Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Autonomic Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,801 records · Page 100Linked to original sources
PubMed1999

[Basic aspects of neuroendocrinoimmunology].

The purpose of this article is to discuss basic aspects of the interplay between the neuroendocrine and the immune systems. Two pathways link the brain and the immune system: the autonomic nervous system and the neuroendocrine outflow via the pituitary. Most of the influence of the brain on immune events is exerted through the hypothalamic-pituitary-adrenal (HPA) axis. Moreover, certain neurotransmitters, neuropeptides, and neurohormones affect immune function both in vivo and in vitro. Receptors for these molecules are present on immune cells. This cell-to-cell communication is bi-directional, since impulses from the immune system can affect many functions of the central nervous system. Cytokines released during the activation of the immune system, in turn, can alter the function of the HPA axis. In this context, we also describe our main findings working with a model of Candida albicans infection in rats exposed to chronic varied stress.

Animals↗
PubMed2001

A-85380 and epibatidine each interact with disparate spinal nicotinic receptor subtypes to achieve analgesia and nociception.

Nicotinic agonists, such as epibatidine (EPI) and A-85380, when administered systemically, elicit analgesia. Intrathecal EPI also produces analgesia accompanied by nociceptive and pressor responses. Since spinal administration of drugs offers a well defined pathway connecting the site of administration with behavioral and autonomic responses, we have compared the responses to intrathecal epibatidine and A-85380 to delineate the role of nicotinic acetylcholine receptors in spinal neurotransmission. Following implantation of intrathecal catheters in rats, we monitored cardiovascular, nociceptive, and antinociceptive responses after administration of various nicotinic receptor agonists. Consistent with A-85380 displacement of epibatidine from isolated spinal cord membranes, A-85380 elicited pressor, nociceptive, and antinociceptive responses similar to EPI. Antinociception was preceded by nociception. Both antinociception and nociception were blocked by mecamylamine, methyllycaconitine, and alpha-lobeline, but dihydro-beta-erythroidine only blocked the antinociceptive response. Whereas prior administration of EPI desensitized the nociceptive and antinociceptive responses to EPI, A-85380 pretreatment only desensitized EPI-elicited nociception and not antinociception. 2-Amino-5-phosphopentanoic acid pretreatment blocked the nociceptive response to A-85380, indicating A-85380 stimulated release of glutamate onto N-methyl-D-aspartate receptors to produce the irritant response of nociception. Intrathecal phentolamine virtually abolished A-85380 antinociception, but had no effect on EPI antinociception. Hence, analgesia can be produced by stimulation of distinct spinal preterminal nicotinic receptor subtypes, resulting in the release of neurotransmitters. In the case of A-85380, these sites primarily appear to be localized on adrenergic bulbospinal terminals. Our data suggest that A-85380 and EPI act at separate preterminal spinal sites as well as on distinct nicotinic receptor subtypes to elicit an antinociceptive response at the spinal level.

Analgesics, Non-Narcotic↗
PubMed1989

[Analysis of follow-up survey in spinocerebellar degeneration].

Spinocerebellar degeneration (SCD) is associated with other various degeneration of the nervous systems such as the optic tract, pyramidal pathway, extrapyramidal system, nuclei of the brain stem and autonomic nervous system as well as changes of heart. The clinical pattern, also have the great variability. We investigated the mode of progression of clinical symptoms and signs in 214 cases of SCD which were examined 2 times at intervals of about 10 years. 79 of 214 cases were reported to be died at the last examination. 135 alive cases included 3 with the Holmes type, 14 with late cortical cerebellar atrophy (LCCA) 10 with Menzel type, 18 with olive-ponto-cerebellar atrophy (OPCA), 33 with spinocerebellar form (SCF), 6 with Friedreich's ataxia, 18 with hereditary spastic paraparesis (HSP) and 33 with the other type. 79 dead cases included 0 with the Holmes type, 6 with LCCA, 5 with Menzel type, 32 with OPCA, 16 with SCF, 1 with Friedreich's ataxia, 4 with HSP and 15 with the other type. The disability of daily living in SCD revealed slower progression in the advanced stage than in the early stage. Every type of SCD had some different progression of disability each other. In the early stage, Friedreich's ataxia showed the highest progression of disability, but in the advanced stage, Holmes type and the OPCA did. Holmes type showed progression of ataxia without any remarkable change of other systems. LCCA showed increase of abnormality in the eye movements, pyramidal tract and autonomic nervous system in addition to the cerebellar system. OPCA involved multiple systems as ataxia worsening, but Menzel type had no remarkable changes of incidence in eye movement disorder.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Changes in coronary blood flow produced by the coronary artery occlusion.

The influence of the occlusion of one coronary artery on coronary blood flow in an intact myocardium was investigated in narcotised dogs with open chest by using the crossed circulation method. Interruption of blood inflow to one of the branches of the left coronary artery under autoperfusion of the coronary bed led to a drop in the blood flow rate in the intact branch of the same artery, which was caused by decreased perfusion pressure. Stabilization of coronary perfusion pressure made it possible to detect the dilatatory reaction of the intact coronary bed to the occlusion of one of the coronary arteries. On the basis of an analysis of the dilatatory reaction, conclusions are drawn about the reflex nature of the observed phenomenon. The results of experiments with selective pharmacological blockade of both parts of the autonomous nervous system suggest that the afferent and efferent pathways run in the sympathetic nervous system.

Afferent Pathways↗
PubMed1997

Extrinsic innervation of the cat prostate gland: a combined tracing and immunohistochemical study.

PURPOSE: The purpose of the present study was to determine the peripheral neural pathways, spinal distribution, sizes, and peptide transmitter content of primary afferent and autonomic efferent neurons that innervate the prostate gland. METHODS: Retrograde transport of the fluorescent dye "fast blue" (injected into the prostate gland) was combined with neurotransmitter immunohistochemistry. Lesions of the pelvic and pudendal nerve were used to determine the peripheral neural pathways. RESULTS: The majority of the afferent innervation arose from the sacral dorsal root ganglia (DRG) and was equally comprised of small, substance P- and calcitonin gene-related peptide-immunoreactive (IR) neurons and large, non-IR neurons. The majority (70%) of the afferent axons traversed the pelvic nerve with the remainder traversing the pudendal nerve. Fewer afferent neurons were located in lumbar DRG; nearly all of these were small, peptidergic neurons. Efferent autonomic neurons were located in the inferior mesenteric ganglia (IMG), sympathetic chain ganglia (SCG), and pelvic plexus ganglia (PPG). Nearly all efferent neurons in the IMG and SCG, but only 2/3 of the PPG neurons, contained dopamine-beta-hydroxylase. Substantial neuropeptide Y innervation was derived from the SCG but not the IMG or PPG. CONCLUSIONS: First, clinical reports suggested that sensory innervation of the prostate would be purely nociceptive in nature (implied by small, peptide-IR neurons). However, the present study suggests that there may also be a substantial, presumably non-nociceptive, afferent innervation (implied by findings of large, non-IR neurons). Second, 3 sources of autonomic efferent innervation exist, each being different in the distribution of transmitter phenotypes. Understanding the physiological role of putative non-nociceptive primary afferent neurons, and the differential roles of the various autonomic neurons, is likely to be important in developing therapies for the treatment of prostatic diseases, such as benign prostatic hyperplasia and prostatodynia.

Amidines↗
PubMed2003

Central serotonin and melanocortin pathways regulating energy homeostasis.

It is now established that the hypothalamus is essential in coordinating endocrine, autonomic, and behavioral responses to changes in energy availability. However, the interaction of key peptides, neuropeptides, and neurotransmitters systems within the hypothalamus has yet to be delineated. Recently, we investigated the mechanisms through which central serotonergic (5-hydroxytryptamine, 5-HT) systems recruit leptin-responsive hypothalamic pathways, such as the melanocortin systems, to affect energy balance. Through a combination of functional neuroanatomy, feeding, and electrophysiology studies in rodents, we found that 5-HT drugs require functional melanocortin pathways to exert their effects on food intake. Specifically, we observed that anorectic 5-HT drugs activate pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (Arc). We provide evidence that the serotonin 2C receptor (5-HT(2C)R) is expressed on POMC neurons and contributes to this effect. Finally, we found that 5-HT drug-induced hypophagia is attenuated by pharmacological or genetic blockade of downstream melanocortin 3 and 4 receptors. We review candidate brain regions expressing melanocortin 3 and 4 receptors that play a role in energy balance. A model is presented in which activation of the melanocortin system is downstream of 5-HT and is necessary to produce the complete anorectic effect of 5-HT drugs. The data reviewed in this paper incorporate the central 5-HT system to the growing list of metabolic signals that converge on melanocortin neurons in the hypothalamus.

Animals↗
PubMed1994

Activated platelet-derived growth factor autocrine pathway drives the transformed phenotype of a human glioblastoma cell line.

Human glioblastoma cells (A172) were found to concomitantly express PDGF-BB and PDGF beta-receptors. The receptors were constitutively autophosphorylated in the absence of exogenous ligand, suggesting the presence of an autocrine PDGF pathway. Neutralizing PDGF antibodies as well as suramin inhibited the autonomous PDGF receptor tyrosine kinase activity and resulted in up-regulation of receptor protein. The interruption of the autocrine loop by the PDGF antibodies reversed the transformed phenotype of the glioblastoma cell, as determined by (1) diminished DNA synthesis, (2) inhibition of tumor colony growth, and (3) reversion of the transformed morphology of the tumor cells. The PDGF antibodies showed no effect on the DNA synthesis of another glioblastoma cells line (U-343MGa 31L) or on Ki-ras-transformed fibroblasts. The present study demonstrates an endogenously activated PDGF pathway in a spontaneous human glioblastoma cell line. Furthermore, we provide evidence that the autocrine PDGF pathway drives the transformed phenotype of the tumor cells, a process that can be blocked by extracellular antagonists.

Antibodies, Monoclonal↗
PubMed1991

Afferent vascular resistance control during hemorrhage in normal and autonomically blocked rabbits.

We examined the role of the arterial and cardiac baroreceptors on the hindquarter conductance and heart rate responses of conscious rabbits bled at approximately 3% blood volume (BV)/min to 80% BV (i.e., 20% BV removed). We used rabbits with both sets of baroreceptors working and when only one or neither sets was working. Each animal was studied with normal effector function and during autonomic blockade (hormonal + local effectors), where release of arginine vasopressin (AVP) and renin (angiotensin II, ANG II) were enhanced. The local response (LR) to hemorrhage was determined in a separate group of neurohumorally blocked rabbits. The estimated constrictor response (ECR) was the difference between the LR and net conductance response. In normal rabbits, the ECR was 49 units, with the estimated arterial-to-cardiac barorecptor drive ratio approximately 2.8:1 and with the two receptor groups acting by simple addition. Both barorecptors contributed to the rise in heart rate, with the relative arterial-to-cardiac baroreceptor drive ratio approximately 4:1. When hemorrhage was performed during autonomic blockade, ECR was 84 units (compared with normal rabbits, P less than 0.01), but blood pressure was poorly maintained and the constrictor effect was not under baroreceptor control. Although the baroreceptors were critical for AVP release during autonomic blockade, they played no role in renin release (ANG II production); the latter was released in large amounts, producing near-maximum constriction, which was unrelated to the afferent input. Thus neurally mediated regulation during hemorrhage has substantial advantages over that mediated primarily through the pressor hormones.

Afferent Pathways↗
PubMed1977

Effects of bradykinin mediated by autonomic efferent nerves.

Intra-arterial injections of bradykinin cause increases in blood pressure and increased impulse rates in single sympathetic efferent fibres. The peptide also causes one or more large bladder contractions, which are associated with increased impulse rates in pelvic nerve efferent fibres whose spontaneous discharges are temporally associated with increases in intravesical pressure. These induced increases in pelvic nerve discharge and intravesical pressure could be abolished or greatly reduced by interference with conduction in pathways which mediate reflex bladder contractions. It is concluded that bradykinin has little direct action on the bladder, and that the large contractions which result from its administration are mediated by the central nervous system.

Action Potentials↗
PubMed1998

Regulation of the Hedgehog and Wingless signalling pathways by the F-box/WD40-repeat protein Slimb.

Members of the Hedgehog (Hh) and Wnt/Wingless (Wg) families of secreted proteins control many aspects of growth and patterning during animal development. Hh signal transduction leads to increased stability of a transcription factor, Cubitus interruptus (Ci), whereas Wg signal transduction causes increased stability of Armadillo (Arm/beta-catenin), a possible co-factor for the transcriptional regulator Lef1/TCF. Here we describe a new gene, slimb (for supernumerary limbs), which negatively regulates both of these signal transduction pathways. Loss of function of slimb results in a cell-autonomous accumulation of high levels of both Ci and Arm, and the ectopic expression of both Hh- and Wg- responsive genes. The slimb gene encodes a conserved F-box/WD40-repeat protein related to Cdc4p, a protein in budding yeast that targets cell-cycle regulators for degradation by the ubiquitin/proteasome pathway. We propose that Slimb protein normally targets Ci and Arm for processing or degradation by the ubiquitin/proteasome pathway, and that Hh and Wg regulate gene expression at least in part by inducing changes in Ci and Arm, which protect them from Slimb-mediated proteolysis.

Amino Acid Sequence↗
PubMed2005

Atropine-induced HRV alteration is not amended by electroacupuncture on Zusanli.

Acupuncture is known to influence autonomic nervous activity. Acupuncture on Zusanli points has been shown to enhance the regularity of gastric myoelectrical activity and accelerate gastric emptying, partly through the vagal pathway, in dogs. The aim of this study was to evaluate whether atropine-induced autonomic nervous alteration, measured by heart rate variability (HRV), could be amended by electroacupuncture on Zusanli points. HRV measurements were recorded in 15 healthy volunteers before, during and after electroacupuncture. Each subject was studied for three sessions in a randomized sequence, which included electroacupuncture on the Zusanli (St 36) points with or without premedication of atropine and placebo stimulation on a non-acupoint. The analysis of low frequency (LF), high frequency (HF) and LF/HF ratios were compared between different sessions. Serum levels of gastrin, motilin and pancreatic polypeptide (PP) levels were also measured. There was an increase in the LF/HF ratio (indicating increased sympathetic activity) during the post-acupuncture period with 2 Hz of electrical stimulation on the Zusanli acupoints. When IV atropine was used immediately before the electroacupuncture, there was a decrease in the LF power and HF power during the acupuncture and post-acupuncture periods. In addition, there was a significant increase in the LF/HF ratio during the acupuncture and post-acupuncture periods. There was a significant decrease in serum PP in the post-acupuncture period after premedication with IV atropine. In conclusion, atropine-induced HRV change might be mediated via the vagal pathway. However, atropine-induced HRV alteration is not amended by electroacupuncture on Zusanli points.

Adult↗
PubMed2006

The mevalonate pathway controls heart formation in Drosophila by isoprenylation of Ggamma1.

The early morphogenetic mechanisms involved in heart formation are evolutionarily conserved. A screen for genes that control Drosophila heart development revealed a cardiac defect in which pericardial and cardial cells dissociate, which causes loss of cardiac function and embryonic lethality. This phenotype resulted from mutations in the genes encoding HMG-CoA reductase, downstream enzymes in the mevalonate pathway, and G protein Ggamma1, which is geranylgeranylated, thus representing an end point of isoprenoid biosynthesis. Our findings reveal a cardial cell-autonomous requirement of Ggamma1 geranylgeranylation for heart formation and suggest the involvement of the mevalonate pathway in congenital heart disease.

Amino Acid Motifs↗
PubMed1982

Diagnostic, pathogenetic, and therapeutic aspects of diabetic neuropathy.

Since nearly all patients with diabetes mellitus will manifest evidence of dysfunction of their peripheral and autonomic nerves, neuropathy can be considered to be the most common of the so-called "late complications of diabetes." Mononeuropathies are uncommon, but can affect virtually any cranial or nerve and are thought to be due to vascular occlusion. Distal symmetrical polyneuropathy usually begins insidiously with the development of sensory symptoms involving the feet. These symptoms progressively ascend and are accompanied by progressive motor dysfunction as well as cardiac, gastrointestinal, and genitourinary manifestations of autonomic neuropathy. Numerous biochemical abnormalities including impaired neural protein synthesis, abnormal axoplasmic transport, disturbed polyol pathway activity, and abnormal myo-inositol metabolism have been described and have been postulated to underlie the development of diabetic peripheral and autonomic neuropathies. At the present time, the available treatments for diabetic neuropathies are largely palliative and are not curative. In the future, a better understanding of the pathophysiologic basis of diabetic neuropathy will undoubtedly lead to the development of more rational therapeutic approaches.

Aging↗
PubMed1999

Autonomous folding of a C-terminal inhibitory fragment of Escherichia coli isoleucine-tRNA synthetase.

We previously reported that C-terminal fragments of Escherichia coli Ile-tRNA synthetase, a monomeric enzyme of 939 amino acids, act as dominant negative inhibitors of the wild-type enzyme in vivo and in vitro. Our experiments suggested that it is possible to block the functional assembly of a monomeric protein by interfering with the folding pathway. We postulated that the inhibitory C-terminal fragments fold autonomously, and in the presence of full-length Ile-tRNA synthetase, trap the N-terminal portion of polypeptide in an unproductive complex. Here, we report the results of experiments aimed at understanding the mechanism of dominant negative inhibition. We have carried out biophysical experiments on fragment 585-939 of Ile-tRNA synthetase, which we previously determined to be the minimal inhibitory unit. Circular dichroism and fluorescence spectroscopy indicate that this fragment forms a compact and stable structure in solution. The secondary structure of this fragment is predominantly alpha-helical, consistent with the crystal structure of Ile-tRNA synthetase from another organism. The C-terminal fragment is capable of forming native-like secondary and tertiary structure after refolding from guanidine HCl. Taken together, the results are consistent with the hypothesis that the inhibitory fragment of Ile-tRNA synthetase forms an independent folding unit.

Circular Dichroism↗
PubMed1983

[Horseradish peroxidase labeled sources of descending propriospinal tracts in the cat].

Propriospinal interneurons with descending axons were labelled after unilateral horseradish peroxidase microinjections to the cat spinal cord at different segmental levels. Main part of long propriospinal units were bilaterally localized in the ventral quadrants (laminae VII, VIII) of cervical segments; some neurons with long ipsilateral projections were also found in the marginal layer (lamina I) and lateral regions of the dorsal horn basis (laminae IV-VI). Propriospinal neurons with short axons were distributed in wider regions of the spinal gray matter. In the lumbar segments a certain trend for concentration of such neurons was found: ipsilaterally--in the lateral part of the dorsal horn basis, intermediate gray and ventral horn and contralaterally--in the ventromedial parts of gray matter. In the cervical segments short neurons with both ipsilateral and contralateral projections are concentrated in lateral parts of gray matter. Some interneurons in the marginal layer, gelatinous substance and intermediolateral sympathetic nuclei were also identified as sources of short descending propriospinal pathways. A certain part of propriospinal neurons has axons of intermediate length; location of such units was to a certain extent similar to the location of long neurons. Correlation of location of propriospinal neuron populations and patterns of synaptic inputs to them as well as correlation of structural and functional characteristics of the neurons are discussed.

Animals↗
PubMed2006

Naive CD4 T cells constitutively express CD40L and augment autoreactive B cell survival.

Chronic engagement of the B cell receptor by soluble autoantigen leads to reduced B cell survival. Using the Ig and hen egg lysozyme double transgenic mouse model, we demonstrate that the survival of soluble autoantigen-engaged B cells is further reduced in mice lacking CD4 T cells or deficient in CD40. Mixed bone marrow chimera experiments reveal that, under homeostatic conditions, the CD40L-CD40 pathway can augment autoreactive B cell survival in a non-cell-autonomous manner. Naive CD4 T cells are shown to constitutively express CD40L mRNA and protein, although cell surface CD40L abundance is low because of engagement with CD40 on other cells. These observations indicate that the CD40L-CD40 pathway can augment the survival of autoantigen-engaged B cells in the absence of T cell activation. We propose that constitutive CD40L expression by naive CD4 T cells influences the composition of the B cell repertoire and may also affect the homeostasis of other cell types such as regulatory T cells in lymphoid organs.

Animals↗
PubMed2002

The battle of the sexes: opposing pathways in sex determination.

In mammals, a primordial gonad forms in XY and XX embryos that develops into a testis or an ovary depending on expression of Sry. Sry induces cell signalling pathways, including proliferation of Sertoli precursors and migration of peritubular myoid and vascular cells from the mesonephros. These events result in increased testis size and testis cord organization. Testis cord formation normally prohibits germ cells from entering meiosis. Ovarian fate is initiated in the absence of Sry, and has been proposed to be dependent upon the presence of meiotic germ cells in the gonad. We have shown that a developmental window exists during which testis development can be experimentally induced in XX gonads. This window closes just prior to the time that germ cells enter meiosis. Based on our work and much work that has preceded it, we suggest that the autonomous entry of germ cells into meiosis initiates the ovarian pathway and blocks testis development. Sry opposes this pathway by initiating testis cord formation prior to meiosis which sequesters germ cells inside cords and arrests them in mitosis. Current experiments in the lab address the hypothesis that cord formation and germ cell entry into meiosis are competing pathways in gonad development.

Animals↗
PubMed2005

Heart induction by Wnt antagonists depends on the homeodomain transcription factor Hex.

Inhibition of canonical Wnt/beta-catenin signaling by Dickkopf-1 (Dkk-1) or Crescent initiates cardiogenesis in vertebrate embryos. However, nearly nothing is known about the downstream effectors of these secreted Wnt antagonists or the mechanism by which they activate heart formation. Here we show that Wnt antagonists in Xenopus stimulate cardiogenesis non-cell-autonomously, up to several cells away from those in which canonical Wnt/beta-catenin signaling is blocked, indicative of an indirect role in heart induction. A screen for downstream mediators revealed that Dkk-1 and other inhibitors of the canonical Wnt pathway induce the homeodomain transcription factor Hex, which is normally expressed in endoderm underlying the presumptive cardiac mesoderm in amphibian, bird, and mammalian embryos. Loss of Hex function blocks both endogenous heart development and ectopic heart induction by Dkk-1. As with the canonical Wnt pathway antagonists, ectopic Hex induces expression of cardiac markers non-cell-autonomously. Thus, to initiate cardiogenesis, Wnt antagonists act on endoderm to up-regulate Hex, which, in turn, controls production of a diffusible heart-inducing factor. This novel function for Hex suggests an etiology for the cardiac malformations in Hex mutant mice and will make possible the isolation of factors that induce heart directly in the mesoderm.

Animals↗

Refine your search to explore more results.