets and a FXase assay was utilized to measure platelet-dependent function. Various agonists as well as normal and mutant fibrinogens and fibrin were evaluated as co-stimuli. Thrombin-stimulated platelets expressed 214 +/- 67 binding sites for thrombin-activated FVIII (FVIIIa) and none of the established soluble agonists enhanced binding site exposure. However, the presence of 5 micro g mL(-1) fibrin increased the number of FVIIIa binding sites/platelet three- to eight-fold (1470 +/- 130, range 600-1800) with a parallel increase in platelet-based FXase assay. Binding site up-regulation was not stimulated by fibrinogen and was blocked by inhibitors of GPIIbIIIa. Mutant fibrin lacking the gamma-chain C-terminal four residues was ineffective while fibrin with altered RGD sequences did stimulate expression of FVIIIa binding sites indicating that co-stimulation is mediated by the fibrin gamma-chain termini. Fibrin-enhanced expression of FVIIIa binding sites was not supported by D364H fibrin, which does not aggregate normally, and was blocked by the GPRP peptide, which inhibits fibrin polymerization. Polymerized fibrin can function as a platelet co-stimulus, up-regulating expression of binding sites for FVIIIa.

Binding Sites↗

PubMed1989

Aggression in male mice: rapid-onset attack of lactating female mice following termination of hyperphysiological testosterone treatment.

Gonadally-intact or castrated and testosterone-(T) treated male mice display aggressive behavior towards olfactory-bulbectomized male (OBM) stimuli, but not towards lactating female (LF) stimuli. By comparison, T-treated female mice display aggressive behavior towards both OBM and LF stimuli. The purpose of the present experiment was to determine if male mice given hyperphysiological T-treatment would display "female-typical" attack of OBM and LF stimuli. Hyperphysiological T-stimulation did not lead to the display of aggressive behavior towards OBM and LF stimuli; only OBM stimuli were attacked, suggesting a qualitative behavioral sex difference in response to T. However, the major finding of this study occurred following the termination of T-treatment. Castrated males that had previously received hyperphysiological T-treatment began to attack LF stimuli within 48 hr of treatment termination. By comparison, castrated males that had previously received physiological T-stimulation, as well as a gonadally-intact control group, generally began to attack LF stimuli 3-4 weeks following treatment-termination/castration. It is suggested that this unusual treatment-termination-induced behavioral display occurs via neurochemical mediation.

Aggression↗

PubMed2001

Regulation of the association between PSTPIP and CD2 in murine T cells.

Prominent in T cells and natural killer cells, CD2 binding protein 1 (CD2BP1) plays an important role in CD2-mediated adhesion and signal transduction. In the current study, we investigated CD2 and PSTPIP (proline, serine, threonine phosphatase interacting protein, murine homologue of CD2BP1) interactions in purified mouse splenic T cells. PSTPIP associated with CD2 in both resting and activated T cells. Following various stimuli, such as concanavalin A, anti-TCRbeta, anti-CD3epsilon, anti-CD3epsilon/phorbol myristate acetate (PMA), IL-2, or PMA/ionomycin, PSTPIP and CD2 expression, as well as their association, increased in a time-dependent fashion. While PSTPIP expression and CD2 expression were comparable across most groups, the PSTPIP-CD2 association stimulated by anti-CD3epsilon alone was significantly greater than with other stimuli. Stimulation by anti-CD3epsilon plus anti-CD28 induced even greater PSTPIP-CD2 association than anti-CD3epsilon treatment alone, indicating that CD28 initiated signals are involved in regulating this interaction. There was no direct association between CD3epsilon or CD28 and PSTPIP. Tyrosine phosphorylated PSTPIP bound poorly to CD2 compared to dephosphorylated PSTPIP, and protein tyrosine phosphatase was shown to affect both phosphorylation of PSTPIP and the CD2-PSTPIP association. In addition to CD2, PSTPIP associated with CD4, CD8, CD54, and CD62L. CD2 and CD4 ligation reciprocally regulated their association with PSTPIP. These findings indicate that T cell activation, particularly through the CD3 and CD28 signal transduction pathways, regulates PSTPIP-CD2 interactions. PSTPIP likely has additional broader effects through interactions with CD4, CD8, CD54, and CD62L, and this may influence T cell responses to antigen.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Effect of low intensity pulsed ultrasound and BMP-2 on rat bone marrow stromal cell gene expression.

To determine how low intensity pulsed ultrasound alters gene expression in rat bone marrow stromal cells and to see if combining this stimulation with BMP-2, cells were pre-cultured for eight days in the presence of 50 microg/ml ascorbic acid and then exposed to either low intensity US or 100 ng/ml BMP-2 or both combined, beginning on the first, third fifth or seventh day of culture so that cells were exposed to the stimuli for one, three, five or seven days. Real time PCR was used to determine the effect of these treatments on gene expression of several genes associated with osteogenesis. The expression of some of the genes (Cbfa-1/Runx2, IGF-receptor, Alk-3, alkaline phosphatase, osteopontin, TGF-beta1, BMP-7) was increased compared to untreated controls. Combination of US and BMP-2 treatment did not lead to synergy of the two stimuli. Cbfa-1 stimulation occurred more quickly with US than with BMP-2. Increases in gene expression were greatest after 3 days exposure to US, with similar results for BMP-2 treatment implying that there may be a time dependence for the stimulus of osteogenic gene expression in stromal cells.

Animals↗

PubMed1985

Localization of visually evoked cortical activity in humans.

The locations of cortical activity evoked by visual stimuli presented at different positions in the visual field are deduced from the scalp topography of visually evoked potentials in humans. To accomplish this, the Laplacian evoked potential is measured using a multi-electrode array. It is shown that the Laplacian response has the following useful attributes for this purpose. It is reference-free. Its spatial resolution is approximately 2 cm referred to the surface of the cortex. Its spatial sensitivity characteristic is that of a spatial band-pass filter. It is relatively insensitive to source--sink configurations that are oriented tangentially to the surface of the scalp. Only modest assumptions about the source--sink configuration are required to obtain a unique inversion of the scalp topography. Stimuli consisting of checkerboard-filled octant or annular octant segments are presented as appearance-disappearance pulses at sixteen different positions in the visual field in randomized order. The locations of evoked cortical activity in the occipital, parietal and temporal lobes are represented on a Mercator projection map for each octant or octant segment stimulated. Lower hemifield stimuli activate cortex which lies mainly on the convexity of the occipital lobe contralateral to the side of stimulus presentation in the visual field. The more peripheral the stimulus is in the visual field, the more rostral is the location of the active cortex. The rostral-to-caudal location of the evoked activity varies from subject to subject by as much as 3 cm on the surface of the occipital cortex. Furthermore, in any single subject there is a substantial amount of hemispheric asymmetry. Upper hemifield stimuli activate cortex that lies on the extreme caudal pole of the occipital lobe. This activity is relatively weak, and in some subjects it is almost unmeasurable. It is suggested that the representation of the upper hemifield in the cortex lies mostly on the inferior and mesial walls of the occipital lobe and possibly within the calcarine fissures. Those locations are inaccessible to the Laplacian analysis because the current generators therein may be oriented tangentially to the surface of the overlying scalp. Posterior parietal lobe activity and/or inferior temporal lobe activity is frequently evoked. Different subjects have different patterns of evoked activity. Unilateral or bilateral posterior parietal lobe activity is the most common pattern. Unilateral inferior temporal lobe activity is a less common pattern.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain Mapping↗

PubMed1985

Cytochrome b translocation to human neutrophil plasma membranes and superoxide release. Differential effects of N-formylmethionylleucylphenylalanine, phorbol myristate acetate, and A23187.

The role of specific granules and cytochrome b in superoxide (O(2)) release was studied by comparing the effects of three different stimuli on normal human neutrophils, neutrophils congenitally deficient in specific granules, and granule-free normal neutrophil cytoplasts. Phorbol myristate acetate (PMA) stimulated normal neutrophils to release more O(2) than did N-formylmethionylleucylphenylalanine (fMet-Leu-Phe), which stimulated greater release than the calcium ionophore A23187. Neutrophils lacking specific granules produced variable amounts of O(2) in response to all stimuli. Stimulation with PMA, fMet-Leu-Phe, and A23187 produced maximal rates of O(2) release that were 32, 55, and 21% of that by normal cells. Likewise, granule-free neutrophil cytoplasts released 24, 20, and 0% of the O(2) released by intact cells. These data suggest that the stimuli require different mechanisms for activation. Three subcellular fractions (azurophil granule rich, specific granule rich, and plasma membrane rich) were separated by Percoll gradients from normal resting and stimulated neutrophils. In resting neutrophils, the cytochrome b content in the plasma membrane was 31% of the total, with the rest in the specific granule-rich fraction. Ten minutes after stimulation, PMA, fMet-Leu-Phe, and A23187 induced translocation of 27, 8, and 49%, respectively, of the cytochrome b from the specific granule-rich fraction to the plasma membrane. Although our data support a role for specific granule factors in A23187-induced O(2) release, there is no correlation between the amount of cytochrome b incorporated into the plasma membrane and the extent of O(2) production activated by the different stimuli.

Calcimycin↗

PubMed1987

Destruction of cultured vascular endothelial cells and red blood cells by immune-activated polymorphonuclear leukocytes.

The cytotoxicity of human polymorphonuclear leukocytes (PMNs) against autologous red blood cells (RBC) and cultured vascular endothelial cells (EC) was investigated. PMNs were activated by phorbol myristate acetate (PMA) together with immune stimuli such as immune complexes and aggregated IgG. In the standard 51Cr-release assay, in which PMA concentration was 5 ng/ml and effector versus target ratio was 5, 76.7% and 34.2% specific 51Cr release was observed from RBC and EC, respectively. Significant levels of 51Cr were released, albeit to a lesser degree, when PMNs were stimulated by immune stimuli. Further experiments which employed various scavengers of oxygen radicals suggested that hydrogen peroxide was the most potent mediator of this cytotoxicity; the implications of these in vitro observations with the pathogenesis of immune vasculitis are of clinical interest.

Antigen-Antibody Complex↗

PubMed1992

Stimulus-specific enhancement of luminol chemiluminescence in neutrophils by phosphatidylserine liposomes.

When stimulated with different stimuli, neutrophils generate various active oxygen species. These active oxygen molecules can be analyzed by luminol chemiluminescence (LCL). Phosphatidylserine (PS)-liposomes increased the formylmethionyl-leucyl-phenylalanine-induced LCL of guinea pig peritoneal neutrophils without affecting their oxygen consumption and superoxide (O2.-) generation. Similar effects of PS-liposomes were also observed in LCL of neutrophils stimulated by phorbol myristate acetate or arachidonic acid but not by opsonized zymosan. Kinetic analysis revealed that the PS-liposome-induced increase in LCL depended on extracellulary generated O2.-. Moreover, the stimulatory effect of PS could be seen only when it formed liposomal membranes. The effect of PS-liposomes was also inhibited by superoxide dismutase, catalase, and deferoxamine, an iron chelator, but not by azide, an inhibitor of myeloperoxidase. Similar enhancement of stimulation-dependent LCL response was also observed with Fe3+ and ADP-Fe3+, but the degree of enhancement was much greater with PS-liposomes than with iron and its complex. The increase in hydroxyl radical generation by PS-liposome-treated neutrophils was confirmed by experiments with EPR spectrometry using spin-trapping agents. These results suggested that the interaction of neutrophils with PS-containing membrane surface might generate reactive oxygen species that enhance the stimulus-dependent LCL response of neutrophils.

Animals↗

PubMed1986

Inhibition of dorsal-horn cell responses by stimulation of the Kölliker-Fuse nucleus.

The Kölliker-Fuse nucleus (KF) in the dorsolateral pons has been shown to be the major source of catecholamine innervation of the spinal cord. This has important implications in terms of pain control mechanisms, since catecholamine-mediated mechanisms are essential for the expression of opiate and other varieties of antinociception. This study examines the effects of KF stimulation on responses of dorsal-horn cells to innocuous and noxious cutaneous stimuli in anesthetized cats. Stimulation of the KF potently inhibits the responses of dorsal-horn cells to both noxious and innocuous stimuli. The threshold for the inhibitory effect is significantly lower for responses to noxious stimuli as opposed to innocuous stimuli. The inhibitory effect is specific to the stimulus site, as evidenced by a marked decrease in the effect following small changes in the position of the stimulating electrode in the brain stem. The latency of the effects indicates a bulbospinal conduction velocity of 4 to 5 m/sec, which is much slower than usual reticulospinal effects and is consistent with a catecholamine-mediated system. The dependence of KF-spinal inhibition on intact biogenic amines was tested by depleting the animals of these amines with reserpine pretreatment. Depletion of biogenic amines resulted in a significant decrease in the KF spinal inhibitory effects, suggesting their dependence on intact noradrenergic stores. The results of these studies are consistent with the idea that the KF-spinal system plays an important noradrenergic-dependent role in the brain-stem modulation of spinal processing of noxious, potentially painful stimuli.

Animals↗

PubMed1983

Effect of Staphylococcus aureus enterotoxin F on human neutrophil oxidative metabolism.

Epidemiologic and animal challenge studies have suggested that SEF may play a critical role in toxic-shock syndrome [1]. However, the pathogenic mechanism of SEF activity is not known. One means by which this toxin could elicit the widespread organ dysfunction observed in toxic-shock syndrome would be by directly promoting PMN production of toxic oxygen species and the resultant secondary endothelial cell damage [2]. To evaluate this possibility, we assayed the effect of SEF on PMN oxidative metabolism. SEF at 0.01-100 ng/ml did not stimulate O2- release or O2 consumption by inactive PMNs. Similarly, incubation of PMNs with 10 ng of SEF/ml for 1 hr neither potentiated nor inhibited cellular O2 consumption stimulated by optimal (10 mg/ml) or suboptimal (0.1 mg/ml) concentrations of opsonized zymosan. Finally, SEF had no effect on O2- release by PMNs stimulated by PMA. PMN viability, as assessed by trypan blue exclusion, was unaffected by SEF. This study did not address the possibility that SEF might indirectly activate PMN oxidative metabolism by promoting leukocytic pyrogen production by monocytes and macrophages [3]. SEF neither directly activated PMN oxidative activity nor potentiated the cellular oxidative response to particulate or soluble stimuli. Consequently, direct stimulation of PMN-derived, O2- mediated damage to endothelial cells is not a tenable hypothesis to explain the mechanism of SEF toxicity.

Bacterial Toxins↗

PubMedDate not supplied

[Reaction of neurons of the medial geniculate body to acoustic stimulation].

Responses of medial geniculate body (MGB) neurons to pure tones and clicks were studied in acute experiments in immobilized cats, preliminary operations being performed under calypsol anaesthesia. MGB units were identified by their reactions to cortical zone AI and brachium of inferior colliculus stimulations. When tonal stimuli were applied relay neurons of pars principalis of MGB usually demonstrated either unimodal tuning curves with narrow frequency band or fragmental ones with several narrow bands. On-response with subsequent inhibition of the background activity or without such an inhibitory period was most frequent type of the reaction (66.6%) of relay MGB neurons to tonal stimulation. The group of relay neurons with the tonic type of reaction (9.1%) was classified for which the duration of tonic response depends on the duration of tonal stimulus. Change of the excitatory reaction to the inhibitory one when the characteristic tone frequency is changed by non-characteristic++ ones is supposed to be a mechanism supplying sharpness of tuning at relay MGB neurons. It is concluded that responses of acoustic cortical neurons to sound stimulation depend to a great extent on the pattern of impulsation that comes from MGB relay units.

Acoustic Stimulation↗