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PubMed1981

Interactions between developing autonomic neurons and their target tissues.

Neurons critically depend on contact with the correct target tissue in order to survive and mature. The number of neurons surviving in a nerve centre directly depends on the size of the peripheral field in innervates. It has been proposed that target tissues release a neurotrophic substance (retrophin) which is internalized by nerve terminals and retrogradely transported to the perikarya where its action results in the survival of appropriate neurons. In the sympathetic nervous system, nerve growth factor probably acts as a retrophin. Similar retrophins must exist for other neuronal systems. In order to identify a parasympathetic retrophin two approaches have been taken. One was to grow appropriate target tissues with radiolabelled amino acids and to determine whether the proteins synthesized and released by these target tissues were retrogradely transported by parasympathetic neurons in vivo. The other approach was to show that a purified neurotrophic factor for the chick ciliary ganglion could be retrogradely transported by parasympathetic neurons. The results have suggested that at least two retrophins are involved in the normal development of the autonomic nervous system: one, nerve growth factor, for the sympathetic nervous system and the other, as yet unnamed, for the parasympathetic system.

Afferent Pathways↗
PubMed2002

RIP4 is an ankyrin repeat-containing kinase essential for keratinocyte differentiation.

The epidermis is a stratified, continually renewing epithelium dependent on a balance among cell proliferation, differentiation, and death for homeostasis. In normal epidermis, a mitotically active basal layer gives rise to terminally differentiating keratinocytes that migrate outward and are ultimately sloughed from the skin surface as enucleated squames. Although many proteins are known to function in maintaining epidermal homeostasis, the molecular coordination of these events is poorly understood. RIP4 is a novel RIP (receptor-interacting protein) family kinase with ankyrin repeats cloned from a keratinocyte cDNA library. RIP4 deficiency in mice results in perinatal lethality associated with abnormal epidermal differentiation. The phenotype of RIP4(-/-) mice in part resembles that of mice lacking IKKalpha, a component of a complex that regulates NF-kappaB. Despite the similar keratinocyte defects in RIP4- and IKKalpha-deficient mice, these kinases function in distinct pathways. RIP4 functions cell autonomously within the keratinocyte lineage. Unlike IKKalpha, RIP4-deficient skin fails to fully differentiate when grafted onto a normal host. Instead, abnormal hair follicle development and epidermal dysplasia, indicative of progression into a more pathologic state, are observed. Thus, RIP4 is a critical component of a novel pathway that controls keratinocyte differentiation.

Animals↗
PubMed1994

Rat spinal cord neurons contain nitric oxide synthase.

We describe the distribution and characteristics of nitric oxide synthase-containing neurons in rat spinal cord using a polyclonal affinity-purified antibody against rat cerebellar nitric oxide synthase. Numerous neurons were stained throughout the entire rostrocaudal extent of the spinal cord. Cell bodies, dendrites and axons stained in a uniform manner. Nitric oxide synthase immunoreactivity was intense in neurons of laminae I-IV and X throughout the entire spinal cord. Neurons in the intermediolateral cell column of the thoracic and lumbar spinal cord were also intensely stained for nitric oxide synthase. The sacral cord demonstrated substantial nitric oxide synthase immunostaining within lamina VII. For the entire cord, scattered neurons in laminae V, VI, VII, and VIII were weakly positive. In addition, punctate nitric oxide synthase staining throughout laminae I, III and surrounding some large motor neurons in the ventral horn suggested the presence of nitric oxide synthase at synapses. Axons and dendritic terminals located in the gray and white matter were also stained. The majority of nitric oxide synthase positive neurons in the intermediolateral cell column were double-labelled by subcutaneously injected FluoroGold confirming that these cells were preganglionic autonomic neurons. Most NADPH-diaphorase-stained neurons were also nitric oxide synthase-positive. The distribution of nitric oxide synthase-containing neurons in spinal cord suggests that nitric oxide plays a role in spinal cord neurotransmission including: preganglionic sympathetic and parasympathetic, somatosensory, visceral sensory and possibly motor pathways. In particular, the autonomic nervous system appears enriched with nitric oxide synthase immunoreactivity. The precise role of each neuron type remains to be demonstrated in physiologic and pathophysiologic paradigms.

Amino Acid Oxidoreductases↗
PubMed2000

The maternal Xenopus beta-catenin signaling pathway, activated by frizzled homologs, induces goosecoid in a cell non-autonomous manner.

In spite of abundant evidence that Wnts play essential roles in embryonic induction and patterning, little is known about the expression or activities of Wnt receptors during embryogenesis. The isolation and expression of two maternal Xenopus frizzled genes, Xfrizzled-1 and Xfrizzled-7, is described. It is also demonstrated that both can activate the Wnt/beta-catenin signaling pathway as monitored by the induction of specific target genes. Activation of the beta-Catenin pathway has previously been shown to be necessary and sufficient for specifying the dorsal axis of Xenopus. beta-Catenin is thought to work through the cell-autonomous induction of the homeobox genes siamois and twin, that in turn bind to and activate the promoter of another homeobox gene, goosecoid. However, it was found that the beta-catenin pathway regulated the expression of both endogenous goosecoid, and a goosecoid promoter construct, in a cell non-autonomous manner. These data demonstrate that maternal Frizzleds can activate the Wnt/beta-catenin pathway in Xenopus embryos, and that induction of a known downstream gene can occur in a cell non-autonomous manner.

Amino Acid Sequence↗
PubMed1998

Origin and neurochemical characteristics of nerve fibres supplying the mammalian vas deferens.

The present paper deals with the origin and neurochemical characteristics of autonomic postganglionic and sensory nerve fibres supplying the mammalian vas deferens. The vas deferens is innervated by postganglionic nerve fibres originating primarily from neurons in pelvic ganglia and, to a lesser extent, from neurons in the inferior mesenteric ganglion and sympathetic chain ganglia as well as by sensory nerve fibres arising from dorsal root ganglia. Three major populations of nerve terminals innervating the organ can be distinguished: (1) noradrenergic fibres; (2) cholinergic fibres containing vasoactive intestinal polypeptide, neuropeptide Y, nitric oxide synthase, and (in the pig) somatostatin, supplying particularly the lamina propria; and (3) non-noradrenergic, presumably sensory fibres, containing calcitonin gene-related peptide and/or substance P. The population of noradrenergic nerves is the most common. In the pig, it can be divided into three subpopulations: a somatostatin-containing, a Leu-enkephalin-containing and a subpopulation immunonegative to these peptides, in descending order of magnitude. In the rat, guinea-pig, and man, NPY seems to be the most common peptide occurring in the noradrenergic axons. In the pig, coexistence patterns of the substances existing within nerve fibres supplying the vas deferens blood vessels are clearly different from those found in nerve fibres innervating the organ wall. The majority of the noradrenergic fibres associated with blood vessels contain neuropeptide Y only, while non-noradrenergic perivascular nerves contain predominantly vasoactive intestinal polypeptide. The possibility of different sources of origin of the particular nerve fibre subpopulations supplying the mammalian vas deferens and its blood vessels is discussed.

Afferent Pathways↗
PubMed1981

Central control and interactions affecting sympathetic and parasympathetic activity.

Current thinking concerning the central control of the autonomic nervous system and the central interactions affecting sympathetic and parasympathetic activity is presented. Among the questions discussed are the following: are there neurons within the common brain stem system which exert an influence on preganglionic parasympathetic neurons and can they be differentiated from neurons which affect sympathetic preganglionic neuron functions? What interactions occur between sympathetic and parasympathetic tone-mediating neurons? In discussing these problems information is presented as obtained by recording from reticular formation (RF) neurons with discharge patterns similar to efferent parasympathetic activity. The general conclusion reached is that there is a common central control; interactions occur in the brain stem as well as peripherally; depending on the functional situation, these two systems can be organized to act either reciprocally or non-reciprocally.

Afferent Pathways↗
PubMed1985

Projections from the nucleus tractus solitarii to the rostral ventrolateral medulla.

Projections from the nucleus tractus solitarii (NTS) to autonomic control regions of the ventrolateral medulla, particularly the nucleus reticularis rostroventrolateralis (RVL), which serves as a tonic vasomotor center, were analyzed in rat by anterograde, retrograde, and combined axonal transport techniques. Autonomic portions of the NTS, including its commissural, dorsal, intermediate, interstitial, ventral, and ventrolateral subnuclei directly project to RVL as well as to other regions of the ventrolateral medulla. The projections are organized topographically. Rostrally, a small cluster of neurons in the intermediate third of NTS, the subnucleus centralis, and neurons in proximity to the solitary tract selectively innervate neurons in the retrofacial nucleus and nucleus ambiguus. Neurons generally located in more caudal and lateral sites in the NTS innervate the caudal ventrolateral medulla (CVL). The RVL, CVL, and nucleus retroambiguus are interconnected. A combined retrograde and anterograde transport technique was developed so as to prove that projections from the NTS to the ventrolateral medulla specifically innervate the region of RVL containing neurons projecting to the thoracic spinal cord or the region of the nucleus containing vagal preganglionic neurons. When the retrograde tracer, fast blue, was injected into the thoracic spinal cord, and wheat germ agglutinin-conjugate horseradish peroxidase (HRP) was injected into the NTS, anterogradely labeled terminals from the NTS surrounded the retrogradely labeled neurons in the RVL and in the nucleus retroambiguus in the caudal medulla. Among the bulbospinal neurons in the RVL innervated by the NTS were adrenaline-synthesizing neurons of the C1 group. When fast blue was applied to the cervical vagus, and HRP was injected into the NTS, anterogradely labeled terminals from the NTS surrounded retrogradely labeled neurons in the rostral dorsal motor nucleus of the vagus, the region of the nucleus ambiguus, the retrofacial nucleus, and the dorsal portion of the RVL, a region previously shown to contain cardiac vagal preganglionic neurons. This combined anterograde and retrograde transport technique provides a useful method for tracing disynaptic connections in the brain. These data suggest that the RVL is part of a complex of visceral output regions in the ventrolateral medulla, all of which receive afferent projections from autonomic portions of the NTS. Bulbospinal neurons in the RVL, in particular the C1 adrenaline neurons, may provide a portion of the anatomic substrate of the baroreceptor and other visceral reflexes.

Afferent Pathways↗
PubMed2006

Abnormal intracellular distribution of NFAT1 in T lymphocytes from patients with systemic lupus erythematosus and characteristic clinical features.

Systemic lupus erythematosus (SLE) presents various clinical features; however, underlying mechanisms remain unclear. In the immunity of SLE, impaired T cell receptor (TCR) signaling and altered cytokine production are in the center of pathogenesis, although, little is known about NFAT (nuclear factor of activated T cells) in lupus T lymphocytes. TCR stimulation activates NFAT1 through Ca2+/calcineurin (Cn) pathway, facilitating nuclear translocation of NFAT1 from cytosol. Therefore, we investigated relationship of disease activity/features and intracellular NFAT1 localization in T lymphocytes from active lupus patients by fractionation. Results showed no significant relationship between disease activity and NFAT1 distribution. However, interestingly, we observed skewed NFAT1 distribution in pellet in patients with active lupus nephritis or pleuritis. In vitro cyclosporin A treatment suggested autonomously activated Ca2+/Cn pathway in lupus T lymphocytes. Considering these results, NFAT1 might be presenting the clinical heterogeneity in SLE.

Adult↗
PubMed2003

Autonomic dysreflexia after spinal cord transection or compression in 129Sv, C57BL, and Wallerian degeneration slow mutant mice.

To study plasticity of central autonomic circuits that develops after spinal cord injury (SCI), we have characterized a mouse model of autonomic dysreflexia. Autonomic dysreflexia is a condition in which episodic hypertension occurs after injuries above the midthoracic segments of the spinal cord. As synaptic plasticity may be triggered by axonal degeneration, we investigated whether autonomic dysreflexia is reduced in mice when axonal degeneration is delayed after SCI. We subjected three strains of mice, Wld(S), C57BL, and 129Sv, to either spinal cord transection (SCT) or severe clip-compression injury (CCI). The Wld(S) mouse is a well-characterized mutant that exhibits delayed Wallerian degeneration. The CCI model is an injury paradigm in which significant the axonal degeneration is due to secondary events and therefore delayed relative to the time of the initial injury. We herein demonstrate that the incidence of autonomic dysreflexia is reduced in Wld(S) mice after SCT and in all mice after CCI. To determine if differences in afferent arbor sprouting could explain our observations, we assessed changes in the afferent arbor in each mouse strain after both SCT and CCI. We show that independent of the type of injury, 129Sv mice but not C57BL or Wld(S) mice demonstrated an increased small-diameter CGRP-immunoreactive afferent arbor after SCI. Our work thus suggests a role for Wallerian degeneration in the development of autonomic dysreflexia and demonstrates that the choice of mouse strain and injury model has important consequences to the generalizations that may be drawn from studies of SCI in mice.

Afferent Pathways↗
PubMed1997

Location, immunohistochemical features, and spinal connections of autonomic neurons innervating the rat seminal vesicles.

With the use of retrograde tracing techniques, selective spinal nerve transections, and immunohistochemistry to label noradrenergic and peptidergic pathways, this study has for the first time defined in detail the autonomic innervation to the rat seminal vesicles. The majority of this innervation originates from the bilateral major pelvic ganglia, whereas very few neurons are located in the accessory, inferior mesenteric, or paravertebral chain ganglia. Neuropeptide Y was the most abundant marker, followed by tyrosine hydroxylase (an enzyme involved in noradrenaline synthesis), and then vasoactive intestinal peptide. Sympathetic axons with tyrosine hydroxylase and neuropeptide Y supplied vascular and nonvascular smooth muscle whereas parasympathetic, cholinergic neuropeptide Y terminals were associated with the glandular epithelium. In contrast, vasoactive intestinal peptide was found only in cholinergic neurons, which may have either parasympathetic or sympathetic spinal connections. The latter were far more prevalent, demonstrating a substantial sympathetic cholinergic innervation to the seminal vesicles. Vasoactive intestinal peptide axons were associated with the glandular epithelia, as well as vascular and nonvascular smooth muscle. Axons associated with the secretory epithelia may regulate secretion or perhaps provide trophic support. Finally, acute damage to preganglionic sacral and lumbar nerves caused a transient increase in glandular weight.

Animals↗
PubMed2001

Pain-autonomic interactions: a selective review.

The nociceptive and the autonomic systems interact at the level of the periphery, spinal cord, brainstem, and forebrain. Spinal and visceral afferents provide converging information to spinothalamic neurons in the dorsal horn and to neurons of the nucleus tractus solitarius and parabrachial nuclei. These structures project to areas involved in reflex, homeostatic, and behavioral control of autonomic outflow, endocrine function, and nociception. These include monoaminergic cell groups of the medulla and pons, periaqueductal gray, hypothalamus, amygdala, insular cortex, and anterior cingulate gyrus. These interactions should be taken into account to understand the complex pathophysiology of chronic pain disorders.

Afferent Pathways↗
PubMed1992

Dissociation of nuclear events on p21 RAS transformation of FDC-P1 myeloid cells: c-jun/AP-1 expression versus c-myc transcription.

We have previously reported transformation to growth factor-independent proliferation in the interleukin-3 (IL-3)-dependent cell line FDC-P1 by high-level expression of the valine 12 Harvey RAS oncogene, following from a nonautocrine mechanism. The present study was undertaken to examine nuclear tertiary messenger, transcriptional response gene expression to deduce the intracellular signaling pathways responsible for this autonomous proliferation. We confirmed other reports that transformed p21RAS-expressing cells constitutively express the transcription factor complex jun/AP-1, in this case resulting from the ongoing expression of the c-jun and c-fos genes in the absence of IL-3. However, the ongoing growth factor independent expression of c-myc by a transcriptional mechanism in FDC-P1 cells expressing p21 RAS cannot be explained by intracellular signaling in the jun/AP-1 (protein kinase C) pathway. This conclusion derives from the observation that c-jun expression mediated via protein kinase C activation with phorbol ester (12-0-tetra decanoylphorbol-13-acetate, TPA) treatment does not lead to c-myc expression in parent FDC-P1 cells. On the contrary, FDC-P1 cells stably transfected with a c-myc gene controlled under the influence of a metallothionein IIA promoter (containing the TPA-responsive element [TRE]) express the transfected MTIIA-c-myc and downregulate the endogenous c-myc in response to protein kinase C activation with TPA. Further, nuclear proteins derived from cells expressing p21 RAS, which bind specifically to the purified c-myc P2 promoter, are not competed in their binding to the motif-rich P2 element by AP-1 oligonucleotide. Therefore, expression of the Harvey RAS oncogene in FDC-P1 myeloid cells leads to at least two pathways of cytoplasmic signaling. One pathway involves protein kinase C and c-jun/AP-1, but another pathway that is protein kinase C-independent appears to mediate c-myc transcription.

Cell Line↗
PubMed1994

Effects of partial and complete ablation of the slow pathway on fast pathway properties in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: The purpose of this study was to prospectively compare the effects of complete and partial ablation of slow pathway function on the fast pathway effective refractory period (ERP). METHODS AND RESULTS: The subjects were 20 patients (mean age 43 +/- 13 years) with atrioventricular nodal reentrant tachycardia (AVNRT), no structural heart disease, and easily inducible AVNRT. Autonomic blockade was achieved with propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). After elimination of AVNRT and during autonomic blockade, the presence of residual slow pathway function was determined by the presence of a single AV nodal echo and/or dual AV nodal physiology. After autonomic blockade and before ablation, the mean fast pathway ERP was 319 +/- 44 msec and the mean slow pathway ERP was 251 +/- 31 msec. After slow pathway ablation and during autonomic blockade, 7 patients had residual slow pathway function and 13 did not. Complete loss of slow pathway function was associated with a shortening of the fast pathway ERP from 334 +/- 35 msec to 300 +/- 62 msec (P < 0.01), while the fast pathway ERP did not change significantly in patients with residual slow pathway function (291 +/- 29 msec vs 303 +/- 38 msec, respectively; P = 0.08). A shortening of 30 msec or more in the fast pathway ERP was observed in 11 of 13 patients who did not have residual slow pathway function, compared to 0 of 7 patients with residual slow pathway function (P < 0.001). CONCLUSION: Shortening of the fast pathway ERP after successful ablation of AVNRT is dependent upon complete loss of slow pathway function. This observation is consistent with electrotonic inhibition of the fast pathway by the slow pathway.

Adult↗
PubMed2004

Urethral evoked sympathetic skin responses and viscerosensory evoked potentials as diagnostic tools to evaluate urogenital autonomic afferent innervation in spinal cord injured patients.

PURPOSE: In most spinal cord injured (SCI) patients the objective assessment of afferent neuronal pathways from the lower urinary tract and the recording of a disturbed urethral sensation and/or desire to void are still difficult. Viscerosensory evoked potentials (VSEPs) might be helpful, but they remain technically difficult to obtain and interpretation is delicate. As a new approach, sympathetic skin response (SSR) of the hand and foot were recorded after electrical stimulation of the posterior urethral mucosa. This technique should allow assessment of the integrity or deterioration of the autonomic afferent pathway. MATERIALS AND METHODS: A total of 20 males and 8 females with SCI somatosensory incomplete 15, somatosensory complete 13 and 6 healthy male volunteers were prospectively examined. During urodynamic examination electrical stimulation (single square pulses of 0.2 ms, 2 to 3-fold sensory threshold, 60 mA in complete SCI patients) of the posterior urethra/bladder neck was performed using a bipolar electrode inserted into a microtip pressure catheter. SSR recordings of the right palm and sole were simultaneously taken using surface electrodes and were analyzed by an electromyography unit. Patient reports on evoked urethral sensations at individual sensory thresholds were simultaneously noted. Additionally, well-known electrophysiological measurements such as pudendal sensory evoked potential and urethral VSEP were recorded to check clinical assessed somatosensory and viscerosensory status, and to compare SSR results with these conventional methods. RESULTS: Electrical stimulation of the posterior urethra evoked clear urethral sensation and SSRs in normal subjects. In 14 of 15 sensory incomplete SCI patients with disturbed urethral sensation SSRs could be recorded as well. Electrically evoked urethral sensations resembled the subjective desire to void at full bladder reported by controls and patients. In 13 sensory complete SCI patients with loss of any urethral sensation SSRs could not be recorded even at maximal electrical stimulation strength. All subjects with electrically induced urethral sensation had positive evoked (supralesional) SSRs of the hand. However, none of the patients with absent urethral sensation presented SSRs. Simultaneously recorded VSEPs could not be recorded clearly in 5 patients and 2 control subjects, whereas SSRs delivered clear results in all controls and patients, matching their reports. CONCLUSIONS: SSR recordings above a spinal lesion level after urethral electrostimulation might provide a useful and technically simple objective diagnostic tool to assess integrity of autonomic (visceral) afferent nerves from the lower urinary tract. Somatosensory deficits are not always paralleled by viscerosensory loss and vice versa. In this study SSRs were superior to VSEPs, the latter being more difficult to record. The subjective sensations reported by subjects during stimulation could be confirmed in an objective way in 100% of cases by positive/negative SSR findings.

Adult↗
PubMed1994

Visceral afferents: their contribution to 'sympathetic dependent' pain.

For 80 years the sympathetic nervous system has been implicated in certain human pains, notably causalgia and reflex sympathetic dystrophy. This assumption has led to the accepted concept of 'sympathetic dependent' pain. In this critical review, the evidence for this assumption is assessed. It is found that the clinical phenomena suggesting sympathetic nerve involvement may be more satisfactorily attributed to effects of neuropeptides released from afferent C-fibres. The evidence also demonstrates that the effects resembling sympathetic dysfunction relate neither to the pain nor to pain relief following sympathetic blockade. The techniques and results of sympathetic blockade have rarely been adequately evaluated, and the apparent efficacy, specificity and mode of action of peripheral sympatholytic drugs are questioned. An alternative explanation is proposed: that visceral afferents subserve a number of human pains, including those that have been considered sympathetically mediated. Problems of terminology are discussed; use of the term 'visceral afferent' is clarified and broadened to include afferents, particularly those related to blood vessels, which travel within autonomic nerves, in addition to the classical visceral afferent innervation of the organs of the great body cavities. The clinico-anatomical evidence reviewed here indicates that this general and widespread system of afferents could subserve certain pains. The relationship between visceral afferents, somatic afferents and autonomic efferents is outlined, and support is found for the unitary nature of the sensory system envisaged by Langley. Conflicting results from experiments on animals and clinical studies in man on the pain-subserving properties of visceral afferents are summarized; these confirm that visceral afferents can, at least on occasions in man, mediate pain not considered typically 'visceral'. This conclusion receives support from a number of clinical observations: not only are diseases of the autonomic nervous system painless, but damage to previously painless autonomic nerves can generate pain, as illustrated by several different conditions; pain from diseases other than of the viscera of the great cavities and which involves the widespread visceral afferents may be alleviated by sympathetic blockade, presumably since afferents travelling within autonomic fibres are simultaneously blocked; and diseases which impair the function of autonomic nerves may be unexpectedly painless. The central nervous system sequelae following involvement of visceral afferents are outlined and found to be relevant to phenomena sometimes seen with causalgia and related conditions: spread of pain; mirror involvement; associated features such as involuntary movements; and referred pain. Visceral afferents are generally clinically silent unless damage occurs.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1981

[Autonomic nervous reflexes elicited by stimulation of muscle nerves in the cat (author's transl)].

The effects on the cardiac and the vesical function of electrical stimulation of muscle hind limb afferent fibers in the gastrocnemius and soleus muscle were tested. Repetitive stimulation of the group III and IV muscle afferent had an excitatory effect on the heart rate through efferent sympathetic cardiac nerves and also an inhibitory effect on the micturition contraction of the bladder through efferent pelvic parasympathetic nerves. Stimulation of hindlimb muscle by algesic chemical substances such as KCl and bradykinin had similar effects on the cardiac and vesical function.

Action Potentials↗
PubMed2003

Interoception: the sense of the physiological condition of the body.

Converging evidence indicates that primates have a distinct cortical image of homeostatic afferent activity that reflects all aspects of the physiological condition of all tissues of the body. This interoceptive system, associated with autonomic motor control, is distinct from the exteroceptive system (cutaneous mechanoreception and proprioception) that guides somatic motor activity. The primary interoceptive representation in the dorsal posterior insula engenders distinct highly resolved feelings from the body that include pain, temperature, itch, sensual touch, muscular and visceral sensations, vasomotor activity, hunger, thirst, and 'air hunger'. In humans, a meta-representation of the primary interoceptive activity is engendered in the right anterior insula, which seems to provide the basis for the subjective image of the material self as a feeling (sentient) entity, that is, emotional awareness.

Afferent Pathways↗