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PubMed1994

Central integration of mechanisms in exercise hyperpnea.

Many hypotheses have been advanced to explain the hyperpnea of exercise and its close relations to the level of metabolic work, expressed as oxygen uptake (VO2) and carbon dioxide production (VCO2). Evidence is presented that a neural central command mechanism from the hypothalamus is important in the driving of both respiration and circulatory adjustments during locomotion or exercise, and that short-term potentiation of neurons in the medulla makes an important contribution. Both are probably augmented by receptors in working muscle and by the effects of increased [K+] acting on the carotid bodies. Feedback from "respiratory" mechanisms, including CO2 and O2 mediated mechanisms and inputs from the lungs, are important in stabilizing ventilation at the level primarily dictated by the major neural mechanisms.

Animals↗

PubMed1996

Decreased interleukin-10 production by neonatal monocytes and T cells: relationship to decreased production and expression of tumor necrosis factor-alpha and its receptors.

The production of IL-10 by human neonatal blood mononuclear leukocytes (BML) stimulated with lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-alpha), antibodies to CD3, or phorbol 12-myristate 13-acetate (PMA) was measured. The production of IL-10 by neonatal BML cultured with LPS or TNF-alpha was approximately 20 and approximately 15%, respectively, of adult BML. The combination of human recombinant TNF-alpha and LPS failed to augment IL-10 production in neonatal BML. The decreased production of IL-10 by neonatal leukocytes was not due to an autocrine feedback mechanism because only low concentrations of IL-10 were found in newborn sera. A connection with TNF-alpha could not be ruled out, because TNF-alpha production by LPS-stimulated newborn BML and the expression of TNF-alpha receptors on newborn monocytes were reduced. Mean +/- SD of concentrations of IL-10 in supernatants from adult and neonatal BML after stimulation with antibodies to human CD3 for 48 or 72 h were 914 +/- 386 and 178 +/- 176 pg/mL, respectively (p < 0.0001). In experiments with enriched populations of neonatal T cells, the addition of PMA failed to augment IL-10 production. This suggested that newborn T cells may be in a different state of activation than adult T cells Thus, IL-10 production in neonatal monocytes and T cells is reduced and this study suggests that the reduction may be secondary in part to regulatory processes involving TNF-alpha and its receptors.

Adolescent↗

PubMed1995

Electromagnetic ossicular augmentation device.

Conventional hearing aids have a number of limitations inherent to amplifying sound in the narrow confines of the external auditory canal. Disadvantages include acoustic feedback, poor fidelity, and the stigmata of aging. Since 1986, Michigan Ear Institute and Smith and Nephew Richards Company have been investigating the feasibility of a new device that converts sound to an electromagnetic field. The efficacy and safety of electromagnetic-induced hearing was sufficient enough to have the Federal Food and Drug Administration approve a pilot study of ten patients with a sensorineural hearing loss in whom a target magnet is implanted beneath the tympanic membrane. A status report of this study and a review of our preceeding investigations are presented in this article.

Audiometry, Pure-Tone↗

PubMed1994

Rising and sitting down in stroke patients. Auditory feedback and dynamic strength training to enhance symmetrical body weight distribution.

The purpose was to study vertical ground reaction force feedback and dynamic knee extensor training used to enhance stroke patients' symmetrical body weight distribution while rising and sitting down. Sixteen healthy subjects and 51 stroke patients participated in the studies. Two vertical strain gauge force transducers attached to two force-measuring platforms were used to measure body weight distribution over the lower limbs. An auditory feedback device, specially developed for training body weight distribution on the paretic leg, employed two electronic balances sensing vertical forces from each foot, separately. Torque of maximal voluntary eccentric and concentric knee extensor and flexor actions at 30, 60, 120, 180 and 240 deg/s was recorded with an isokinetic dynamometer together with surface electrodes from the quadriceps and hamstring muscles. When instructed to rise with even body weight on each lower limb, the stroke patients loaded the paretic leg more than when rising habitually, indicating that stroke patients have a latent motor capacity. Stroke patients' own estimations on visual analogue scales of body weight distributed on the paretic leg correlated with measured loading of the paretic leg in rising. After six weeks of training with auditory feedback of vertical ground reaction forces in the acute phase after stroke, the patients improved their loading of the paretic leg compared to a control group. The patients distributed body weight over the lower limbs nearly symmetrically while rising and while sitting down. The peak torque was not greater, however, than in the control group, rising with an asymmetrical body weight distribution. This implies that the patients after feedback training were better at using the knee extensor torque of the paretic leg to attain symmetrical body weight distribution over the lower extremities. Changes in improvement of physical performance and sitting to standing were greater than in the control group. No differences between groups were seen in performance of activities of daily living. Body weight distribution over the limbs in rising and in sitting down was re-tested on average 33 months after end of training. The symmetrical weight distribution after feedback training was not maintained over time. Knee extensor strength improved after six weeks of eccentric and concentric training, starting on average 27 months after stroke. The increase in strength was related to enhanced activation of agonist EMG activity. Eccentric training seems to be superior to concentric training with reference to a) improved body weight distribution over the lower limbs in rising, to b) increased knee extension torque and to c) increased agonist EMG activity without a concomitant, augmented EMG activity of the antagonistic knee flexor muscles. It was concluded that stroke patients have a latent motor capacity, that six weeks auditory feedback training promotes symmetrical body weight distribution which, however, is not consistent over time and that isokinetic eccentric training is superior to concentric training with reference to weight distribution in rising, knee extension torque and EMG activity.

Adult↗

PubMed2005

Effects of deliberate control on verbal and facial expressions of pain.

The 'facial feedback hypothesis' suggests that inhibiting or exaggerating pain displays produces parallel effects on subjective experience. Research on the regulation of emotional expressions suggests that the act of self-regulation may be detectable in the properties of facial behavior. Both issues were examined in this study. Healthy young volunteers were videotaped while they were exposed to electric shocks varying in intensity. Participants in the Augment group were instructed to exaggerate their facial reactions to the shocks. Participants in the Attenuate group were instructed to inhibit their reactions. Controls simply responded to the shocks. All groups rated the pain of each shock on numeric, sensory and affective scales. In subsequent phases, judges rated the intensity of pain displays for all participants, and facial reactions were measured with the Facial Action Coding System. Results provided no support for the facial feedback hypothesis. Judges' ratings of participants' pain indicated that the augment instructions produced distinct alterations in pain expression. The control and inhibit groups showed linear increases in pain expression with increasing pain intensity, which did not differ significantly. Fine-grained analysis of participants' facial behavior provided evidence that pain augmentation was accompanied by topographic changes in pain expression. Parallels with existing studies, methodological issues and practical implications of the findings are discussed.

Adult↗

PubMed2005

Differences in the gestational pattern of mRNA expression of the Rnd family in rat and human myometria.

Uterine myometrial contractility remains a poorly characterized area of research in reproductive physiology. Rnd1, a novel member of the GTP-binding Rho protein family, inhibits Ca(2+)-sensitization by specifically interfering with a RhoA/Rho-activated kinases-dependent mechanism in smooth muscle. In addition to Rnd1, there are two other members, Rnd2 and Rnd3, in the Rnd family of Rho proteins. In the present comparative study of myometrial contractility in rats and humans, we found that all three Rnd mRNAs were expressed in nonpregnant rat myometrium and in nonpregnant human myometrial tissues. Although all three mRNA levels increased significantly after gestation in rat myometria, only Rnd1 expression was significantly greater after gestation in human samples. In the ovariectomized rat, administration of estrogen and/or progesterone increased the expression of all Rnd mRNAs. These results suggest that universal Rnd family up-regulation during pregnancy in rats may have an important role for negative-feedback control of uterine contraction during gestation by inhibiting RhoA-mediated increase in Ca(2+) sensitivity of contractile elements. Such increases in Rnd levels may be due to augmented levels of reproductive steroids in rats. Our data also point to gestational differences between rats and humans in Rnd isoform patterns.

Adult↗

PubMed1987

Pituitary and adrenocortical responses to the ovine corticotropin releasing hormone in depressed patients and healthy volunteers.

It has been suggested that limbic system-hypothalamic "overdrive" may be the underlying mechanism causing an augmented secretion of corticotropin releasing hormone (CRH), heightened adrenocortical responsiveness to corticotropin (adrenocorticotropic hormone) (ACTH), and alteration in cortisol feedback regulatory mechanisms as demonstrated by the dexamethasone suppression test. We examined pituitary and adrenocortical responses after morning administration of ovine CRH (oCRH) in 26 depressed patients and 11 healthy volunteers. Basal plasma ACTH concentrations were similar in both groups, whereas patients had a significantly diminished cumulative ACTH response after administration of oCRH. In contrast, basal total cortisol concentrations and cumulative cortisol responses to oCRH were similar in depressed patients and controls. Patients with melancholic features demonstrated the most profound ACTH blunting after oCRH, whereas patients separated according to dexamethasone suppression test results had similar ACTH and cortisol responses to oCRH. The present results extend data from prior studies utilizing oCRH in the evening and demonstrate a dysregulation of the functional integrity of the hypothalamic-pituitary-adrenocortical axis in depressive illness after a morning oCRH test at both central and peripheral hypothalamic-pituitary-adrenocortical axis sites.

Adrenocorticotropic Hormone↗

PubMed2005

Volatile anesthetics disrupt frontal-posterior recurrent information transfer at gamma frequencies in rat.

We seek to understand neural correlates of anesthetic-induced unconsciousness. We hypothesize that cortical integration of sensory information may underlie conscious perception and may be disrupted by anesthetics. A critical role in frontal-posterior interactions has been proposed, and gamma (20-60 Hz) oscillations have also been assigned an essential role in consciousness. Here we investigated whether general anesthetics may interfere with the exchange of information encoded in gamma oscillations between frontal and posterior cortices. Bipolar electrodes for recording of event-related potentials (ERP) were chronically implanted in the primary visual cortex, parietal association and frontal association cortices of six rats. Sixty light flashes were presented every 5s, and ERPs were recorded at increasing concentrations of halothane or isoflurane (0-2%). Information exchange was estimated by transfer entropy, a novel measure of directional information transfer. Transfer entropy was calculated from 1-s wavelet-transformed ERPs. We found that (1) feedforward transfer entropy (FF-TE) and feedback transfer entropy (FB-TE) were balanced in conscious-sedated state; (2) anesthetics at concentrations producing unconsciousness augmented both FF-TE and FB-TE at 30 Hz but reduced them at 50 Hz; (3) reduction at 50 Hz was more pronounced for FB-TE, especially between frontal and posterior regions; (4) at high concentrations, both FF-TE and FB-TE at all frequencies were at or below conscious-sedated baseline. Our findings suggest that inhalational anesthetics preferentially impair frontal-posterior FB information transfer at high gamma frequencies consistent with the postulated role of frontal-posterior interactions in consciousness.

Anesthetics, Inhalation↗

PubMed1991

Differential regulation of brain aromatase by androgen in adult and fetal ferrets.

The contribution of androgens to the regulation of aromatase activity (AA), measured by quantifying the in vitro formation of [3H]estrone from 19-[3H]hydroxyandrostenedione precursor, was studied in equivalent microdissected brain regions of adult and fetal ferrets. In adulthood, AA was similar in the bed nucleus of the stria terminalis, medial (M) and lateral (L) preoptic area (POA), medial (MA) and lateral amygdala (LA), ventromedial hypothalamus (VMH), and parietal cortex of gonadectomized males and females given no concurrent steroid treatment. Daily sc injections of the androgen dihydrotestosterone propionate significantly stimulated AA in MPOA, MA, and VMH of adult males and in MA of females; a similar trend was seen in MPOA and VMH of females. By contrast, no evidence of androgenic regulation of AA was obtained in these three brain regions microdissected from fetuses killed on embryonic day 35 (E35; 41-day gestation). Transplacental administration of the antiandrogen flutamide beginning on day E24 failed to affect AA in MPOA, LPOA, MA, LA, or parietal cortex, although this treatment significantly reduced AA in bed nucleus of the stria terminalis of fetal males. The results suggest that the responsiveness of aromatizing enzymes to androgenic induction is similar in several subcortical brain regions of adult ferrets of both sexes. In breeding males such an action of androgen may augment the neural production of estrogen, which has previously been implicated in the control of sexual behavior and the feedback regulation of LH secretion. By contrast, androgen apparently contributes minimally to the regulation of AA in brain regions of fetal ferrets, particularly in the MPOA, in which a sexually dimorphic nucleus differentiates in males around E37 in response to estrogen produced locally.

Androgens↗

PubMed2004

Signals and mechanisms of compensatory lung growth.

Growth of the lung involves unique structure-function interactions not seen in solid organs. Mechanical feedback between the lung and thorax constitutes a major signal that sustains developmental as well as compensatory lung growth. After the loss of lung units as by pneumonectomy (PNX), increased mechanical stress and strain on the remaining units induce adaptive responses to augment oxygen transport, including 1) recruitment of alveolar-capillary reserves, 2) remodeling of existing tissue, and 3) regenerative growth of acinar tissue when strain exceeds a critical threshold. Alveolar hypoxia, hormones, and growth factors may feed into the mechanical feedback system to modify an existing growth response but are unlikely to initiate compensatory growth in the absence of sufficient mechanical signals. Whereas endogenous post-PNX alveolar growth preserves normal structure-function relationships, experimental manipulation of selected metabolic pathways can distort these relationships. Finally, PNX widens the disparity between the rapidly adapting acini and slowly adapting conducting airways and blood vessels, leading to disproportionate airflow and hemodynamic dysfunction and secondary hypertrophy of the right ventricle and respiratory muscles that limits overall organ function despite regeneration of gas exchange tissue. These are key concepts to consider when formulating approaches to stimulate or augment compensatory growth in chronic lung disease.

Adaptation, Physiological↗

PubMed1994

Characterization of platelet-activating factor synthesis in glomerular endothelial cell lines.

Platelet-activating factor synthesis in two transformed lines of glomerular endothelial cells was characterized and contrasted with platelet-activating factor production in macrovascular-derived endothelial cells as well as with glomerular cells of mesenchymal origin. Platelet-activating factor synthesis was assessed in intact cells and in cell-free preparations. Glomerular endothelial cells constitutively synthesize bio-active alkyl-PAF, and this basal activity can be chronically augmented by various inflammatory and thrombotic agents. In contrast, thrombin-mediated platelet-activating factor formation in bovine pulmonary aortic endothelial cells as well as in glomerular mesangial cells is acute and transient. The potential role of anti-inflammatory prostanoids to function as negative feedback modulators of thrombin- or endothelin-mediated platelet-activating factor synthesis was also investigated, as the synthesis of platelet-activating factor is often associated with the formation of these prostanoids. Indomethacin augmented receptor-mediated platelet-activating factor synthesis while prostanoids of the E and I series reduced agonist-stimulated PAF synthesis. In summary, the unique capacity of glomerular endothelial cells to respond to inflammatory stimuli with sustained platelet-activating factor synthesis is a clear indication of this cell's pivotal role in augmenting the inflammatory response in the limited environment of the glomerulus.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed1998

ACTH responses to hypotension and feedback inhibition of ACTH increased by chronic progesterone treatment.

During pregnancy, arterial pressure, baroreceptor sensitivity, and adrenocorticotropic hormone (ACTH) responses to hypotension are decreased. Basal ACTH and cortisol are increased in pregnancy, suggesting a reduction in cortisol feedback inhibition of ACTH. Acute treatment with progesterone decreases arterial pressure, baroreflex-mediated responses, and corticosteroid feedback effects on ACTH. These experiments test the hypothesis that chronic increases in progesterone produce changes in arterial pressure, ACTH responses to stress, and feedback inhibition of ACTH similar to pregnancy. Ewes were treated with progesterone for 60-80 days. This increase in plasma progesterone (to 7.6 +/- 0.4 ng/ml) did not alter basal ACTH, cortisol, arterial pressure, or heart rate. However, ACTH and AVP responses to hypotension were augmented in progesterone-treated ewes compared with untreated ewes. Chronic progesterone treatment resulted in greater inhibition of ACTH by cortisol. Because chronic progesterone treatment did not decrease the ACTH response to hypotension or attenuate the feedback control of ACTH secretion, these results suggest that the changes in pituitary-adrenal control during pregnancy do not reflect a simple effect of progesterone alone.

Adrenocorticotropic Hormone↗

PubMed1995

Galanin neurons exhibit estrogen receptor immunoreactivity in the female rat mediobasal hypothalamus.

Galanin has been shown to augment the hypothalamic luteinizing hormone releasing hormone and pituitary luteinizing hormone release and to play an important role in the feedback effects of ovarian steroids on pituitary hormone secretion. To further characterize estrogen effects on galanin, we tested for the existence of estrogen receptors in arcuate nucleus galanin-producing cells. Hypothalamic vibratome sections from colchicine-pretreated female rats were double immunolabeled for estrogen receptor and galanin. Neurons which exhibited immunoreactivity for either estrogen receptor or galanin were distributed throughout the hypothalamus; and a population of neurons, located predominantly in the mediobasal hypothalamus, displayed immunoreactivity for both galanin and estrogen receptor. These results raise the possibility that estrogen may act directly on galanin-producing arcuate nucleus neurons to regulate pituitary hormone secretion.

Animals↗

PubMed1996

Glycine effects on glutamate-receptor elicited acetylcholinesterase release from slices and synaptosomes of the spinal ventral horn.

To study the mechanisms by which glutamate-elicited acetylcholinesterase release (GEAR) might play a part in the pathogenesis of excitotoxically triggered motor neurone disease, and to investigate the interaction of GEAR with spinal glycinergic mechanisms, we measured acetylcholinesterase (AChE) and cholinergic markers, after stimulating ventral horn slices and synaptosomes from the mouse spinal cord, with both glutamate- and glycine-receptor agonists. Glutamate (GLU), kainate and AMPA, as well as glycine (GLY) evoked dose-related, calcium-dependent liberation of soluble forms of AChE from both slices and synaptosomes. GLY-evoked AChE release showed remarkable age-related postnatal changes. In the immature slice of the ventral horn. GLY potentiated the GEAR response in the presence of strychnine, suggesting N-methyl-D-aspartate (NMDA) receptor involvement, and was also able to evoke a strychnine-sensitive AChE release in the absence of exogenous GLU. After the 28th postnatal day, nearly all the AChE secreted was released either after the activation of non-NMDA glutamate receptors or by strychnine-sensitive GLY-evoked AChE release mechanisms. Both GEAR and GLY-evoked AChE release might impair the negative feedback loop which modulates the overactivation of motor neurones, and cause prolonged extracellular rises of soluble AChE. These effects might augment the vulnerability of motor neurones to excitotoxic stress, promote fiber outgrowth, and eventually accelerate the metabolic exhaustion of lower motor neurones. It is possible that the mechanisms described are operative at the spinal cord of ALS/MND patients.

Acetylcholinesterase↗

PubMed2000

Spike-and-wave discharges of absence seizures as a transformation of sleep spindles: the continuing development of a hypothesis.

OBJECTIVES: This review aims to offer a critical account of recent scientific developments relevant to the hypothesis which Pierre Gloor proposed in the 1970s for the generation of spike and wave discharges (SWDs) of primary generalized absence seizures. RESULTS: According to this hypothesis SWDs develop in the same circuits, which normally generate sleep spindles, by an initially cortical transformation of one every two or more spindle waves to a 'spike' component of SWDs, while the next one or more spindle waves are eliminated and replaced by a slow negative wave. This hypothesis was based on experiments in feline generalized penicillin epilepsy showing the possibility of transition from spindles to SWDs, when cortical neurons become hyper-responsive to thalamocortical volleys, which normally induce spindles, and thus engage feedback cortical inhibition, rebound excitation, recurrent intracortical dissemination of excitation during the 'spike' and strong excitation of thalamus for further augmentation of a brain wide synchronous oscillation. In the 1980s, electrophysiological studies in vitro and in vivo revealed the basic features of spindle rhythm generation by neurons in nucleus reticularis thalami and thalamocortical-corticothalamic oscillatory reverberations. CONCLUSIONS: In the light of this knowledge, experimental studies in several genetic and pharmacological animal models of absence seizures, clinical observations and theoretical studies in computer models have considered, tested, modified and challenged this hypothesis. It may still be found useful in the era of dynamic digital EEG analysis of SWDs and its current sources.

Animals↗

PubMed1982

Changes in control of renin release in congestive heart failure in dogs: response to acute and chronic vasodilator therapy.

Neural control of renin secretion is an important physiologic mechanism, but alterations in the central nervous system feedback and control of renin release in heart failure have not been investigated. Accordingly we studied conscious dogs after volume overload (arteriovenous fistula) or chronic myocardial infarction. Acute infusion of nitroprusside was used to test the renin response to arterial hypotension and decreased central blood volume. Hydralazine and prazosin administration were used to test the response to chronic vasodilator administration. After 4 weeks of volume overload or 3 weeks after myocardial infarction, the renin response to a graded hypotensive stimulus was blunted. After 7 days of hydralazine or prazosin administration, plasma renin activity remained elevated and blood volume increased from baseline values. Our results indicate a decrease in the neural feedback control of renin release after chronic volume overload or myocardial infarction. However, chronic vasodilator administration still resulted in sustained augmented renin secretion and an increase in blood volume.

Animals↗

PubMed1992

IL-1 receptor antagonist protein production and gene expression in rheumatoid arthritis and osteoarthritis synovium.

IL-1 can participate in the perpetuation of arthritis through direct stimulation of synoviocytes and augmentation of matrix degradation. Hence, local production of the IL-1R antagonist protein (IRAP) might be an important negative feedback signal that regulates synovitis. We assessed synovial IRAP production in synovia from 30 individuals, by using a specific mAb and the immunoperoxidase staining method. IRAP was detected in 11 of 12 rheumatoid arthritis (RA) synovial tissues (ST) and was located primarily in the sublining, particularly in perivascular regions enriched for macrophages. Some staining was observed in the intimal lining of the synovium, although this was significantly less than in the sublining (p less than 0.05). Nine of 12 osteoarthritis (OA) tissues were positive for IRAP. In contrast to RA, the staining was observed primarily in the synovial lining in OA, with only minimal sublining IRAP being detected. Synovia from four patients without arthritis were negative (three autopsy specimens and one post-traumatic sample). Of the other two patients with miscellaneous diagnoses, one sample was negative (tenosynovitis) and one was positive (seronegative inflammatory arthritis) (sublining). Studies of serial sections and double-immunostaining experiments indicated that macrophages are the major cells containing immunoreactive IRAP. IRAP gene expression in vivo was determined by performing in situ hybridization on ST from 17 arthritis patients. RNA sense IRAP probes did not hybridize to any tissues. Anti-sense IRAP probes bound to two of nine RA tissues, two of six OA tissues, one of one seronegative inflammatory arthropathy tissue, and none of one flexor tenosynovitis tissue. As with immunoreactive protein, IRAP mRNA was primarily localized to cells in the synovial lining in OA but was more prominent in perivascular lymphoid aggregates in RA and seronegative inflammatory arthropathy. Northern blot analysis was performed on RNA isolated from nine ST. The appropriately sized IRAP band was identified in six of nine samples (five of six RA and one of three OA). Supernatants from cultured RA and OA ST cells contained immunoreactive and biologically active IRAP. Hence, IRAP gene expression and protein production occur in RA and OA synovium, albeit in different distributions.

Amino Acid Sequence↗

PubMed2003

Three-peptide control of pulsatile and entropic feedback-sensitive modes of growth hormone secretion: modulation by estrogen and aromatizable androgen.

The present review highlights a simplified perspective of growth hormone (GH) secretory control, which incorporates the individual and joint effects of final-common signals that converge on somatotrope cells. Critical peptidyl effectors are GH-releasing hormone (GHRH), GH-releasing peptide (GHRP, ghrelin), and somatostatin. The latter three-peptide ensemble mediates stimulation, inhibition, and feedback suppression of GH secretion via homologous and heterologous interactions. Pubertal sex steroids putatively act via post-aromatized estrogen (e.g., testosterone converted to estradiol by aromatase) to augment sensitivity to GHRH, potentiate GHRP action, and mute somatostatin restraint. The dynamic interactions in this three-peptide network, rather than the activity of any single effector, subserve core adaptations in GH secretion across development.

Androgens↗