ON THE EFFERENT PATHWAY OF THE REFLEX PULMONARY TEMPERATURE FALL BY NASAL IRRITATION IN RABBITS.
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Ammonia↗
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Notch signaling controls proliferation through cell-autonomous and non-autonomous mechanisms in the Drosophila eye.
During Drosophila eye development, localized Notch signaling at the dorsal ventral (DV)-midline promotes growth of the entire eye field. This long-range action of Notch signaling may be mediated through the diffusible ligand of the Jak/STAT pathway, Unpaired (Upd), which was recently identified as a downstream target of Notch. However, Notch activity has not been shown to be cell-autonomously required for Upd expression and therefore yet another diffusible signal may be required for Notch activation of Upd. Our results clarify the Notch requirement, demonstrating that Notch activity at the DV-midline leads to cell-autonomous expression of Upd as monitored in loss and gain-of-function Notch clones. In addition, mutations in the Jak/STAT pathway interact genetically with the Notch pathway by suppressing Notch mediated overgrowth. N(act) clones show non-autonomous effects on the cell cycle anterior to the furrow, indicating function of the Jak/STAT pathway. However, cell-autonomous effects of Notch within and posterior to the furrow are independent of Upd. Here, Notch autonomously maintains cells in a proliferative state and blocks photoreceptor differentiation.
Animals↗
Mutations in erupted, the Drosophila ortholog of mammalian tumor susceptibility gene 101, elicit non-cell-autonomous overgrowth.
The reproducible pattern of organismal growth during metazoan development is the product of genetically controlled signaling pathways. Patterned activation of these pathways shapes developing organs and dictates overall organismal shape and size. Here, we show that patches of tissue that are mutant for the Drosophila Tsg101 ortholog, erupted, cause dramatic overproliferation of adjacent wild-type tissue. Tsg101 proteins function in endosomal sorting and are required to incorporate late endosomes into multivesicular bodies. Drosophila cells with impaired Tsg101 function show accumulation of the Notch receptor in intracellular compartments marked by the endosomal protein Hrs. This causes increased Notch-mediated signaling and ectopic expression of the Notch target gene unpaired (upd), which encodes the secreted ligand of the JAK-STAT pathway. Activation of JAK-STAT signaling in surrounding wild-type cells correlates with their overgrowth. These findings define a pathway by which changes in endocytic trafficking can regulate tissue growth in a non-cell-autonomous manner.
Amino Acid Sequence↗
Nitric oxide and the autonomic regulation of cardiac excitability. The G.L. Brown Prize Lecture.
Cardiac sympathetic imbalance and arrhythmia; Nitric oxide-cGMP pathway and the cholinergic modulation of cardiac excitability; Nitric oxide-cGMP pathway and the sympathetic modulation of cardiac excitability; Functional significance of nitric oxide in the autonomic regulation of cardiac excitability; Summary; References. Experimental Physiology (2001) 86.1, 1-12.
Animals↗
Assessment of autonomic nervous function in elderly subjects with or without postprandial hypotension.
To examine the role of autonomic nervous dysfunction in postprandial hypotension (PPH) in elderly persons, we non-invasively assessed autonomic nervous function in 50 elderly subjects with or without PPH, defined as a reduction of more than 20 mmHg in systolic blood pressure (SBP) after a meal. The heart rate response to the reduction of SBP during head-up tilt was less and the coefficient of variation of R-R intervals was smaller in subjects with PPH than in those without PPH. The responses to cold pressor test, hyperventilation test, and mental arithmetic test were normal in all subjects. The magnitude of deltaSBP after meal ingestion closely correlated with deltaSBP during tilt-table examination, but did not correlate with the results of the cold pressor test, hyperventilation test, or mental arithmetic test. Stepwise multiple regression analysis revealed that the magnitude of the BP reduction and heart rate increase during the tilt-table test were independent predictors of the magnitude of deltaSBP after meal ingestion. The results indicate that impaired afferent pathways of baroreflexes, including baroreceptors, may play an important role in the pathogenesis of postprandial hypotension in the elderly and that the magnitude of the fall in SBP during tilt-table testing may be related to the degree of the postprandial reduction in BP in elderly persons.
Aged↗
Reversible inactivation of the dorsal vagal complex blocks lipopolysaccharide-induced social withdrawal and c-Fos expression in central autonomic nuclei.
Peripheral administration of lipopolysaccharide (LPS), a potent activator of the immune system, induces symptoms of behavioral depression, such as social withdrawal, concommitant with increases in c-Fos expression in central autonomic network nuclei. Previous studies implicated vagal visceral sensory nerves in transduction of immune-related signals relevant to for the induction of social withdrawal, a symptom of behavioral depression. Vagal sensory nerves terminate in the dorsal vagal complex (DVC) of the brainstem, a region that functions to integrate visceral signals and may also play a role in modulating arousal and affect. The objective of the current study was to determine whether the DVC contributes to immunosensory pathways driving symptoms of social withdrawal associated with LPS-induced behavioral depression, using a reversible lesion technique to temporarily inactivate the DVC. To assess the effects of DVC inactivation on LPS-induced social withdrawal and the subsequent changes in brain activation, we used behavioral assessment of social withdrawal, and analyzed c-Fos expression, a marker of neuronal activation, in the central nucleus of the amygdala (CEA), bed nucleus of the stria terminalis (BST), hypothalamic paraventricular nucleus (PVN), and ventromendial preoptic area (VMPO). Two hours following intraperitoneal LPS injection, there was a significant increase in c-Fos immunoreactivity in forebrain regions in animals treated with LPS. DVC inactivation completely blocked LPS-induced social withdrawal and dramatically reduced LPS-induced Fos expression in all four forebrain regions assessed. Collectively, these findings support the idea that the DVC acts as an immune-behavior interface between the peripheral stimuli and brain areas involved in modulating social behavior.
Acute-Phase Reaction↗
[A light-independent function of the retina of rabbits. Examination on the energetic part of the visual pathway (author's transl)].
In this study a light-independent function of the retina of rabbits could be proved. For this purpose, the energetic part of the visual pathway was utilized, and its influence on the maturation of the testicles was examined. As a criterion of maturation, the pattern of the phosphatid-fatty acids was ascertained. The subdivision of the energetic part of the visual pathway into a photo-energetic and an autonomic-energetic component is proposed.
Animals↗
Low lumbar CSF levels of homovanillic acid and 5-hydroxyindoleacetic acid in multiple system atrophy with autonomic failure.
Low lumbar CSF concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in patients with multiple system atrophy attended by autonomic failure (MSA) reflect decreased activity in central dopaminergic and serotonergic pathways. These neurochemical changes are consistent with the neuropathological involvement in MSA and distinguish such patients from those with pure autonomic failure who have normal CSF metabolite levels.
Adult↗
Neural control of intraocular pressure.
Efferent and afferent pathways by which the central nervous system (CNS) may control intraocular pressure (IOP) are considered. As experience with pharmaceutical agents has suggested, the targets for autonomic influence on ocular tension are both aqueous formation and resistance to outflow. The afferent input to the brain must be served by sensory fibers which are sensitive to intraocular pressure levels or which respond to changes in intraocular pressure. The location and physiology of such receptors is discussed.
Afferent Pathways↗
Autonomic responsiveness in obesity with and without hypertension.
Evidence from animals models of obesity, eg the ob/ob mouse, and from studies in man are consistent with the autonomic regulation of brown tissue being one of the principal pathways involved in the normal thermogenic regulation of energy balance. Studies in man on other components of the sympathetic nervous system do not suggest generalized autonomic abnormalities in obese patients. Patients placed on a reduced carbohydrate intake show a fall in metabolic rate, a reduction in cardiovascular indices of sympathetic activity and a fall in venous noradrenaline concentrations. The hypotensive effect is accompanied by a precipitous fall in hydroxy-methoxymandelic acid excretion. These changes are not nearly so evident in those obese patients who are also hypertensive so there may be altered control of catecholamine metabolism in obese hypertensive patients.
Animals↗
Inhibition of Caenorhabditis elegans vulval induction by gap-1 and by let-23 receptor tyrosine kinase.
During induction of the Caenorhabditis elegans hermaphrodite vulva, a signal from the anchor cell activates the LET-23 epidermal growth factor receptor (EGFR)/LET-60 Ras/MPK-1 MAP kinase signaling pathway in the vulval precursor cells. We have characterized two mechanisms that limit the extent of vulval induction. First, we found that gap-1 may directly inhibit the LET-60 Ras signaling pathway. We identified the gap-1 gene in a genetic screen for inhibitors of vulval induction. gap-1 is predicted to encode a protein similar to GTPase-activating proteins that likely functions to inhibit the signaling activity of LET-60 Ras. A loss-of-function mutation in gap-1 suppresses the vulvaless phenotype of mutations in the let-60 ras signaling pathway, but a gap-1 single mutant does not exhibit excess vulval induction. Second, we found that let-23 EGFR prevents vulval induction in a cell-nonautonomous manner, in addition to its cell-autonomous role in activating the let-60 ras/mpk-1 signaling pathway. Using genetic mosaic analysis, we show that let-23 activity in the vulval precursor cell closest to the anchor cell (P6.p) prevents induction of vulval precursor cells further away from the anchor cell (P3.p, P4.p, and P8.p). This result suggests that LET-23 in proximal vulval precursor cells might bind and sequester the inductive signal LIN-3 EGF, thereby preventing diffusion of the inductive signal to distal vulval precursor cells.
Amino Acid Sequence↗
Preganglionic C-fibres: a major component of the sacral autonomic outflow to the colon of the cat.
The sacral preganglionic pathways to the colon and urinary bladder of the cat were studied with electrophysiological techniques. Peak conduction velocities in preganglionic fibres to the colon ranged from 0.5 to 1.4 m/sec, whereas maximum velocities in the bladder pathway were between 8 to 10 m/sec. Thresholds for electrical stimulation of preganglionic axons to the colon were 7 to 10 times higher than thresholds for bladder efferents. It is concluded that the sacral parasympathetic inputs to the colon and bladder are composed, respectively, of non-myelinated and myelinated fibres.
Animals↗
Swallow-evoked action potentials in vagal preganglionic efferents.
Swallow-evoked potentials in the preganglionic vagal fibers were studied using the single-fiber recording technique in anesthetized opossums. Swallows were evoked by tactile pharyngeal stimulation or electrical stimulation of the cut central end of the superior laryngeal nerve (SLN). Swallowing activity was recorded by the mylohyoid electromyogram and esophageal motility. Sixty-six fibers were studied in which swallowing evoked action potentials. The latencies (from the onset of mylohyoid activity) of evoked responses in different fibers varied from 100 ms to 5 s. The discharge rate of the evoked response was 3-8 action potentials per burst. Each burst lasted 1.1 +/- 0.02 (SE)s. The latencies of evoked spike bursts showed a bimodal distribution. In 34 fibers the latencies were less than 1 s, and in 32 fibers the latencies ranged between 1 and 5 s; these are the short- and long-latency fibers, respectively. Short-latency fibers could easily be distinguished from long-latency fibers based on the influence of SLN-stimulus frequency. Short-latency discharges had low thresholds of activation and were sensitive to changes in the frequency of SLN stimulation, since their latencies decreased and their discharge rate increased with increasing SLN-stimulus frequency. On the other hand, the latencies and discharge rates of long-latency discharges were not modified with changing SLN stimulus frequencies. The conduction velocities of 6 short- and 9 long-latency fibers were 5.64 +/- 0.12 and 5.78 +/- 0.12 (SE) m/s, respectively (P greater than 0.05). The relationship between the latencies of swallow-evoked discharges in the short- and long-latency fibers and the esophageal smooth muscle responses suggested that the short-latency discharges may correlate with the latency of initial inhibition, and the long-latency fibers may correlate with latencies of peristaltic contractions. Based on these temporal relationships, we speculate that vagal efferent fibers showing swallow-evoked, short-latency discharges make contact with intramural inhibitory neurons. They may mediate deglutitive inhibition in the body of the esophagus, relaxation of the lower esophageal sphincter, and receptive relaxation of the fundus of the stomach. The fibers showing late discharges make contact with intramural excitatory neurons and participate in their sequential activation. This dual pathway of activation may be responsible for physiological esophageal peristalsis.
Animals↗
Medial preoptic area afferents to periaqueductal gray medullo-output neurons: a combined Fos and tract tracing study.
We have shown recently that the medial preoptic area (MPO) robustly innervates discrete columns along the rostrocaudal axis of the midbrain periaqueductal gray (PAG). However, the location of PAG neurons responsive to MPO activation is not known. Anterograde tract tracing was used in combination with Fos immunohistochemistry to characterize the MPO --> PAG pathway anatomically and functionally within the same animal. Focal electrical or chemical stimulation of MPO in anesthetized rats induced extensive Fos expression within the PAG compared with sham controls. Fos-positive neurons were organized as 2-3 longitudinal columns. The organization and location of these columns overlapped remarkably well with the distribution of fibers and terminals in PAG labeled by Phaseolus vulgaris leucoagglutinin (PHA-L) injected into the same MPO stimulation site. This indicates that MPO inputs may terminate on the soma or proximal dendrites of neurons exhibiting elevated Fos. A second series of experiments investigated whether MPO stimulation excited PAG neurons with descending projections to the medulla. Retrograde labelling of PAG neurons projecting to the medial and lateral regions of the rostroventral medulla (RVM) was combined with MPO-induced Fos expression. The results showed that a substantial population (37-53%) of Fos-positive PAG neurons projected to the ventral medulla. This indicates that MPO stimulation engages PAG-medullary output neurons. Taken together, these results suggest that the MPO --> Pag --> RVM projection constitutes a functional pathway. This circuit may coordinately regulate neuroendocrine, motor, and autonomic adjustments necessary for the elaboration of sexual behaviors.
Afferent Pathways↗
Prenatal development of peptidergic primary afferent projections to mouse lumbosacral autonomic preganglionic cell columns.
To examine the prenatal development of spinal visceral reflexes, primary sensory nerve fibers immunoreactive for calcitonin gene-related peptide (CGRP) were examined in the spinal cord, particularly in the autonomic preganglionic nuclei of mouse embryos. On embryonic day 16 (E16), CGRP-immunoreactive fibers were first observed in the sacral intermediolateral nucleus (IML) of the parasympathetic division as well as in the lumbar central autonomic nucleus (CA) of the sympathetic division, where they appeared in proximity to preganglionic neuronal perikarya immunoreactive for choline acetyltransferase or nitric oxide synthase. Most of the CGRP-immunoreactive varicosities were negative for substance P. Substance P-immunoreactive varicosities were scattered in these nuclei, but no appositions were seen on the preganglionic neuronal perikarya. On E18, CGRP-immunoreactive fibers were more abundant in the sacral IML and the lumbar CA. Co-expression of substance P and CGRP was frequently observed in the varicosities very close to the preganglionic neuronal perikarya on E18. CGRP-immunoreactive fibers were also observed in the lumbar IML on E18, although significantly fewer were found in this nucleus compared with the sacral IML. In contrast to the upper lumbar level, no fibers immunoreactive for CGRP were observed in the IML at the thoracic level. These results suggest that peptidergic primary sensory fibers grow to project to the selective targets of autonomic preganglionic neurons during the embryonic period. The potential direct connections between the peptidergic primary sensory fibers and preganglionic neurons innervating the pelvic viscera might provide a circuit for spinal visceral reflexes active in embryos.
Afferent Pathways↗
Pathophysiology of pain.
OBJECTIVE: To review the pain pathways in the central and peripheral nervous system and the actions of drugs used to treat pain. DESIGN: An overview of pain pathways is presented, beginning in the periphery and progressing centrally, and the ascending and descending pathways are described in detail. RESULTS: The nociceptive pathway, consisting of the classic three-neuron chain, is now understood to be a dual system at each level, and the sensation of pain is thought to arrive in the central nervous system with the discriminative component of pain ("first pain") carried separately from the affective-motivational component of pain ("second pain"). In addition to spinal control mechanisms of nociceptive transmission, descending pathways that originate in three major areas--the cortex, thalamus, and brain stem--can modify functions at the spinal level. At every level of the nervous system, a close relationship prevails between somatic pain pathways and visceral pathways. This relationship likely accounts for the transmission of visceral pain and also for autonomic responses to somatic pain and somatic responses to visceral pain. CONCLUSION: By understanding the pathways of pain and the transmitters involved, prevention and treatment of pain will be improved.
Afferent Pathways↗
Simvastatin therapy normalizes sympathetic neural control in experimental heart failure: roles of angiotensin II type 1 receptors and NAD(P)H oxidase.
BACKGROUND: In a previous study, we showed that simvastatin (SIM) therapy normalized sympathetic outflow and cardiovascular reflex regulation in chronic heart failure (CHF). However, the precise neural and cellular pathways for these effects are unknown. We hypothesized that SIM exerts its beneficial effect on autonomic function in CHF by downregulating central angiotensin II (Ang II) and superoxide mechanisms. METHODS AND RESULTS: Experiments were carried out on 36 male New Zealand White rabbits, 13 normal and 23 CHF. All rabbits were identically instrumented to record mean arterial pressure, heart rate, and renal sympathetic nerve activity (RSNA). Echocardiography was used to monitor cardiac function. Reverse transcription-polymerase chain reaction, Western blotting, and lucigenin-enhanced chemiluminescence were used to measure gene expression of Ang II type 1 receptor and NAD(P)H oxidase subunits and NAD(P)H oxidase activity in the rostral ventrolateral medulla. Compared with the CHF control group, SIM significantly reduced the central Ang II-induced pressor and sympathoexcitatory responses, decreased baseline RSNA (57.3+/-3.2% to 22.4+/-2.1% of maximum, P<0.05), increased baroreflex control of heart rate (gain(max), 1.6+/-0.3 to 4.5+/-0.2 bpm/mm Hg, P<0.05), and increased RSNA (gain(max), 1.7+/-0.2% to 4.9+/-0.6% of maximum/mm Hg, P<0.01). Importantly, SIM improved left ventricular function (EF, 32.4+/-4.1% to 51.7+/-3.2%, P<0.05). SIM also downregulated mRNA and protein expression of Ang II type 1 receptor and NAD(P)H oxidase subunits and inhibited NAD(P)H oxidase activity in the rostral ventrolateral medulla of CHF rabbits. Chronic intracerebroventricular infusion of Ang II completely abolished the aforementioned effects of SIM in CHF rabbits. CONCLUSIONS: These data strongly suggest that SIM normalizes autonomic function in CHF by inhibiting central Ang II mechanisms and therefore the superoxide pathway. These data also demonstrate that SIM improves left ventricular function in pacing-induced CHF rabbits.
Animals↗
Functional organization of central pathways regulating the cardiovascular system.
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Animals↗