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PubMed1976

Automatic recording and evaluation of neuronography.

The introduction in the 60' s of the Nerve Excitability Test (NET) by Laumans and Jongkees for the diagnosis of Bell's palsy stimulated an interest of quantitative testing of the facial nerve. In 1970 Yanagihara reported the Evoced Myography (EMG; i.e. NET is combined with EMG). Starting with electrophysiological basis of the impulse spread of peripheral nerves May, in 1971, extended this concept by including supraliminal stimuli, i.e. Maximal Stimulation Test (MST), for diagnostic purposes. This method eventually developed into what is known as neuronography (Esslen, Huffmann, Ehrenberger, Satoh). It is undoubtedly a refinement in the question of prognosis of Bell's palsy. Continuing the original concept of May we have developed an electronic device with which to carry out automatically the neuronography that demonstrates an evaluation on a numeric display. We use the conventional bipolar negative square wave for a 1 ms stimulation. We stimulate the angle of the mandible, where the ramus marginalis can be readily found in all patients. Neuronography and Evoked Myography provide earlier a more precise prognosis of facial palsy than Nerve Excitability Test (NET). We developed an electronic device for the Maximal Stimulation Test (MST) of May, M., that is automatic. The device counts the spikes of the evoked myogram. A time window is related to the stimulus to exclude stimulus noise and background muscle noise from the counter. Only spikes seen in this window are processed. The number of spikes generated per stimulus is the measurement of the live axons in a stimulated nerve.

Electronic Data Processing↗

PubMed1992

Noradrenergic inputs enhance the response of neurosecretory cells to osmotic stimulation.

Extracellular recordings from neurosecretory cells in the hypothalamic paraventricular nucleus (PVN) displayed either an excitation or no response following electrical stimulation (5 Hz) of the A1 noradrenergic region of the ventrolateral medulla, and exhibited either an increase or no effect in neuronal activity in response to intracarotid injections of hypertonic saline (0.2 M, 0.05 ml). The neurons responded to both the electrical and osmotic stimuli, A1 region stimulation at the subthreshold current (80-90% of the threshold required to evoke the response) significantly enhancing the facilitatory response caused by the osmotic stimulation. These results suggest that the A1 region may serve to potentiate the responsiveness of PVN neurosecretory cells in response to changes in plasma osmolality.

Animals↗

PubMed1996

Basal and touch-evoked fos-like immunoreactivity during experimental inflammation in the rat.

Fos-immunoreactivity can readily be induced in spinal cord neurones by noxious, but to a much more limited extent, by innocuous peripheral stimuli. The present study has investigated whether low intensity stimuli and electrical stimulation of A beta afferents elicit greater c-fos expression during the behavioural sensory hypersensitivity generated by experimental peripheral inflammation. We have examined the time-course of c-fos expression after inflammation produced by either an intra-plantar injection of the irritant turpentine oil or of complete Freund's adjuvant (CFA). In the former case, a significant initial expression in all dorsal horn laminae was followed by a gradual decrease, whereas after CFA injection, an initial expression limited to the superficial laminae subsequently extended into the deep laminae, with a decrease at 24 h and an increase in labelling at later times. Low intensity touch stimuli repeated for 10 min, when applied at 24 h and 48 h after CFA injection, elicited a significant increase in the number of Fos-immunoreactive neurons in both the superficial and deep laminae of the dorsal horn compared to non-inflamed animals. Electrical stimulation of the sciatic nerve 24 h post-CFA injection, at a strength sufficient only to activate A beta-afferents fibres (100 microA, 50 microseconds, 10 min), also elicited a significant increase in labelling relative to the same stimuli applied in control animals, especially in laminae V-VI. The present results demonstrate that low intensity cutaneous stimuli elicit a significantly greater increase in c-fos expression in dorsal horn neurons during peripheral inflammation and that A beta-afferent input contributes to this, a finding that may relate to the allodynia experienced during inflammation.

Afferent Pathways↗

PubMed1991

Olfactory associative conditioning in infant rats with brain stimulation as reward: II. Norepinephrine mediates a specific component of the bulb response to reward.

One of the circuits modified by early olfactory learning is in the olfactory bulb. Specifically, response patterns of mitral-tufted cells are modified by associative conditioning during the early postnatal period. In addition, previous work has demonstrated that mitral-tufted cell single units respond to both olfactory conditioned stimuli and rewarding stimulation of the medial forebrain bundle-lateral hypothalamus (MFB-LH). The present study suggests that norepinephrine beta-receptor activation is required for early olfactory learning using MFB-LH stimulation as reward. Propranolol injected before odor-MFB-LH pairings blocks the acquisition of conditioned behavioral responses and their neural correlates to the conditioned odor. Furthermore, propranolol blocks a specific class of the mitral-tufted cell responses to MFB-LH reward stimulation. The relationship of this response to reward and early learning is discussed.

Aging↗

PubMed1999

Dendritic cells and MPIF-1: chemotactic activity and inhibition of endogenous chemokine production by IFN-gamma and CD40 ligation.

We have examined the biological activity of the CC chemokine myeloid progenitor inhibitory factor 1 (MPIF-1) on human dendritic cells. MPIF-1 has chemotactic activity on dendritic cells derived from either peripheral blood monocytes or cord blood CD34+ progenitors. However, chemokine treatment did not induce further cell activation or maturation. In addition, MPIF-1 is constitutively released by monocyte-derived dendritic cells but not macrophages or monocytes (resting or stimulated). The proinflammatory stimuli lipopolysaccharide and tumor necrosis factor alpha, which induced the release of monocyte chemotactic protein-1, macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and interleukin-8, did not affect MPIF-1 release. In contrast, CD40 ligation and interferon-gamma treatment, while stimulating the production of the other chemokines, caused a pronounced reduction of MPIF-1 transcript and protein release. Thus, in dendritic cells the regulation of the production and release of MPIF-1 is distinct in comparison to other CC and CXC chemokines.

Antineoplastic Agents↗

PubMed1998

Ca2+ signaling by cholinergic and alpha1-adrenergic agonists is up-regulated in lacrimal and submandibular glands in a murine model of Sjögren's syndrome.

Innervation of the lacrimal gland of MRL/Mp-Fas-lpr/lpr (MRL/lpr), a murine model for Sjögren's syndrome, is unaltered with the onset or progression of the lymphocytic infiltration. To determine whether lacrimal and submandibular gland cells are able to respond to external stimuli, acini were prepared from MRL/lpr (diseased) and MRL/Mp-+/+ (MRL/+, control) mice at 4, 8, and 12 weeks of age and loaded with the fluorescent dye fura-2 to monitor changes in the intracellular Ca2+ concentration ([Ca2+]i) in response to cholinergic and alpha1-adrenergic stimulation, two major stimuli of lacrimal gland protein secretion. Cholinergic-induced [Ca2+]i increase was up-regulated 3- and 4-fold in lacrimal gland acini isolated from 8- and 12-week-old MRL/lpr mice, respectively, compared to 4-week-old animals, but was not up-regulated in age-matched MRL/+ control mice. Similarly, alpha1-adrenergic-induced [Ca2+]i increase was up-regulated 7- and 12-fold in acini isolated from 8- and 12-week-old MRL/lpr mice, respectively, compared to 4-week-old animals, but was not up-regulated in MRL/+ mice. Cholinergic-induced [Ca2+]i increase in submandibular gland acini of MRL/lpr and MRL/+ mice was the same at all ages. In contrast, alpha1-adrenergic-induced [Ca2+]i increase was up-regulated 3-fold in acini from 12-week-old MRL/lpr mice, compared to 4-week-old mice, but was not up-regulated in age-matched MRL/+ mice. We conclude that the Ca2+ signaling portion of cholinergic and alpha1-adrenergic pathway in the lacrimal gland and the Ca2+ signaling portion of alpha1-adrenergic pathway in the submandibular gland is up-regulated with the onset and progression of the lymphocytic infiltration in the MRL/lpr murine model of Sjögren's syndrome.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

[Analysis of the mechanisms of refractivity of the pituitary-adrenal system in rat ontogeny].

In the course of postnatal ontogeny of rats, the synthesis and secretion of corticosterone after birth first decline, then increase by the 3d week of development, reaching by puberty the level seen in adult animals. During stressor stimulation with "neurogenic" stimuli (sound, swinging), the response on the part of the pituitary-adrenal system (PAS) is detectable only at the age of 3 weeks, whereas during immobilization of the animals with paw stretching and fixation it is detectable since the first day of life. The chemical stimulants of the adrenal cortex (ACTH), of the pituitary (vasopressin) and of the hypothalamus (insulin) activate the peripheral and central components of the PAS at varying age periods and to varying degree. This indicates that during early postnatal ontogenesis, the character of a stressor stimulus and line of its effect on different components of the system play the key roles.

Adrenal Cortex↗

PubMed2006

Effect of electrical stimulation of the internal capsule on nociceptive neurons responding to orofacial stimuli in the medullary dorsal horn of the rat.

Internal capsule (IC) stimulation has been used clinically to alleviate central pain. However, the neuronal mechanisms underlying pain relief by IC stimulation are poorly understood. In order to elucidate the analgesic mechanism, the effect of IC conditioning stimulation on nociceptive neurons in the rat medullary dorsal horn was investigated in the present study. Rats were anaesthetized with N(2)O-O(2) (2:1) and 0.5% halothane and were immobilized with pancuronium bromide. Two kinds of nociceptive neurons, wide dynamic range (WDR) and nociceptive specific (NS) neurons, responding to noxious stimulations of the face and oral structures were recorded in the trigeminal caudal nucleus and the medial reticular subnuclei. A test stimulus with a single rectangular pulse (2ms in duration, 5-70V) was applied to the centre of the receptive field. Responses in 55.9% of the WDR neurons and in 60% of the NS neurons were inhibited by conditioning stimuli to the ipsilateral IC with trains of 33 pulses (100-300microA) at 330Hz. The percents of peak inhibitory effects on WDR neurons and NS neurons were 78.1+/-25.0% (n=19) and 89.0+/-13.6% (n=3), respectively. The inhibitory effect continued for conditioning-test intervals of up to 500ms. Effective sites for conditioning stimulation were concentrated in the lateral side of the IC. These findings suggest that modulation of nociceptive transmission by IC stimulation occurs at second-order neurons via a presynaptic phenomenon by corticofugal fibers in the IC.

Animals↗

PubMed2000

Quantitative, rather than qualitative, differences in CD69 upregulation in human blood eosinophils upon activation with selected stimuli.

BACKGROUND: The study aimed to investigate whether CD69 expression on granulocytes is subject to specific regulation by inflammatory mediators, and, if so, to identify these factors in relation to eosinophil activity markers such as the EG2 epitope and ECP release. METHODS: Peripheral blood leukocytes from healthy donors were used. The surface and intracellular distribution of CD69 was investigated with a whole-blood cell-membrane permeabilization technique, the FOG method, and flow cytometry. In vitro stimulation was performed with GM-CSF, IL-5, IL-5 plus eotaxin, LPS, and fMLP. RESULTS: A preformed intracellular pool of CD69 was demonstrated in both eosinophils and neutrophils, but not in monocytes. Almost no resting eosinophils, neutrophils, or monocytes expressed CD69 on the cell surface. However, in vitro stimulation with selected stimuli increased the proportion of CD69-positive eosinophils to various extents, with GM-CSF being the most and fMLP the least efficient stimulus. The neutrophils did not respond under these conditions. Increased expression of the EG2 epitope and initiation of degranulation preceded CD69 upregulation. CONCLUSIONS: Eosinophils and neutrophils from healthy donors have a preformed intracellular pool of CD69, which is mobilized on the cell surface on eosinophils, but not on neutrophils, to various extents by selected stimuli. Monocytes, however, do not have a preformed intracellular pool of CD69. Our data indicate that a kinetic order exists among the EG2 expression, the degranulation process, and CD69 upregulation. Due to a quantitative, rather then a qualitative, upregulation of CD69 by stimuli associated with both allergic and bacterial inflammation, CD69 may be a potential activity marker of clinical value.

Adolescent↗

PubMed1989

Relationship between hormonal, GTP and Ins(1,4,5)P3-stimulated Ca2+ uptake and release in pancreatic acinar cells.

Electrically permeabilized rat pancreatic acini were used to evaluate the contributions of GTP and Ins(1,4,5) P3 to hormone-stimulated Ca2+ uptake and release from intracellular pools. Treatment of permeabilized acini with Ca2+-mobilizing hormones, GTP or GTP[S] resulted in stimulation of an ATP-dependent, VO4(2-)-sensitive Ca2+ uptake into a non-mitochondrial intracellular pool. GTP and GTP[S] also augmented the hormone-mediated stimulation of Ca2+ uptake. Including oxalate in the uptake medium increased Ca2+ uptake into this pool but did not modify the stimulation of Ca2+ uptake induced by hormones or GTP. Ins(1,4,5)P3 released all the extra Ca2+ accumulated as a result of hormone, GTP or GTP[S] stimulation. Hence, these stimuli activated the Ca2+ pump localized in the membrane of the hormone and Ins(1,4,5)P3-sensitive Ca2+ pool. Including 2,3-diphosphoglyceric acid (PGA) [an inhibitor of Ins(1,4,5)P3 hydrolysis] in the incubation medium blunted the GTP and GTP[S]-stimulated Ca2+ uptake. In the presence of PGA, the hormones inhibited Ca2+ accumulation, and GTP and GTP[S] augmented this effect. Accordingly, PGA stabilized the Ins(1,4,5)P3-evoked Ca2+ release from intracellular pools. Only in the presence of PGA was it possible to demonstrate hormonally-evoked Ca2+ release from permeabilized cells. GTP, and more importantly GTP[S], augmented the hormone-evoked Ca2+ release. Hormones and Ins(1,4,5)P3 in the presence or absence of GTP or GTP[S] released Ca2+ from the same intracellular pool. The extent of Ca2+ release caused by the combination of hormones and GTP or GTP[S] was similar to that evoked by Ins(1,4,5)P3 alone. Taken together, these results suggest that GTP or GTP[S] facilitates stimulation of phospholipase C by hormones. Such stimulation results in stimulation of protein kinase C and increased levels of Ins(1,4,5)P3 and is sufficient to explain the effects of GTP and GTP[S] on Ca2+ uptake and release from pancreatic acinar cells.

Adenosine Triphosphate↗

PubMed1976

Modification of stimulated lacrimal gland flow by sympathetic nerve impulses in rabbit.

This study was undertaken to determine if sympathetic nerve impulses modify lacrimal gland fluid (LGF) flow, which was continuously recorded from a cannula in the excretory duct of the lacrimal gland in rabbits anesthetized with pentobarbital sodium. The preganglionic trunk of the superior cervical ganglion was stimulated with electrical stimuli during pilocarpine-induced and reflexly induced secretion. Stimuli equal to or 6-8 times stronger than the intensity that produced maximal pupil dilation caused inhibition followed by poststimulus enhancement of LGF flow when the prestimulus LGF flow was greater than 3.0 mul/min. When the prestimulus LGF flow was less than 0.8 mul/min, the stronger stimulation enhanced LGF flow but the weaker stimulation produced inhibition followed by poststimulus enhancement of LGF flow. Although no measurements of lacrimal gland blood flow were made, the alterations in these responses, which occurred during alpha- and beta-adrenergic blockade, were consistent with the changes in sympathetically induced blood flow that occur during alpha- and beta-blockade in other organs.

Animals↗

PubMed1983

Re-evaluation of cortical and thalamic responses evoked by stimulation of the cerebellar fastigial nucleus in the cat.

In view of the discrepancies in reports about the cerebral responses induced by stimulation of the cerebellar fastigial nucleus in the cat, attempts were made to re-evaluate the effects of stimulation of the fastigial nucleus in the cerebral cortex and thalamus of cats anesthetized with pentobarbital. Stimulation of the fastigial nucleus elicited responses of low amplitude bilaterally in the medial portion of the precruciate cortex in 7 out of 25 animals studied. The responses were mainly composed of a positive wave which reversed its polarity at a depth between 250 and 500 microns from the cortical surface. Presumable relay cells for the responses were detected in the ventromedial nucleus and the medial area of the ventrolateral nucleus of the thalamus. Thalamic neurones showed a tendency to repetitive spike generation with variable latencies after fastigial stimulation, while conditioning stimuli applied to the midbrain reticular formation apparently counteracted it, enhancing the probability of generation of a single spike at a shorter latency. The effect of pentobarbital anesthesia on the fastigio-thalamic transmission is discussed in relation to the inconstant appearance of cortical responses after fastigial stimulation.

Animals↗

PubMed2003

Determination of the eicosanoid response to inflammatory stimuli in whole blood and its pharmacological modulation ex vivo.

Recognition of pathogens by immune cells initiates the release of numerous signaling molecules, including cytokines and eicosanoids. Here, we describe a simple procedure by which eicosanoids such as prostaglandin E(2) (PGE(2)), leukotriene B(4) (LTB(4)) and thromboxane B(2) (TxB(2)) can be measured using commercial enzyme immunoassays (EIAs) in the supernatant of whole blood stimulated with inflammatory stimuli. This is illustrated for numerous stimuli. The kinetics by which lipopolysaccharide (LPS) induces cyclooxygenase (COX)-2 expression in this setup were determined by quantitative reverse transcription polymerase chain reaction (RT-PCR). The eicosanoid response of the blood of 160 healthy volunteers to 1 microg/ml LPS was measured. To determine whether the action of a drug in vivo is represented ex vivo in the eicosanoid response of blood, one volunteer took a standard dose of a number of commercially available cyclooxygenase inhibitors on different days and the eicosanoid response of his blood to LPS was determined before ingestion as well as 2 and 6 h afterwards. The efficacy of the different pharmaceuticals on cyclooxygenase but not lipoxygenase products or cytokines could be monitored ex vivo. Similarly, ex vivo eicosanoid release was measured in blood from 10 volunteers who had taken 50 mg flurbiprofen. The method described extends approaches for studying whole blood cytokine release to the lipid mediators formed from arachidonic acid. These important signaling molecules represent targets for pharmacological intervention, which can now be monitored in vitro, as well as ex vivo employing the same model. Furthermore, the assay could be used to characterize the immune status of patient groups or to monitor the course of disease.

Adult↗

PubMed2004

Age-related endocrine dysfunction in nonhuman primates.

Peculiarities of functioning of some parts of the endocrine system (the pineal gland, pancreatic gland, hypothalamic-pituitary-adrenal axis, and hypothalamic-pituitary-testicular axis) in an aging nonhuman primate model (Papio hamadryas and Macaca mulatta) are described in this article. It has been established that basal activity of some endocrine functions (glucocorticoid, corticotropic, pancreatic, male estradiol producing) varies little with age. Other functions significantly decrease (DHEA/DHEAS-producing, pineal, testicular) or increase (male gonadotropic) with age. In contrast with basal activity, pronounced age-related changes in response to specific stimuli were detected in all endocrine functions. Old baboons and rhesus monkeys exhibited a delay of the normalization of the pituitary-testicular axis, adrenal cortex, and pancreatic gland function after their activation in response to specific stimuli, such as LHRH, CRH, ACTH, and glucose. Old monkeys also demonstrate decreased HPA axis sensitivity to glucocorticoid regulation by negative feedback and the HPT axis to inhibitory effect of prolonged administration of LHRH agonist. Age-related changes in reactions of endocrine functions in response to specific stimulating and inhibiting stimuli indicate impaired resiliency of these functions. Age-related endocrine changes perhaps play a pathophysiological role in age function disorders of hormonocompetent tissues and organs and age pathology.

Aging↗

PubMed1999

NADPH oxidase is functionally assembled in specific granules during activation of human neutrophils.

In addition to the extracellular production of O2- by NADPH oxidase in neutrophils stimulated by soluble stimuli, the intracellular formation of oxygen reactive species has been described. Cytochrome b559, the redox component of the NADPH oxidase complex, is mainly associated with specific granule membrane in resting neutrophils. We examined whether these granules could be a site for intracellular production of O2-. Phorbol myristate acetate (PMA)-stimulated neutrophils were fractionated by differential centrifugation, and generation of O2- was detected in both the granule and the plasma membrane-enriched fractions, but more in the granules. Translocation of p47phox and p67phox, two cytosolic components of the NADPH oxidase, was also quantitatively more important in the granules than in the plasma membrane fraction. After separation of the specific from the azurophil granules, p47phox and p67phox were found to be present only in the specific granules of PMA-activated cells. As a control, the production of O2- was studied in retinoic acid-differentiated NB4 cells that lack specific granules. During stimulation of NB4 cells with PMA, only the plasma membrane-enriched fraction was the site of O2- production. Together, these results indicate that NADPH oxidase can be functionally assembled in specific granules.

Cell Membrane↗

PubMed1992

On the possibility of independent activation of bilateral mismatch negativity (MMN) generators.

Event-related potential (ERP) studies on auditory selective attention have suggested that the neuronal traces underlying the mismatch negativity (MMN) develop separately for left and right ear inputs. We investigated whether this feature of the MMN could be exploited to activate the MMN generators in each hemisphere independently. Given the location of the MMN sources, this would allow separate assessment of left and right hemisphere auditory cortical structures. The MMN was elicited in a dichotic oddball paradigm using stimuli and conditions of stimulation that should optimize transmission of left and right ear stimuli to the contralateral auditory cortices. The MMN demonstrated no interhemispheric asymmetries, indicating that the bilateral MMN generators were symmetrically involved. The results of a supplementary experiment provide evidence for the simultaneous existence of multiple traces for MMN generation.

Acoustic Stimulation↗

PubMed1986

Short and long latency reflexes in human muscles following electrical and mechanical stimulation.

Electromyographic (EMG) recordings were made during slight voluntary contraction or during rest in various human muscles following electrical and mechanical stimulation. The electrical stimuli used in most of these experiments were square wave pulses with the duration of 100 microseconds given at a frequency of 3 Hz on cutaneous and mixed nerves. The mechanical stimuli were constant stretches of the muscle induced by taps of the electromechanical reflex hammer. The aims of the series of studies were to investigate the characteristic features of electrically and mechanically elicited muscular responses, the correspondence between electrically and mechanically elicited responses, the short latency response following muscle afferent stimulation and the modifications of the electrically elicited responses. The electrical stimulation during slight voluntary activity caused short and long latency excitatory phases in averaged and rectified EMG with the onset latencies much shorter than the voluntary reaction time. The responses were considered reflexive. The most constant short and long latency reflexes following electrical stimulation were found in the first dorsal interosseus muscle in the hand and in the extensor digitorum brevis in the foot. The mean onset latency for the short latency reflex was 30.9 +/- 1.7 ms (SD) and for the long latency reflex 50.9 +/- 2.8 ms in the hand muscle. In the foot muscle the mean short latency reflex latency was 54.9 +/- 4.1 ms and the long latency reflex latency was 80.5 +/- 5.5 ms. The onset latencies of the short and long latency reflexes during slight voluntary activity following stretching and following cutaneous nerve stimulation corresponded in the first dorsal interosseus muscle. It was concluded that they are generated at least partly via mutual pathways. The stretches given to the triceps brachii muscle during various head positions, different elbow angles and during the Jendrassik maneuver revealed short latency reflex facititations. The lesser degree of the facilitation was caused by the tonic neck reflex and the Jendrassik maneuver caused the greater degree of the facilitation. The short latency reflex following muscle afferent stimulation (the H-reflex) was elicited in the flexor carpi radialis muscle with a mean latency of 15.4 +/- 0.5 ms. The amplitude of the 50% H-reflex was modified by contracting or by stretching of the muscle. Voluntary contraction increased the 50% H-reflex amplitude about 30% and the passive stretching decreased it to about 80% of the control value. The patients with different central nervous system disorders showed abnormal electrically elicited short and long latency reflexes. The s

Adult↗

PubMed1990

[Neuropeptide-mediated transmission of nociceptive information and its regulation. Novel mechanisms of analgesics].

Substance P and somatostatin may be transmitters of nociceptive information, which are involved in the transmission of pressure and heat nociceptive information, respectively, in the spinal dorsal horn. Calcitonin gene-related peptide, which is present in the primary sensory neurons having substance P or somatostatin, may function as a pain-promoting substance and be involved in the production of inflammation-induced hyperalgesia. The descending noradrenergic system plays a role in inhibiting nociceptive transmission in the spinal dorsal horn, and inhibits the release of substance P evoked by noxious mechanical stimulation. Persistent noxious stimuli increase the release of Met-enkephalin from the nucleus reticularis gigantocellularis, which promotes the activity of the descending noradrenergic system. Morphine activates the descending noradrenergic system, acting on the nucleus reticularis gigantocellularis. Morphine also activates the descending serotonergic system, which inhibits the release of somatostatin evoked by thermal noxious stimulation.

Analgesics↗