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Effects of afferent stimulation on local synthesis of protein in CA1 pyramidal cell dendrites were studied using light microscope autoradiography. Tissue was fixed with paraformaldehyde immediately after 3 min exposure to 3H-leutine in order to trap 3H associated with macromolecules. The rate of 3H-leucine incorporation into dendrites of resting hippocampal slices was 10% the rate of incorporation Ninety percent of the incorporation into the into cell somata. somata was inhibited by cycloheximide 300 #I none of the incorporation into dendrites was blocked by cycloheximide. extramitochondrial synthesis Thus, there is no measurable of protein in the dendrites of the resting slice. Slices were exposed to 50 carbachol and the Schaffer collateral afferents to the CA1 pyramidal cells were stimulated intermittently at 10 Hz over a 20 min period. In this case, 3H incorporation into dendrites was increased almost threefold over resting levels, with no effect on label over the cell somata. There was no associated increase in uptake of free 3H-leucine, and the increase in label was completely blocked by cycloheximide. Thus, associating carbachol and afferent stimulation appears to activate de novo protein synthesis in the dendrites. Neither the carbachol alone nor the Schaffer collateral stimulation alone increased synthesis. The activation of dendrite synthesis was completely blocked by 5 #I atropine, and also by 50 o-aminophosphonovalerate. It did not occur when carbachol was paired with steady stimulation of the Schaffer collaterals at 1 Hz for 20 min, rather than with the patterned high-frequency stimulation. Thus, associating a cholinergic agonist with a level of neural activity that occurs in CA3 and CA1 pyramidal cells during behavior Muller et al., 1987 ; initiates local proexploratory tein synthesis in target dendrites. This effect is dependent on muscarinic cholinergic receptors and NMDA-type glutamate receptors. The possible relationship of this phenomenon to mechanisms of learning is discussed. [Key words: ACh, dendrities, hippocampus, learning, synthesis] NMDA, protein.
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PATIENT POPULATION This was a prospective evaluation of all infants aged 3 months or younger who presented to Primary Children's Medical Center, Salt Lake City, Utah, with SVT between August 1995 and October 1997. Infants with atrial flutter were excluded. Approval for this study was obtained from the institutional review board at the University of Utah and Primary Children's Medical Center, and parental consent was obtained. We evaluated data at presentation including age, tachycardia rate and QRS morphology, signs and symptoms of congestive heart failure, and mechanism of successful and sustained tachycardia termination. All infants had either a 12-lead electrocardiogram ECG ; or rhythm strip in tachycardia and a 12-lead ECG in sinus rhythm to evaluate for the presence of ventricular preexcitation. The association of ventricular preexcitation and SVT establishes the diagnosis of Wolff-Parkinson-White syndrome WPW ; . A complete echocardiogram was performed to evaluate for congenital heart disease and to assess ventricular function. INITIAL ESOPHAGEAL EP STUDY During the initial hospitalization, an esophageal EP study was performed on all infants in the absence of antiarrhythmic medication. The technique for performing an esophageal EP study has been described previously.1-3 Parental informed consent was obtained and intravenous access was secured. The study was performed with all patients in the fasting state and with some patients under light sedation by means of intravenous midazolam hydrochloride 0.1 mg kg ; . An esophageal pacing electrode was placed through the infant's nostril to a depth estimated by the infant's length.2 Using the esophageal pacing catheter, premature atrial extrastimuli and incremental atrial pacing were performed to induce SVT. Tachycardia was initiated with esophageal pacing in all patients, although isoproterenol hydrochloride 0.1 g kg per minute ; was used in 1 infant in whom SVT was not initiated in the baseline state. To determine the tachycardia mechanism, the ventriculoatrial VA ; interval was measured on the esophageal lead. The VA esophageal interval is measured from the onset of the earliest QRS to the rapid deflection of the atrial electrogram recorded from the esophageal lead during tachycardia Figure 1 ; . The VA esophageal interval is the time in milliseconds that it takes the electrical impulse to travel backwards from the ventricle to the atrium during SVT. A VA esophageal interval of less than 70 milliseconds excludes.
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Data were analyzed with the statistical package SPSS 6.1.2 SPSS Inc., Chicago, IL ; . All results are expressed as means SEM. Kruskal-Wallis H-tests were used for screening significant differences between the groups. When P was 0.05, Mann-Whitney U-tests were applied to compare the individual groups. The significance levels were adapted with Bonferroni's conservative correction. The dose-response curves obtained from the pulmonary function tests were analyzed with the GLM univariate procedure, providing regression analysis and analysis of variance for one dependent variable by two factors and or variables the groups and the carbachol concentration.
Figure 15 Expression of NK cell receptors on CD4 + T cells. The frequencies of A ; CD4 + CD28null and B ; CD4 + CD28 + T cells expressing the indicated receptors. The results are based on data from 4-23 screened patients. Only 4 patients were analyzed for NKp30, NKp44 and NKp46. In order to confirm the differentiated phenotype of the CD4 + CD28null T cell populations investigated in Paper IV we identified these cells as CD57 positive. CD57 is also found on NK cells and on highly differentiated CD8 + T cells [52]. The regulatory function of CD57 on T cells and NK cells is not clear. 2B4 CD244 ; interacts with CD48 and stimulate or inhibit cytotoxicity and IFN- secretion by NK cells, dependent on their differentiation activation status [275]. 2B4 has also been described to be expressed by the CD28 negative population of CD8 + T cells, but without activating properties [276, 277]. On CD4 + T cells the expression of 2B4 has been demonstrated on those cells expressing KIRs, which we and other have shown to be the CD28null subset [16, 27], Paper I. The regulatory function of 2B4 on CD4 + T cells is however hitherto unknown. In Paper IV we describe 2B4 to be expressed by most cells of the CD4 + CD28null T cell subset. DNAM-1 can enhance cytolysis by NK cells and CD8 + T cells when ligated with polio virus receptor PVR, CD155 ; or Nectin-2 CD112 ; . Additionally, DNAM-1 has been shown to drive Th1 differentiation and proliferation of DNAM-1-transfected nave CD4 + T cells [278-280]. Also a study by Dardalhon and colleagues suggested DNAM1 to be a specific marker for Th1 cells in mice [281]. In line with the Th1 profile of CD4 + CD28null T cells, DNAM-1 was expressed by a majority of these cells, and as could be expected, by a fraction of the CD4 + CD28 + T cells, possibly displaying a Th1 phenotype.
Capsaicin cont. ; The effect of neonatal capsaicin treatment on the innervation of the pulp of rat incisors. 401, 40P, 1988 Selective and non-selective actions of capsaicin on afferent fibres of the neonatal rat spinal cord-tail preparation in vitro. 401, 58P, 1988 Calcium and the effects of capsaicin on afferent fibres in a neonatal rat isolated spinal cord-tail preparation. 406, 37P, 1988 Autonomic reflexes in the rat are regulated by capsaicin-sensitive afferents. 409, 69P, 1989 Further evidence for the origin of circulating calcitonin gene-related peptide in the rat. 412, 297, 1989 Extracellular sodium and desensitization of nociceptive fibres by capsaicin in the neonatal rat spinal cord tail in vitro. 414, 21P, 1989 Resiniferatoxin: a capsaicin-like activator of peripheral fibres of the neonatal rat tail in vitro 418, 150P, 1989 Antinociceptive effects of capsaicin on the spinal cord: studies in the halothane-anaesthetized rat and neonatal rat in vitro. 423, 77P, 1990 The effect of neonatal capsaicin treatment on the distribution of neurokinin binding sites in rat bladder. 423, 79P, 1990 Antinociception induced by the capsaicin analogue, olvanil: peripheral and central sites of action studied in vivo in adult rats and in vitro using neonatal rat. 424, 60P, 1990 Capsaicin-sensitive afferents activate a sympathetic intestinointestinal inhibitory reflex in dogs. 425, 133, 1990 In viivo and in vitro capsaicin treatment reduces endothelium-dependent vascular relaxation to acetylcholine in the rat. 427, 31P, 1990 Capsaicin and sensory neuropeptide stimulation of goblet cell secretion in guinea-pig trachea. 431, 629, 1990 Captopril Captopril reduces L-type calcium current in isolated guinea-pig ventricular myocytes. 418, 167P, 1989 Carbachol Oscillations of free cytosolic calcium evoked by cholinergic and catecholaminergic agonists in rat parotid acinar cells. 406, 35, 1988 Properties of calcium stores and transient outward currents in single smooth muscle cells of rabbit intestine. 409, 385, 1989 Carbon dioxide Concentration of carbon dioxide, interstitial pH and synaptic transmission in hippocampal formation of the rat. 396, 247, 1988 Effect of carbon dioxide on heat production of frog skeletal muscles. 397, 643, 1988 A dynamic analysis of the ventilatory response to carbon dioxide inhalation in man. 398, 423, 1988 An effect of carbon dioxide on the behaviour of an ant, Messor wasmanni. 401, 98P, 1988 Influences on the cardiovascular response to graded levels of systemic hypoxia of the accompanying hypocapnia in the rat. 410, 381, 1989 and carbenicillin.
Data are time-averaged values during baseline t 1500 min ; and stimulation t 240360 min paired analysis of area under the curve AUC ; during baseline and stimulation. GH, growth hormone.
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1. Olin J, Masand P. Psychostimulants for depression in hospitalized cancer patients. Psychosomatics 1996; 37: 5762 Woods SW, Tesar GE, Murray GB, et al. Psychostimulant treatment of depressive disorders secondary to medical illness. J Clin Psychiatry 1986; 47: 1217.
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Gation for other purposes, and 50 children with atopic asthma 35 boys and 15 girls; mean age 8.32.8 yrs, range 515 yrs ; seen at the Paediatric Pulmonary Outpatient Clinic of the University Children's Hospital in Berne, Switzerland, were selected as study patients. Standardized case histories and physical examinations were performed by trained paediatricians in collaboration with the family doctor. Inclusion criteria were that the child was free from respiratory symptoms and had not had any signs of viral infections or vaccinations during the previous 6 weeks. Asthma was diagnosed by: a history of recurrent wheezy attacks; elevated immunoglobulin E IgE ; levels paper radioimmunosorbent test PRIST ; positive specific IgE radioallergosorbent test RAST for one or more allergens; and the documentation of airway obstruction Raw ; , which reversed with sympathomimetics. At the time of testing, the patients were in a symptom-free interval, with no signs of asthma, and the last acute asthma episode was at least 2 weeks before examination. Bronchodilator treatment was withheld 12 h before and inhaled steroids or disodium cromoglycate 24 h before the test. None of the patients were on xanthine treatment, systemic steroids, or oral 2-agonist. All of the subjects' parents gave their informed consent for the examinations and investigations, and the study was approved by the local Ethics Committee. Study design In healthy and asthmatic children, we determined whether the frequency and damping properties of the postocclusional pressure transients changed at lower provocation doses of carbachol than the end-interrupter resistance. After baseline lung function measurements whole body plethysmography and interrupter technique ; , cumulative doses of inhaled carbachol were administered and the provocation dose at which each parameter changed significantly from the baseline mean was determined. Following this challenge, salbutamol was given in order to test the reversibility of the induced airway obstruction. For safety reasons, patients with airway resistance of more than 200% of the predicted value at baseline were excluded from the carbachol challenge and therefore the study ; . Baseline lung function tests Functional abnormalities were evaluated by wholebody plethysmography using an air-conditioned, constant volume, variable pressure whole-body plethysmograph Jaeger, Wrzburg, Germany ; . The technique has been described previously [15]. Lung function data were expressed as a percentage of predicted values [16]. Functional residual capacity FRC ; at resting level was taken as an estimate of the degree of pulmonary hyperinflation, and Raw as an estimate of the degree of bronchial obstruction. The interrupter technique The airflow interruptions were performed using the Bronchoscreen Jaeger, Wrzburg, Germany ; , a computerized apparatus with a combined nebulizer-shutter.
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Recording, experimental recording sessions began. During the experimental recording day, all rats were subjected to 30 trials of a two-way active avoidance learning task between 9: 15 and 9: 45 A.M. ; . Immediately after these learning trials, 10 rats received control saline 50 nl ; and 10 rats received carbachol 50 ng in microinjection into the Pwave generator. After microinjection, rats were selectively deprived of REM sleep during a six-hour polygraphic recording session 10: 00 A.M. to 4: 00 P.M. ; . REM sleep deprivation was achieved by observing the ongoing polygraphic record and awakening rats within 2-3 seconds of the onset of each REM sleep episode. At the end of the six-hour polygraphic recordings, rats were retested for 30 learning trials between 4: 05 P.M. and 4: 50 P.M. ; . Results: Based on the polygraphic records, our sleep deprivation technique selectively eliminated 90-97% of REM sleep. In the retest trials, rats that received the control saline microinjection SRD ; did not show any learning improvement compared to their earlier test trials. In contrast, rats that received the carbachol microinjection CRD ; showed a significant improvement P 0.001 ; in retest trials compared to their earlier test trials and the retest trials of the SRD group. Conclusions: The results presented here demonstrate that post-training REM sleep deprivation impairs improvement of learning performance in retest trials. Most significantly, these results demonstrate, for the first time, that activation of the P-wave generator, by carbachol microinjection, prevented the memory impairing effects of post-training REM sleep deprivation. This evidence supports our hypothesis that activation of the P-wave generator during REM sleep deprivation enhances a physiological process of memorization that naturally occurs during post learning REM sleep. Research supported by NIH grants NS34004 and MH59839 and caverject!
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First Published Online September 13, 2005 Abbreviations: COX, Cyclooxygenase; EE, eutopic endometriotic stromal; EI, ectopic endometriotic stromal; FBS, fetal bovine serum; MCP, monocyte chemoattractant protein; NE, normal endometrial stromal; NF- B, nuclear factor- B; NSAID, nonsteroidal antiinflammatory drug; PR, progesterone receptor; RANTES, regulated on activation, normal T cell expressed and secreted. JCEM is published monthly by The Endocrine Society : endo-society ; , the foremost professional society serving the endocrine community and carbachol!
FIG. 6. CaM antagonists reduced carbachol-stimulated PLC activity in 1321N1 cells. An IP assay was performed with 1321N1 cells. Results are reported as % conversion of [3H]inositol phospholipids to [3H]inositol phosphates. Data shown are % conversion in the absence of agonist Basal ; , % conversion following 20 min treatment with 1 mM carbachol CCh ; , and % conversion in carbachol-stimulated samples minus unstimulated samples representing net carbachol-stimulated IP hydrolysis Cch-Basal ; . A, 1321N1 cells were pre-treated for 10 min with 1% Me2SO Vehicle ; , 100 M W-13 W-13 ; , or 100 M fluphenazine. W-13 and fluphenazine pre-treatments significantly reduced total carbachol-stimulated IP hydrolysis as well as net carbachol-stimulated IP hydrolysis compared with vehicle pre-treated controls * , p 0.001 ; . B, cells were treated with 1% Me2SO 10 min pre-stimulation Vehicle ; , with 100 M W-13 10 min pre-stimulation pre-treatment ; , with 100 M W-13 concurrent with stimulation concurrent ; , or with 100 M W-13 10 min post-stimulation post-treatment ; . W-13 treatments significantly reduced total carbachol-stimulated IP hydrolysis as well as net carbachol-stimulated IP hydrolysis compared with vehicle pre-treated controls * , p 0.001 ; by 42% with pre-treatment, 58% with concurrent treatment, and 32% with post-treatment. Experiments were performed in triplicate with n 3 and cefprozil.
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