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PubMed1992

Evidence of impaired afferent vagal function in patients with diabetes gastroparesis.

Two patients, a 28-year-old male and a 70-year-old female, with chronic insulin dependent diabetes mellitus and evidence of autonomic neuropathy were studied using cortical evoked responses following esophageal balloon and electrical stimulation. Both patients had symptomatic gastroparesis, poor gastric emptying, and reduced gastroduodenal motility including abnormal results of scintigraphy and manometry. There was slowing of afferent vagal conduction but good evoked potential responses were recorded even though one patient could not feel electrical stimulation of either the proximal or distal esophagus. It is improbable that the gastric symptoms are due to an afferent autonomic neuropathy, but symptoms may well be related to impairment of motor vagal pathways. Nevertheless, afferent vagal pathways are involved in severe diabetes mellitus. The clinical significance of this delay in conduction velocity of afferent pathways remains to be established.

Adult↗
PubMed2006

Autonomic regulation of pacemaker activity: role of heart nitric oxide synthases.

In autonomic-blocked rats treated with NG-nitro-L-arginine methyl ester (L-NAME, 7.5 mg/kg), heart rate increased 18% and mean arterial pressure increased 48%. Thyroidectomy, along with autonomic blockade, hampered the chronotropic response but did not modify the effect on blood pressure. After 150 min of autonomic blockade, the experimental end point, total nitric oxide (NO) production by heart NO synthases (NOS) decreased 61%: from 54 to 21 nmol NO.min-1.g heart-1. Mitochondrial NOS (mtNOS) and sarcoplasmic reticulum endothelial NOS activities decreased 74% and 52%, respectively. Mitochondria isolated from whole heart showed a well-coupled oxidative phosphorylation with high respiratory control and ADP-to-O ratios, decreased mtNOS activity (55-60%), and decreased mtNOS protein expression (70%). Immunohistochemistry with anti-inducible NOS antibody linked to gold particles localized mtNOS at the inner mitochondrial membranes. Histochemical right atrial NOS (NADPH-diaphorase) decreased 55% after heart denervation. The effects of autonomic denervation on the NO system were partially prevented by thyroidectomy performed simultaneously with autonomic blockade. Western blot analysis indicated a very rapid mtNOS protein turnover (half time=120 min) with a process of protein expression that was upregulated by thyroidectomy and a degradation process that was downregulated by the autonomic nervous system. The observations suggest that NO-mediated pathways contribute to pacemaker heart activity, likely through the NO steady-state levels in the right atrium and the whole heart.

Animals↗
PubMed1985

Autonomic mechanisms regulating myocardial contractility in conscious animals.

In this review some of the issues and controversies involved in the neural control of the myocardial inotropic response to stress have been discussed. For example, it is surprising that either direct or reflex activation of the sympathetic nerves induces a relatively small increase (20-40%) in the left ventricular inotropic state when compared with the three-five-fold increase associated with maximal dynamic exercise. Studies contrasting the levels of circulating catecholamines with the left ventricular inotropic responses induced by hemorrhage, exercise and exogenously administered catecholamines, suggest that the catecholamine concentration at the synaptic cleft is the primary determinant of the left ventricular inotropic response. Although parasympathetic neural activation alone appears to have little direct influence on the left ventricular inotropic state and central nervous system integration of the autonomic nervous system usually insures there is a reciprocal relationship between sympathetic and parasympathetic neural activity, the potential for parasympathetic inhibition of the response to sympathetic or sympathomimetic augmentation of the intropic response exists. The importance of sympathetic-parasympathetic nervous system interaction in physiologic and pathologic conditions has yet to be defined. It is this type of knowledge of the interactions of reflex pathways which will be critical to the full understanding of autonomic reflex control of myocardial performance under physiologic and pathologic conditions.

Anesthesia↗
PubMed2005

Protein-tyrosine phosphatase 1B deficiency protects against Fas-induced hepatic failure.

Genetic disruption of protein-tyrosine phosphatase 1B (PTP1B) in mice leads to increased insulin sensitivity and resistance to weight gain. Although PTP1B has been implicated as a regulator of multiple signals, its function in other physiological responses in vivo is poorly understood. Here we demonstrate that PTP1B-null mice are resistant to Fas-induced liver damage and lethality, as evident by reduced hepatic apoptosis in PTP1B-null versus wild type mice and reduced levels of circulating liver enzymes. Activation of pro-apoptotic caspases-8, -9, -3, and -6 was attenuated in livers from PTP1B-null mice following Fas receptor stimulation, although components of the death-inducing signaling complex were intact. Activation of anti-apoptotic regulators, such as the hepatocyte growth factor/Met receptor tyrosine kinase, as well as Raf, ERK1/2, FLIP(L), and the NF-kappaB pathway, was elevated in response to Fas activation in livers from PTP1B-null mice. Using PTP1B-deficient primary hepatocytes, we show that resistance to Fas-mediated apoptosis is cell autonomous and that signals involving the Met, ERK1/2, and NF-kappaB pathways are required for cytoprotection. This study identifies a previously unknown physiological role for PTP1B in Fas-mediated liver damage and points to PTP1B as a potential therapeutic target against hepatotoxic agents.

Animals↗
PubMed2006

Which pathways must be spared in the injured human spinal cord to retain cardiovascular control?

Cardiovascular abnormalities following spinal cord injury are attributed to autonomic instability caused by a combination of changes occurring within the spinal cord, including loss of descending autonomic control and plastic changes within spinal and peripheral circuits. Previous animal studies have shown that localized disruption of the descending vasomotor pathways results in cardiovascular changes similar to those observed following cord injury. However, the location of these pathways in humans is uncertain. This chapter presents clinical and histopathological findings from individuals with spinal cord injury that associates a common area of white matter destruction with severe cardiovascular symptoms. These data provide evidence that descending vasomotor pathways in the human spinal cord project through the dorsal aspects of the lateral funiculus.

Adult↗
PubMed1996

Monosynaptic projections from the nucleus tractus solitarii to C1 adrenergic neurons in the rostral ventrolateral medulla: comparison with input from the caudal ventrolateral medulla.

The rostral ventrolateral medulla (RVL) contains reticulospinal adrenergic (C1) neurons that are thought to be sympathoexcitatory and that form the medullary efferent limb of the baroreceptor reflex pathway. The RVL receives direct projections from two important autonomic regions, the caudal ventrolateral medulla (CVL) and the nucleus tractus solitarii with immunocytochemical identification of C1 adrenergic neurons in the RVL to compare the morphology of afferent input from these two autonomic regions into the RVL. NTS (n = 203) and CVL (n = 380) efferent terminals had similar morphology and vesicular content, but CVL efferent terminals were slightly larger than NTS efferent terminals. Overall, efferent terminals from either region were equally likely to contact adrenergic neurons in the RVL (21% for NTS, 25% for CVL). Although efferents from both regions formed both symmetric and asymmetric synapses, NTS efferent terminals were statistically more likely to form asymmetric synapses than CVL efferent terminals. CVL efferent terminals were more likely to contact adrenergic somata than were NTS efferents, which usually contacted dendrites. These findings 1) support the hypothesis that a portion of NTS efferents to the RVL may be involved in sympathoexcitatory, e.g., chemoreceptor, reflexes (via asymmetric synapses), whereas those from the CVL mediate sympathoinhibition (via symmetric synapses); and 2) provide an anatomical substrate for differential postsynaptic modulation of C1 neurons by projections from the NTS and CVL. With their more frequent somatic localization, CVL inhibitory inputs may be more influential than excitatory NTS inputs in determining the discharge of RVL neurons.

Animals↗
PubMed1999

Autonomic dysreflexia presenting as a severe headache.

Hypertension, bradycardia, and severe headache have been associated with autonomic dysreflexia. Autonomic dysreflexia affects those with spinal transection above the level of T6 after plastic changes of the afferent pathways. This restructuring in the presence of noxious stimuli below the level of the lesion leads to autonomic dysreflexia. The onset of the first episode of autonomic dysreflexia has been documented as soon as 30 days and as late as 13 years after the injury. This report presents a case study of a paraplegic man 8 years after injury with autonomic dysreflexia associated with a urinary tract infection.

Adult↗
PubMed1983

Segmental distribution and central projections of renal afferent fibers in the cat studied by transganglionic transport of horseradish peroxidase.

The segmental and central distributions of renal nerve afferents in adults cats and kittens were studied by using retrograde and transganglionic transport of horseradish peroxidase (HRP). Transport of HRP from the central cut ends of the left renal nerves labelled afferent axons in the ipsilateral minor splanchnic nerves and sensory perikarya in the dorsal root ganglia from T12 to L4. The majority of labeled cells (85%) were located between L1 and L3. A few neurons in the contralateral dorsal root ganglia were also labeled. Labeled cells were not confined to any particular region within a dorsal root ganglion. Some examples of bifurcation of the peripheral and central processes within the ganglion were noted. A small number of preganglionic neurons, concentrated in the intermediolateral nucleus, were also identified in some experiments. In addition, many sympathetic postganglionic neurons were labeled in the renal nerve ganglia, the superior mesenteric ganglion, and the ipsilateral paravertebral ganglia from T12 to L3. Transganglionic transport of HRP labeled renal afferent projections to the spinal cord of kittens from T11 to L6, with the greatest concentrations between L1 and L3. These afferents extended rostrocaudally in Lissauer's tract and sent collaterals into lamina I. In the transverse plane, a major lateral projection and a minor medial projection were observed along the outer and inner margins of the dorsal horn, respectively. From the lateral projection many fibers extended medially in laminae V and VI forming dorsal and ventral bundles around Clarke's nucleus. The dorsal bundle was joined by collaterals from the medial afferent projection and crossed to the contralateral side. The ventral bundle extended into lamina VII along the lateroventral border of Clarke's nucleus. Some afferents in the lateral projection could be followed ventrally into the dorsolateral portion of lamina VII in the vicinity of the intermediolateral nucleus. In the contralateral spinal cord, labeled afferent fibers were mainly seen in laminae V and VI. These results provide the first anatomical evidence for sites of central termination of renal afferent axons. Renal inputs to regions (laminae I, V, and VI) containing spinoreticular and spinothalamic tract neurons may be important in the mediation of supraspinal cardiovascular reflexes as well as in the transmission of activity from nociceptors in the kidney. In addition, the identification of a bilateral renal afferent projection in close proximity to the thoracolumbar autonomic nuclei is consistent with the demonstration in physiological experiments of a spinal pathway for the renorenal sympathetic reflexes.

Animals↗
PubMedDate not supplied

Function of the autonomic nervous system in patients with hepatic encephalopathy.

To obtain further pathophysiological details concerning the development of cardiovascular disturbances in severe liver disease, the state of the autonomic nervous system, the function of the baroreceptor reflex pathway and the responsiveness of the cardiovascular system to noradrenaline, angiotensin II and isoprenaline were investigated in 11 patients with hepatic encephalopathy and in 10 healthy control subjects. Increased plasma levels of noradrenaline and adrenaline and an attenuated increase in heart rate in response to atropine were found in patients with hepatic encephalopathy. These changes and the hemodynamic disturbances tended to be more pronounced in patients with hepatic encephalopathy Grades III-IV as compared to hepatic encephalopathy Grades I-II. The increase in systolic blood pressure induced by infusion of noradrenaline (400 ng per kg per min) and angiotensin II (20 ng per kg per min) was higher in the patients than in healthy control subjects (hepatic encephalopathy Grades I-II: p less than 0.001; hepatic encephalopathy Grades III-IV: p less than 0.02). The changes in mean and diastolic blood pressure in response to angiotensin II were more pronounced in hepatic encephalopathy grades I-II than in hepatic encephalopathy Grades III-IV (p less than 0.02). The decrease of heart rate in response to blood pressure increase in patients with hepatic encephalopathy was not different from control subjects except a smaller decrease during angiotensin II infusion in hepatic encephalopathy grades III-IV (p less than 0.05). The responsiveness to isoprenaline was diminished (p less than 0.001). The present results indicate that the increased activity of the sympathetic nervous system in hepatic encephalopathy is associated with decreased parasympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

The neuronal connections of the frontal ganglion of the cockroach Periplaneta americana. A histological and iontophoretical study.

The frontal ganglion of the cockroach Periplaneta americana was studied histologically and its neuronal pathways were mapped by use of axonal cobalt iontophoresis. Neurons and fiber tracts of the frontal ganglion are directly linked with different regions of the central nervous system (tritocerebrum, protocerebrum, subesophageal ganglion) and with the more caudal parts of the stomatogastric nervous system (hypocerebral ganglion, nervus oesophagei).

Animals↗
PubMed1982

Neurogenic and psychological factors in coronary heart disease: an introductory overview.

Some of the major nervous and psychological factors affecting the functioning of the heart are briefly reviewed. Emphasis is placed on the autonomic nervous system and its response to stressful situations. Possible pathways by which mental processes and behaviour might influence cardiovascular pathology and sudden death are outlined. Differences observed in the pattern of response are emphasized, as are the factors upon which these differences depend. The Type A behaviour pattern is considered and the importance of marital and social support is also discussed.

Autonomic Nervous System↗
PubMed1999

Unusual autonomic ganglia: connections, chemistry, and plasticity of pelvic ganglia.

The pelvic ganglia provide the majority of the autonomic nerve supply to reproductive organs, urinary bladder, and lower bowel. Of all autonomic ganglia, they are probably the least understood because in many species their anatomy is particularly complex. Furthermore, they are unusual autonomic ganglia in many ways, including their connections, structure, chemistry, and hormone sensitivity. This review will compare and contrast the normal structure and function of pelvic ganglia with other types of autonomic ganglia (sympathetic, parasympathetic, and enteric). Two aspects of plasticity in the pelvic pathways will also be discussed. First, the influence of gonadal steroids on the maturation and maintenance of pelvic reflex circuits will be considered. Second, the consequences of nerve injury will be discussed, particularly in the context of the pelvic ganglia receiving distributed spinal inputs. The review demonstrates that in many ways the pelvic ganglia differ substantially from other autonomic ganglia. Pelvic ganglia may also provide a useful system in which to study many fundamental neurobiological questions of broader relevance.

Animals↗
PubMed1987

The effect of muscarinic and beta-adrenergic blockade on cysteamine-induced gastrin secretion by the isolated perfused rat stomach.

Cysteamine-induced duodenal ulceration in rats is accompanied by increased circulating gastrin. Although cysteamine appears to exert a direct action on the gastrin cell some groups have provided evidence for an involvement of the autonomic nervous system. The current experiments were performed to determine whether beta-adrenergic or cholinergic (muscarinic) pathways are involved in the acute effect of cysteamine on gastrin secretion in the isolated perfused rat stomach. Cysteamine (1 mM) increased gastrin (IRG) secretion to a maximum ranging between 100% and 192% above basal. A cysteamine concentration of 5mM resulted in peak levels ranging between 150% and 1050% above basal. Addition of atropine or propranalol did not influence the responses obtained. The present results, therefore, do not support a role for either cholinergic or beta-adrenergic pathways in cysteamine-induced gastrin release at the level of the stomach and suggest that in vivo such autonomic effects are mediated extrinsically.

Animals↗
PubMed1994

The Caenorhabditis elegans locus lin-15, a negative regulator of a tyrosine kinase signaling pathway, encodes two different proteins.

The Caenorhabditis elegans locus lin-15 negatively regulates an intercellular signaling process that induces formation of the hermaphrodite vulva. The lin-15 locus controls two separate genetic activities. Mutants that lack both activities have multiple, ectopic pseudo-vulvae resulting from the overproduction of vulval cells, whereas mutants defective in only one lin-15 activity appear wild-type. lin-15 acts non-cell-autonomously to prevent the activation of a receptor tyrosine kinase/ras signaling pathway. We report here the molecular characterization of the lin-15 locus. The two lin-15 activities are encoded by contiguous genomic regions and by two distinct, non-overlapping transcripts that may be processed from a single mRNA precursor by trans-splicing. Based on the DNA sequence, the 719- and 1,440-amino acid lin-15 proteins are not similar to each other or to known proteins. lin-15 multivulva mutants, which are defective in both lin-15 activities, contain deletions and insertions that affect the lin-15 genomic region.

Amino Acid Sequence↗
PubMed2003

Anterior spinal artery syndrome complicated by the ondine curse.

BACKGROUND: Anterior spinal artery (ASA) syndrome results in motor palsy and dissociated sensory loss below the level of the lesion, accompanied by bladder dysfunction. When the cervical spine is involved, breathing disorders may be observed. OBJECTIVE: To describe the polysomnographic findings in a patient with cervical ASA syndrome complicated by a sleep breathing disorder. SETTING: Unit of neurology at a sleep center. Patient A 30-year-old man had an ischemic lesion that affected the anterior cervical spinal cord (C2-C6) bilaterally because of an ASA thrombosis. He developed ASA syndrome associated with respiratory impairment during sleep. RESULTS: The polysomnographic study during sleep showed a severe sleep disruption caused by continuous central apneas that appeared immediately after falling asleep. Treatment by intermittent positive pressure ventilation normalized the respiratory pattern and sleep architecture. CONCLUSIONS: The sleep breathing pattern was compatible with central alveolar hypoventilation due to automatic breathing control failure caused by a lesion of the reticulospinal pathway, which normally activates ventilatory muscles during sleep. This autonomic sleep breathing impairment resembles that found as a complication in patients who undergo spinothalamic tract cervical cordotomy for intractable pain. This surgical complication is known as the Ondine curse.

Adult↗
PubMed2000

Ovarian steroid action in the serotonin neural system of macaques.

The serotonin neural system plays an important role in cognitive, emotional and endocrine processes. If the ovarian hormones, oestrogen and progesterone, alter serotonin neural transmission, then functional changes in all of these systems would follow. Therefore, information on the effects of oestrogen and progesterone at a molecular level in the serotonin neural system was sought using non-human primates. Serotonin neurons express nuclear oestrogen receptor beta (ER beta) and progesterone receptors (PRs) which are gene transcription factors. Within serotonin neurons, the regulation of three genes related to serotonin neurotransmission was examined. The mRNA for tryptophan hydroxylase (TPH), the committal enzyme in serotonin synthesis, increased significantly with oestrogen treatment and remained elevated when progesterone was added to the oestrogen regimen. Serotonin reuptake transporter (SERT) mRNA decreased significantly with oestrogen treatment and addition of progesterone had no further effect. 5-HT1A autoreceptor mRNA decreased significantly with oestrogen treatment and addition of progesterone caused a further decrease. Little or no regulation of postsynaptic 5-HT1A, 5-HT2A or 5-HT2C receptor mRNAs was observed in hypothalamic target neurons. TPH protein is increased by oestrogen treatment and remains elevated with addition of progesterone in a manner similar to TPH mRNA. Medroxyprogesterone (MPA) blocked the stimulatory effect of oestrogen on TPH protein and tamoxifen reduced TPH protein levels below that observed in spayed monkeys. Together these data indicate that ovarian hormones and their synthetic analogues could modify cognitive and autonomic neural functions by acting on the serotonin neural pathway.

Animals↗
PubMed2006

Developmental cell death during Xenopus metamorphosis involves BID cleavage and caspase 2 and 8 activation.

Elimination of tadpole organs during Xenopus metamorphosis is largely achieved through apoptosis, and recent evidence suggest involvement of the mitochondrial death route and bax-initiated caspase-3 and -9 deployment. However, events upstream of the activation of Bax are unknown. In other models, proteins of the BH3-only group such as BID are known to assure this function. We show that Xenopus bid transcript levels increase at metamorphosis in larval cells destined to disappear. This increase correlates with an abrupt rise in Caspase-2 and -8 mRNA levels and an enhanced activity of Caspase-2 and -8. In BIDGFP transgenic animal's tail regression is accelerated. The cleavage of BIDGFP fusion protein during natural or T(3)-induced metamorphosis was specifically inhibited by caspase-8 inhibitors. Our results show that tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BID and Caspases-2 and -8.

Animals↗