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At least 163 records · Page 9Linked to original sources
PubMed1993

An animal model for the study of brain transmittor release in response to spinal cord stimulation in the awake, freely moving rat: preliminary results from the periaqueductal grey matter.

Electrical spinal cord stimulation (SCS) is an important method in the treatment of certain chronic pain syndromes which are difficult to manage with conventional techniques. The indications for this procedure have gradually narrowed to neuropathic pain states, especially those of peripheral origin, ischaemic pain due to peripheral vascular disease, and treatment-resistant angina pectoris. In spite of the clinical use of this method for more than 20 years, the mechanisms underlying the pain alleviating effect remain largely unknown. For the effect on ischaemic pain, recent animal research indicates a mediation via autonomic pathways. Concerning the effect on neuropathic pain progress in knowledge has been scanty. Data from spinal microdialysis in decerebrated or anaesthetized animals indicate the possible importance of serotonin and substance P in the dorsal horn for pain inhibition by SCS. However, data from experiments on anaesthetized animals are, for several reasons, not likely to truely reflect the mechanisms active in conscious humans under treatment with SCS. To avoid the influence of anaesthesia and to approach the clinical situation, we have developed an animal model enabling simultaneous SCS and supraspinal microdialysis in awake, freely moving rats. The animal model is described and some preliminary data indicating a release of gamma-amino butyric acid (GABA) induced by SCS in the periaqueductal grey matter (PAG), are presented.

Animals↗
PubMed1994

Breast carcinoma: a collective disorder.

The development and differentiation of the epithelial component of glandular tissues such as the breast is regulated by two apparently unrelated processes. One of these is presumed to be epithelial cell collective autonomous, that is, it is mediated by gene products which act directly on the epithelial cells. An important component of autonomous regulation is the functional expression of homotypic cell-cell adhesion molecules such as cadherins. The second process is non-autonomous and involves an inductive effect of the neighboring mesenchymal cell collective. An important component of non-autonomous regulation is the aggregation/condensation of mesenchyme closely associated with the epithelium. We propose that molecular alterations in autonomous and non-autonomous pathways are important causes and indicators respectively of breast cancer progression and that these two fundamental regulators of epithelial collective organization are in fact inter-dependent. For example, we show that the expression of hepatocyte growth factor (HGF), an epithelially targeted mesenchymally derived morphogenic factor is regulated by mesenchymal cell density (condensation) and by factors released from epithelial cells. Breast epithelial cells produce factors which inhibit and stimulate HGF expression. The inhibitory factor is transforming growth factor beta (TGF-beta) and the activation state of TGF-beta is a crucial element in HGF homeostasis. The balance of negative and positive HGF regulators is markedly affected by the growth conditions and differentiation state of the epithelial cells. The expression of the HGF receptor, met, is high in normal breast epithelial cells and in dedifferentiated (ER negative) tumor cells but is reduced or lost in ER positive well differentiated epithelial cells. Our results indicate that the expression of at least one epithelial morphogen, HGF, is inter-dependently regulated by mesenchymal condensation and by factors released by neighboring epithelial cells.

Breast Neoplasms↗
PubMed1994

The mind and the immune system.

Stress-induced brain-mediated immunoregulation is effected by two pathways: autonomic outflow and (neuro)endocrine outflow. Particular attention is given to the interaction-effects of chronic an acute stress. Recent data have established that cells of the immune system produce neuro-peptides and hormones. In concert with cytokines released by these immune cells the brain can be informed on the nature of ongoing immune activity. The significance of conditioning of immune responses is discussed.

Autonomic Nervous System↗
PubMed1995

Immunohistochemical correlation of human adrenal nerve fibres and thoracic dorsal root neurons with special reference to substance P.

Applying a double-labelling immunofluorescence technique, six types of substance P-containing nerve fibres were distinguished in the human adrenal gland according to the immunohistochemical colocalization of (I) calcitonin gene-related peptide (CGRP), (II) cholecystokinin, (III) nitric oxide synthase, (IV) dynorphin, (V) somatostatin, and (VI) vasoactive intestinal polypeptide. Fibre populations I to IV in their mediator content resembled the respective subpopulations of primary sensory neurons in human thoracic dorsal root ganglia, while populations V and VI revealed no correspondence with dorsal root neurochemical coding. Nerve fibres with the combination substance P/nitric oxide synthase occurred only in the adrenal cortex, whereas all other fibre types were present in both cortex and medulla. As revealed by immuno-electron microscopy, substance P-immunolabelled axon varicosities (a) exhibited synaptic contacts with medullary chromaffin cells or with neuronal dendrites, (b) were directly apposed to cortical steroid cells and (c) were separated from fenestrated capillaries only by the interstitial space. These findings provide immunochemical support for an assumed sensory innervation of the human adrenal gland, and additionally suggest participation of substance P in efferent autonomic pathways. Furthermore, the results are indicative for a differentiated involvement of substance P in the direct and indirect regulation of neuroneuronal and neuroendocrine interactions.

Adolescent↗
PubMed1997

Electrodermal activity in patients with Parkinson's disease.

Peripheral sympathetic activity was investigated in 25 Parkinson's disease (PD) patients and 27 healthy subjects by measuring the skin resistance level (SRL) and skin resistance response (SRR) at the palm of the hand during rest, auditory stimulation and patellar tendon tapping. Blood flow to the hand was also monitored. Normal responses were obtained from all the 27 healthy subjects with both stimuli. All but one of the 25 PD patients responded to sound, six patients failed to respond to patellar tendon tapping and one patient failed to respond to both stimuli. The SRRs (when detectable) of PD patients were always smaller in amplitude than those of normal subjects. It was also observed that while an electrodermal response was present, no vasomotor response could be elicited by either stimulus in some patients. The opposite was true in some other patients. When response latencies were evaluated, it was found that although the mean latency of SRRs evoked by tendon taping was shorter than the mean latency of responses to auditory stimuli in normal subjects, this was not the case in PD patients. SRR mean latency to patellar tendon tapping was significantly longer in PD patients compared with that in normal subjects. Mean latencies of responses to auditory stimuli were the same for both normal subjects and patients. The ratio of the SRR amplitude to SRL (i.e. relative change in SRL) during both types of stimulation was significantly smaller in PD patients than in normal subjects. All the above findings were also true when blood flow to the tissue was interrupted briefly. These findings support the conjecture that the abnormal peripheral sympathetic neural responses associated with PD may arise from a functional disorder in the basal ganglia that influence the efferent autonomic pathway, from impairment of the intermediolateral column of the spinal cord, and possibly from cognitive deficits.

Acoustic Stimulation↗
PubMed2006

The cold face test: a non-baroreflex mediated test of cardiac vagal function.

Application of cold to the face evokes potent bradycardia and a pressor response, similar to the diving reflex. However, the role of the baroreceptors in this response is unclear. Ten healthy controls and two patients with baroreflex impairment were recruited. A cold face test (CFT) was induced by the application of three cold packs (0.5 degrees C) to the face. Heart rate (ECG), blood pressure (Finapres) and skin temperature (forehead electrode) were recorded continuously. All data were analyzed using unpaired Students t-tests, and expressed as mean +/- SD. In all controls, CFT induced bradycardia. The mean onset latency was 5.6 +/- 4.6 s, and the maximal bradycardia was seen at 35.8 +/- 15.8 s. Systolic blood pressure increased in eight controls, with a mean onset latency of 18.8 +/- 16.6 s and a peak rise at 38.7 +/- 22.7 s. In the controls, bradycardia preceded the pressor response. The heart rate and blood pressure changes during CFT had a longer latency than baroreflex evoked responses. Moreover, one subject had bradycardia despite a fall in blood pressure. The two patients had abnormal Valsalva ratios and no change in heart rate during tilt, indicating impairment of the baroreflex. However, both their heart rate and blood pressure responses to CFT were normal. These data are further evidence of the limited role of the baroreflex in the autonomic responses to CFT. They suggest that the CFT may be of use in assessing the integrity of the efferent cardiovascular autonomic pathways in patients with suspected baroreflex impairment.

Adult↗
PubMed2006

Demyelinating disorders: update on transverse myelitis.

Transverse myelitis (TM) is a focal inflammatory disorder of the spinal cord. Perivascular monocytic and lymphocytic infiltration, demyelination, and axonal injury are prominent histopathogic features of TM. The clinical manifestations of TM are consequent to dysfunction of motor, sensory, and autonomic pathways. At peak deficit, 50% of patients with TM are completely paraplegic (with no volitional movements of legs), virtually all have some degree of bladder dysfunction, and 80% to 94% have numbness, paresthesias, or band-like dysesthesias. Longitudinal case series of TM reveal that approximately one third of patients recover with little to no sequelae, one third are left with a moderate degree of permanent disability, and one third have severe disability. Recent studies have shown that the cytokine interleukin-6 may be a useful biomarker, as the levels of interleukin-6 in the cerebrospinal fluid of acute TM patients strongly correlate with and are highly predictive of disability. Clinical trials testing the efficacy of promising axonoprotective agents in combination with intravenous steroids in the treatment of TM are currently underway.

Biomarkers↗
PubMed1993

Specificity of pseudorabies virus as a retrograde marker of sympathetic preganglionic neurons: implications for transneuronal labeling studies.

The purpose of the present study was to examine the specificity of the Bartha strain of pseudorabies virus (PRV) as a CNS retrograde marker. This information is critical in assessing whether this virus has potential value as a specific transneuronal marker. The model system chosen for analysis was the intermediolateral cell column (IML)--the principal site of origin of sympathetic preganglionic neurons (SPNs). Two experiments were performed. The first experiment established the usefulness of this model system and the second examined the properties of PRV as a retrograde cell body marker. In the first experiment, injections of two different conventional retrograde cell body markers (cholera toxin-beta subunit (CTb) and Fluoro-Gold) were made in two ipsilateral sympathetic structures (viz., stellate ganglion and adrenal gland) in the same rat. This experiment established that (1) heterogenous SPNs originate in the same cell clusters that form the IML at the T4-T8 levels and 2) SPNs innervate specific sympathetic targets with almost none providing a dual innervation of the stellate ganglion and adrenal gland. This mosaic arrangement of target-specific SPNs makes the IML an excellent CNS site for this type of study. The second experiment followed the same paradigm: PRV was injected into the stellate ganglion and CTb into the adrenal gland (and vice versa). These experiments established that PRV infections of one functional class of SPNs did not produce infections in nearby, functionally unrelated SPNs and did not cause a reduction in the SPN cell population, except under conditions of severe gliosis. These two properties increase the probability that Bartha PRV may be used as a specific retrograde transneuronal marker of central autonomic pathways.

Animals↗
PubMed1976

Effects of acute administration of delta9-tetrahydrocannabinol on pulmonary hemodynamics of anesthetized dogs.

I.v. administration of delta9-THC (2.5 mg/kg) To anesthetized dogs resulted in a decrease in heart rate, pulmonary blood flow (PBF), and a significant increase in pulmonary artery pressure (PAP) and total pulmonary vascular resistance (PVR). The increase in PVR to delta9-THC was significantly reduced by cardiac pacing, and was virtually abolished either by bilateral vagotomy or by pretreatment with hexamethonium. The data indicated the delta9-THC induced elevation of PVR was mediated via reflexogenic mechanisms involving afferent vagi and efferent autonomic pathways.

Animals↗
PubMed1986

Beta-adrenoceptors in the rat parotid gland enlarged by salivariectomy and bulk diet. Effects of denervation.

The numbers of beta-adrenergic receptors and level of cyclic AMP (cAMP) of the parotid gland of adult female rats were determined 4 weeks after introduction of a regimen that induced a 2-fold increase in gland weight. This regimen consisted of ablation of the submandibular-sublingual glands and substitution of the normal chow diet with a bulk diet consisting of 50% inert cellulose and 50% ground solid chow. There was a 2.4-fold increase in number (density) of beta-adrenoceptors in the enlarged parotid gland when comparison was made with parotid glands of control rats. The beta-adrenoceptor present in the enlarged and normal glands was of the beta 1 subtype. Removal of either autonomic pathway at the time of partial salivariectomy and dietary substitution was followed by a small reduction in number of beta-adrenoceptors (4-9% with either denervation), but when both nerves were removed the reduction was 25%; in magnitude, these changes were generally similar to those observed with denervated parotid glands of chow-fed rats. The norepinephrine concentration of the enlarged gland was much less than that of normal glands (reduced 38%); sympathectomy of normal or enlarged parotid glands resulted in a marked lowering of norepinephrine concentrations (to 1-5% of control levels); parasympathectomy had no effect on norepinephrine concentration of enlarged parotid glands but caused a decrease in that of the parotid of normal size. Apparently, the number of beta-adrenoceptors depends on the degree of activity of both the parasympathetic and sympathetic nerves to the parotid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Induction of Fos-like immunoreactivity in rat oxytocin neurons following insulin injections.

Double immunostaining for oxytocin (OT) and Fos was used to study the oxytocinergic system of the rat hypothalamic paraventricular nucleus (PVN) following intraperitoneal insulin injections. The expression of c-fos in the PVN appeared about 3 h after insulin treatment and was very high after 5 h while no labelling was observed in isotonic saline-injected animals. Twelve to 18% of OT neurons expressed Fos-like immunoreactivity and these activated neurons were found in both the magno- and the parvocellular compartments of the PVN suggesting that the OT neuron responses to insulin induced disturbances are complex and involve hormonal as well as autonomic pathways.

Animals↗
PubMed1988

Bombesin-like peptides: neuropeptides with mitogenic activity.

In recent years, a remarkable advance has been made in identifying the extracellular factors that control cell proliferation in a variety of cells. Bombesin-like peptides (BN-LP) are neuropeptides involved in the regulation of many important functions, including sensory transmission, regulation of central autonomic pathways, thermoregulation, pituitary, gastric, and pancreatic secretion, food intake, and satiety. They also may stimulate cellular proliferation in a developmental and tissue-specific manner. Their role in pathogenesis appears to be related to their properties as growth factors, especially in the lung, where BN-LP are proposed to induce growth of normal and neoplastic epithelial cells. The formulated hypothesis of control of SCLC growth by BN-LP will be tested using specific synthetic BN antagonists. Neuronal modulation of the release of BN-LP from neuroepithelial bodies and paracrine effects of BN-LP as sensory neurotransmitters indicate possible pathways of nervous system involvement in tissue development, proliferation, and differentiation, as well as repair processes and wound healing.

Animals↗
PubMed2006

Enhanced neuronal activation in central autonomic network nuclei in aged mice following acute peripheral immune challenge.

Infection is associated with activation in central autonomic nuclei involved in mediating coordinated host defense responses. Aged mice showed exaggerated sickness behavior following peripheral injection of pro-inflammatory bacterial lipopolysaccharide (LPS), but is unknown whether central autonomic network responses are concomitantly increased. To assess whether aged mice exhibit enhanced neural response to LPS, we compared neural responses using c-Fos immunohistochemistry in aged BALB/c mice (22-24 months) with those of young adult peers (3-6 months). Intraperitoneal LPS challenge induced robust expression of c-Fos protein in central autonomic regions, including catecholaminergic neurons in the pons and brainstem, as well as in barrier-associated areas including the circumventricular organs. The numbers of c-Fos positive neurons were significantly greater in the aged compared to the young adult mice. These findings show age-associated enhancement of response to inflammation in the blood-brain chemosensory interfaces as well the central autonomic pathways involved in the elaboration of sickness symptoms, which may contribute to exaggerated sickness and poorer outcomes of infectious disease in the elderly.

Age Factors↗
PubMed2006

The trifecta of aging in Caenorhabditis elegans.

Insulin signaling, mitochondrial respiration, and dietary restriction share conserved roles not only in the regulation of lifespan, but also in the timing and control of diverse functions such as reproduction, stress resistance and metabolism. These autonomous pathways differ in their dependence on known transcription factors and in their temporal requirements, but converge to manipulate the core set of physiological systems necessary for extended lifespan in worms. Recent work suggests that components of these pleiotrophic pathways might be manipulated specifically for their effects on aging without affecting additional downstream functions. Examination of these findings will help us to understand how the molecular mechanisms of distinct pathways can unite in the regulation of longevity.

Aging↗
PubMed2005

Current knowledge in the neurophysiologic modulation of obesity.

Obesity is today one of the commonest of life-threatening diseases in developed countries and generally results from an imbalance between energy intake and energy expenditure. Although there is increasing evidence for a genetic basis of obesity in some clinical syndromes, this seems to be the cause only in a limited number of patients and obesity is far from being considered as a gene-related disease. Eating is a complex and multifactorial process involving autonomous pathways that transfer sensory and motor information between the entire length of the digestive tract and the central nervous system. Modulation of the amount of energy that we take in as food involves several mechanisms and networks that connect the brain with the gut, this process being key to the regulation of body weight over time, as well as to the modification of long-term eating behaviors. Furthermore, this axis is closely coupled to other systems that are involved in energy homeostasis, namely, food preference, energy expenditure, and lifestyle. The identification of several neuropeptides that modulate eating behavior in various ways, along with studies performed in animal models, have focused attention on the role of these molecules and their clinical implications in the development of obesity in humans.

Animals↗
PubMed2003

NMDA receptor regulation of nNOS phosphorylation and induction of neuron death.

Stimulation of NMDA receptors activates neuronal nitric oxide synthase (nNOS) and the production of nitric oxide (NO). Dephosphorylation of nNOS increases nNOS enzymatic activity. We have examined the regulation of nNOS phosphorylation in rat cortical neurons following NMDA receptor activation. We show that nNOS is constitutively phosphorylated and that NMDA receptor activation decreases the level of nNOS phosphorylation by a mechanism that is blocked specifically by NMDA receptor antagonists and inhibitors of the Ca2+-regulated phosphatases calcineurin and PP1/PP2A. Using quantitative digital microscopy, we show that NMDA receptor activation induces the accumulation of nitrotyrosine, a measure of nNOS activity, and TdT-mediated fluorescein-dUTP nick end labeling (TUNEL) positivity, a measure of cell death. A calcineurin inhibitor blocked the increase in both TUNEL and nitrotyrosine positivity. Notably, TUNEL was increased in those neurons that were most strongly positive for nitrotyrosine. We conclude that NMDA receptor activation induces death of neurons by a cell autonomous pathway involving nNOS dephosphorylation by a calcineurin-dependent mechanism.

Animals↗
PubMed2005

The basic physiology and pathophysiology of melatonin.

Melatonin is a methoxyindole synthesized and secreted principally by the pineal gland at night under normal environmental conditions. The endogenous rhythm of secretion is generated by the suprachiasmatic nuclei and entrained to the light/dark cycle. Light is able to either suppress or synchronize melatonin production according to the light schedule. The nycthohemeral rhythm of this hormone can be determined by repeated measurement of plasma or saliva melatonin or urine sulfatoxymelatonin, the main hepatic metabolite. The primary physiological function of melatonin, whose secretion adjusts to night length, is to convey information concerning the daily cycle of light and darkness to body physiology. This information is used for the organisation of functions, which respond to changes in the photoperiod such as the seasonal rhythms. Seasonal rhythmicity of physiological functions in humans related to possible alteration of the melatonin message remains, however, of limited evidence in temperate areas in field conditions. Also, the daily melatonin secretion, which is a very robust biochemical signal of night, can be used for the organisation of circadian rhythms. Although functions of this hormone in humans are mainly based on correlative observations, there is some evidence that melatonin stabilises and strengthens coupling of circadian rhythms, especially of core temperature and sleep-wake rhythms. The circadian organisation of other physiological functions could depend on the melatonin signal, for instance immune, antioxidative defences, hemostasis and glucose regulation. Since the regulating system of melatonin secretion is complex, following central and autonomic pathways, there are many pathophysiological situations where the melatonin secretion can be disturbed. The resulting alteration could increase predisposition to disease, add to the severity of symptoms or modify the course and outcome of the disorder.

Adaptation, Physiological↗
PubMed2005

Role of chromatin modification in flowering-time control.

The regulation of the FLC locus provides a plant model of how chromatin-modifying systems have emerged as important components in the control of a major developmental switch, the transition to flowering. Genetic and molecular studies have revealed that three systems of FLC regulation (vernalization, FRI and the autonomous pathway) all influence the state of FLC chromatin. Histone H3 trimethylation at lysine 4 and histone acetylation are associated with active FLC expression, whereas histone deacetylation and histone H3 dimethylation at lysines 9 and 27 are involved in FLC repression. These chromatin modifications provide an additional level of regulation of gene expression beyond that of the transcription factors that recruit RNA polymerase to target genes.

Arabidopsis↗