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PubMed1993

Amygdaloid CRF pathways. Role in autonomic, neuroendocrine, and behavioral responses to stress.

The results of numerous studies have provided compelling evidence that CRF plays an important function in the amygdala. Stimulation of the amygdala produces physiological changes similar those observed after central injections of CRF. Central injections of CRF activate neurons in the amygdala as measured by increases in c-fos protein expression. Destruction of cells or injections of CRF antagonist in the amygdala can attenuate some of the central effects of CRF. The amygdala is the origin of major CRF-containing pathways in the brain. Amygdaloid CRF neurons project to widespread regions of the basal forebrain and brain stem. These amygdaloid pathways mainly arise from the central amygdaloid nucleus where there are a large number of CRF immunoreactive neuronal perikarya. Glucocorticoid and CRF-binding protein are located in cells of the central amygdaloid nucleus. CRF neurons in the central nucleus send their axons to the bed nucleus of the stria terminalis, lateral hypothalamus, midbrain central gray, raphe nuclei, parabrachial region, and the nucleus of the solitary tract. Tract tracing studies have suggested that amygdaloid CRF neurons also innervate CRF neurons in some of these regions and, furthermore, that CRF neurons in some of these areas project back to the CRF neurons in the amygdala. Thus, the amygdala is part of a network of brain nuclei interconnected by CRF pathways. In addition, amygdaloid CRF neurons may project directly to dopaminergic, noradrenergic, and serotonergic neurons, which have widespread projections throughout the neuroaxis.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1996

The expression pattern of the transcription factor Phox2 delineates synaptic pathways of the autonomic nervous system.

Many transcription factors, and most prominently among them, homeodomain proteins, are expressed in specific groups of cells in the developing nervous system in patterns that suggest their involvement in neural fate determination. How various aspects of neural identity are controlled by such transcription factors, or sets of them, is still mostly unknown. It has been shown previously that Phox2 is such a homeodomain protein, expressed exclusively in differentiated groups of neurons or their precursors, and that its expression correlated with that of the noradrenaline synthesis enzyme dopamine-beta-hydroxylase. Here we confirm this striking correlation at the single-cell level with the use of an anti-Phox2 antibody. Moreover, we uncover a second, nonmutually exclusive correlative clue to the Phox2 expression pattern: a high proportion of Phox2-expressing cells are involved in, or located in areas involved in, synaptic circuits, i.e., that of the medullary control reflexes of autonomic functions. This suggests that Phox2 could be involved in the establishment of these circuits.

Animals↗
PubMed1966

Central pathways of some autonomic reflex discharges.

1. Electrical stimulation of spinal sensory nerves evoked discharges in inferior cardiac and renal nerves. In the anaesthetized cat both an early and a late response could be recorded in each nerve.2. For any one afferent input the central delay of the late cardiac nerve response was significantly less than that of the late renal nerve response. The central delay of the early responses was similar for both nerves. In the spinal cat only the early response was present.3. Cooling the floor of the 4th ventricle abolished the late responses in renal nerves, but left reflex volleys in white rami and intercostal nerves unchanged.4. Stimulation in the brain stem evoked responses in both cardiac and renal nerves which had a shorter latency than the reflexes evoked in these nerves by stimulating dorsal roots.5. The late responses could be abolished by lesions in the cervical spinal cord.6. Such evidence led to the conclusion that there are two pathways for reflex discharge into inferior cardiac and renal nerves, one involving a supraspinal relay and the other confined to the spinal cord.

Animals↗
PubMed1994

Shortening of fast pathway refractoriness after slow pathway ablation. Effects of autonomic blockade.

BACKGROUND: Shortening of the anterograde effective refractory period (ERP) of the fast pathway has been reported after radiofrequency ablation of the slow pathway. We hypothesized that ERP shortening may be related to autonomic changes, possibly catecholamine release, as a result of ablation. METHODS AND RESULTS: To test this, 10 consecutive patients with atrioventricular node reentry undergoing slow pathway ablation were given autonomic blockade before the ablation procedure. This was achieved by atropine 0.03 mg/kg and propranolol 0.15 mg/kg IV supplemented by half the initial dose after ablation and before the final study. A control group of 10 patients underwent the protocol without autonomic blockade. Before ablation, autonomic blockade did not alter the ERP of either the fast pathway (295 +/- 22 versus 298 +/- 26 milliseconds) or the slow pathway (264 +/- 36 versus 269 +/- 38 milliseconds). Autonomic blockade obscured dual pathway physiology in 2 patients and brought it out in another 2 without dual pathway physiology initially. Slow pathway ablation shortened the ERP of the fast pathway for the group as a whole (331.5 +/- 54 versus 305.5 +/- 60 milliseconds, mean +/- SD, n = 20, P < .04). There was no difference in degree of ERP shortening in control patients (23.5 +/- 58 milliseconds) or autonomic blockade patients (25.5 +/- 52 milliseconds). CONCLUSIONS: These data suggest that shortening of the ERP of the fast pathway after slow pathway ablation is not mediated by autonomic changes.

Adult↗
PubMed2006

OsFY, a homolog of AtFY, encodes a protein that can interact with OsFCA-gamma in rice (Oryza sativa L.).

FCA and FY are flowering time related genes involved in the autonomous flowering pathway in Arabidopsis. FCA interacts with FY to regulate the alternative processing of FCA pre-mRNA. The FCA/FY interaction is also required for the regulation of FLC expression, a major floral repressor in Arabidopsis. However, it is not clear if the regulation of this autonomous flowering pathway is also present in monocot plants, such as rice. Recently, alternative RNA processing of OsFCA was observed in rice, which strongly suggested the existence of an autonomous flowering pathway in rice. In this work, we cloned the cDNA of the autonomous flowering pathway gene OsFY from rice. The predicted OsFY protein contained a conserved 7 WD-repeat region and at least two Pro-Pro-Leu-Pro motifs compared to Arabidopsis FY. The protein-protein interaction between OsFY and OsFCA-gamma, the key feature of their gene function, was also demonstrated using the yeast two-hybrid system. The GenBank database search provided evidence of expression for other autonomous pathway gene homologs in rice. These results indicate that the autonomous flowering pathway is present in monocots, and the regulation through FY and FCA interaction is conserved between monocots and dicots.

Amino Acid Sequence↗
PubMed1993

Basic mechanisms in autonomic nervous responses in specific and nonspecific nasal hyperreactivity.

The nasal mucosa and the autonomic nervous regulation of protective reflexes plays an important role for the protection of the lower airways. Increasing experimental evidence from both animal models and humans suggests that the organization of the autonomic nervous pathways is more complicated than previously assumed. Thus a number of biologically active peptides are known to be present in the autonomic pathways and coexist with the classical transmitters. The neuropeptides have experimentally been shown to play an important role in the pathophysiological events in both specific and nonspecific hyperreactivity.

Animals↗
PubMed2003

The need for winter in the switch to flowering.

Vernalization is the process whereby the floral transition is promoted through exposure of plants to long periods of cold temperature or winter. A requirement for vernalization aligns flowering with the seasons to ensure that their reproductive phase occurs in favorable conditions. The mitotic stability of vernalization, suggestive of an epigenetic mechanism, has intrigued researchers for many years. Genetic analysis of the vernalization requirement in Arabidopsis has identified key floral repressor genes, FRI and FLC. The action of these floral repressors is antagonized by vernalization and the activity of a set of genes grouped into the autonomous floral pathway. Analysis of the vernalization pathway has defined a series of epigenetic regulators crucial for "cellular-memory" of the cold signal, whereas the autonomous pathway appears to function in part through posttranscriptional mechanisms. The mechanism of the vernalization requirement, which is now being explored in a range of plant species, should uncover the evolutionary origins of this key agronomic trait.

Arabidopsis↗
PubMed2004

Interleukin-1beta can mediate growth arrest and differentiation via the leukemia inhibitory factor/JAK/STAT pathway in medullary thyroid carcinoma cells.

Interleukin-1beta (IL-1beta) is a pleiotropic cytokine that can induce several cellular signal transduction pathways. Here, we show that IL-1beta can induce cell cycle arrest and differentiation in the human medullary thyroid carcinoma (MTC) cell line, TT. IL-1beta induces cell cycle arrest accompanied by morphological changes and expression of the neuroendocrine marker calcitonin. These changes are blocked by the MEK1/2 specific inhibitor U0126, indicating that MEK1/2 is essential for IL-1beta signaling in TT cells. IL-1beta induces expression of leukemia inhibitory factor (LIF) and activation of STAT3 via the MEK/ERK pathway. This activation of STAT3 could be abrogated by treatment with anti-LIF neutralizing antibody or anti-gp130 blocking antibody, indicating that induction of LIF expression is sufficient and essential for STAT3 activation by IL-1beta. In addition to activation of the LIF/JAK/STAT pathway, IL-1beta also induced an MEK/ERK-mediated intracellular cell-autonomous signaling pathway that is independently sufficient for growth arrest and differentiation. Thus, IL-1beta activates the MEK/ERK pathway to induce growth arrest and differentiation in MTC cells via dual independent signaling mechanisms, the cell-extrinsic LIF/JAK/STAT pathway, and the cell-intrinsic autonomous signaling pathway.

Antigens, CD↗
PubMed1999

Nitric oxide and target-organ control in the autonomic nervous system: anatomical distribution, spatiotemporal signaling, and neuroeffector maintenance.

Recent neuroanatomical studies, neurochemical coding and physiological findings of multiple cotransmitter actions and/or receptor patterns, and the characterization of synaptic molecules and nitrergic (NOergic) signaling mechanisms may help for a better understanding of target-organ control in the autonomic nervous system. Thus, nitric oxide (NO) synthase, which generates the freely diffusible and short-lived messenger NO and expression of neurotrophic proteins (e.g., neurotrophins, glial cell-line-derived neurotrophic factor, fibroblast growth factors) in autonomic neural pathways or target organs suggest unique actions in autonomic neurotransmission. In central NOergic pathways, NO may serve as spatial (volume) messenger within hierarchically ordered autonomic neuron pools and convergent/divergent pathways for synchronized autonomic outflow. Likewise, NO modulates intraganglionic and interaxonal transmission and postganglionic activity including long-term potentiation. In the visceral targets, NO appears to be a spatial modulator in local intrinsic networks or at varicose terminals. In endocrine glands, NO possibly acts as synaptic coactivator or inhibitor, as a cotransmitter affecting stimulus-coupled exocytosis, or as a local vasoactive signal. The short-term neural messenger NO may also induce diffusible target-derived long-term neurotrophic signals, thereby supporting neuroeffector maintenance and plasticity, if not synaptic efficacy, in autonomic target-organ control.

Animals↗
PubMed2005

Comparative anatomical study of the autonomic cardiac nervous system in macaque monkeys.

The main aim of this study was to clarify the general morphology of the autonomic cardiac nervous system in macaque monkeys. A submacroscopic comparative anatomical study of the autonomic cardiac nervous system was performed by examining 22 sides of 11 bodies of four species of macaque monkeys, including some previously unreported species (pig-tailed and stump-tailed monkeys), under a surgical stereomicroscope. The following results were obtained. 1) The basic arrangement of the autonomic cardiac nervous system is constant in all examined macaques. 2) A superior cardiac nerve originating from the superior cervical ganglion was not observed, whereas the thoracic cardiac nerve originating from the sympathetic trunk/ganglia under the cervicothoracic ganglion was rarely observed in all the examined macaques. 3) The main cardiac nerve is the middle cardiac nerve originating from the middle cervical ganglion, similar to the situation in humans. 4) Although the superior, inferior, and thoracic cardiac branches of the vagus nerve were consistently observed, the left thoracic cardiac branch is rarely absent because of its lower origin to the heart. 5) The cranial autonomic nerves tend to distribute into the heart medially (arterial porta), and the caudal autonomic nerves tend to distribute into the heart laterally (venous porta). To comprehend the comparative morphological and evolutionary changes more completely, these results were compared with our previous studies and some references. Consequently, differences in the sympathetic cardiac nerves of macaques and humans are recognized, in spite of the similar morphologies of the vagal cardiac branches. These differences include the composition of the cervicothoracic ganglion, the lower positions of the middle cervical and cervicothoracic ganglia, and the narrow range for the origin of the cardiac nerves in macaques compared to that in humans.

Anatomy, Comparative↗
PubMed2003

Serotonin2 receptors in the nucleus tractus solitarius: characterization and role in the baroreceptor reflex arc.

1. There is a general agreement concerning the key role of the baroreceptor reflex in blood pressure homeostasis. It is also well accepted that baroreceptor afferent messages are first integrated within the nucleus tractus solitarius (NTS) and that an excitatory amino acid, probably glutamate, is the principal neurotransmitter of corresponding afferents fibers. However, important points concerning the processing of baroreceptor messages within the NTS remain to be clarified, in particular the possible modulatory role of other neuroactive substances at this particular level in the medulla oblongata. 2. In this context, the present review focuses on serotonin, and the possible facilitatory influence of NTS serotonergic afferents and receptors on the baroreceptor reflex arc. Relevant pharmacological, electrophysiological, immunohistochemical, and biochemical data, are presented and discussed. They can be summarized as follows. 3. The selective destruction of the nodose ganglion-NTS serotonergic pathway produces a long-term increase in blood pressure variability, similar to that caused by baroreceptor denervation. 4. Microinjection of picomolar doses of 5-HT into the NTS elicits the typical responses of baroreceptor activation. 5. The cardiovascular effects elicited by local microinjections of specific agonists and antagonists into the NTS of intact rats and of animals that underwent nodose ganglionectomy indicate that the baroreceptor-like effects of locally administered 5-HT are mediated by the activation of postsynaptic 5-HT2 receptors. 6. The medullary pathways which mediate NTS 5-HT2 receptor-evoked responses are similar to those involved in the baroreceptor reflex arc. 7. Pharmacological and electrophysiological studies suggest that the cardiovascular effects of intra-NTS 5-HT involve the 5-HT2A receptor subtype expressed by NTS barosensitive neurons that receive polysynaptic vagal afferents 8. Intra-NTS microinjection of a subthreshold dose of DOI, a 5-HT2 receptor agonist, which, on its own, does not produce any cardiovascular changes, significantly enhances the bradycardiac component of the baroreflex. 9. Altogether, the data summarized above show that, in the NTS, 5-HT acting at 5-HT2A receptors exerts a facilitatory influence on the baroreceptor reflex, especially on the cardiac component of this reflex. 10. Convergent pharmacological and electrophysiological data indicate that, in the NTS, functional interactions between NMDA- and 5-HT2A-receptors coexpressed by the same neurons probably underlie the facilitatory influence of 5-HT upon the baroreceptor reflex. 11. Under physiological conditions, the 5-HT2A receptor-mediated facilitatory modulation of the cardiovagal component of the baroreflex might be triggered by 5-HT released from nodose ganglion-NTS serotoninergic afferent neurons and/or for serotoninergic projections originating in raphe nuclei. The latter possibility might notably occur during recovery after physical exercise and/or during the "freezing" reaction in stressed animals.

Afferent Pathways↗
PubMed1993

Skin potential recordings during cystometry in spinal cord injured patients.

In order to investigate autonomic mechanisms associated with bladder filling and bladder contraction, skin potentials from the hands and the feet of 32 spinal cord injured patients were recorded during cystometry. All had a complete clinical loss of motor and sensory function below the lesion, but in 3 patients, the autonomic lesion was electrophysiologically assessed as incomplete. In patients with a complete autonomic lesion, any rise in intravesical pressure associated with bladder hyperreflexia induced SP responses below the level of the lesion. SP responses were never obtained during bladder filling, as the intravesical pressure remained low. These results tend to confirm those of Guttmann and Whitteridge, but differ in so far as SP responses at the foot were a regular finding in all paraplegic and in most tetraplegic patients. Furthermore, bladder contraction failed to elicit SP responses below the level of the lesion in patients with an incomplete autonomic lesion. This study emphasises the importance of assessing the integrity of the autonomic nervous pathways when dealing with autonomic mechanisms in spinal cord injured patients. The possible relation between SP responses and bladder neck dysfunction is further discussed.

Cystoscopy↗
PubMed2006

Reflex regulation of airway smooth muscle tone.

Autonomic nerves in most mammalian species mediate both contractions and relaxations of airway smooth muscle. Cholinergic-parasympathetic nerves mediate contractions, whereas adrenergic-sympathetic and/or noncholinergic parasympathetic nerves mediate relaxations. Sympathetic-adrenergic innervation of human airway smooth muscle is sparse or nonexistent based on histological analyses and plays little or no role in regulating airway caliber. Rather, in humans and in many other species, postganglionic noncholinergic parasympathetic nerves provide the only relaxant innervation of airway smooth muscle. These noncholinergic nerves are anatomically and physiologically distinct from the postganglionic cholinergic parasympathetic nerves and differentially regulated by reflexes. Although bronchopulmonary vagal afferent nerves provide the primary afferent input regulating airway autonomic nerve activity, extrapulmonary afferent nerves, both vagal and nonvagal, can also reflexively regulate autonomic tone in airway smooth muscle. Reflexes result in either an enhanced activity in one or more of the autonomic efferent pathways, or a withdrawal of baseline cholinergic tone. These parallel excitatory and inhibitory afferent and efferent pathways add complexity to autonomic control of airway caliber. Dysfunction or dysregulation of these afferent and efferent nerves likely contributes to the pathogenesis of obstructive airways diseases and may account for the pulmonary symptoms associated with extrapulmonary disorders, including gastroesophageal reflux disease, cardiovascular disease, and rhinosinusitis.

Animals↗
PubMed2006

TRPV1 receptor mediates glutamatergic synaptic input to dorsolateral periaqueductal gray (dl-PAG) neurons.

The purpose of this study was to determine the role of transient receptor potential vanilloid type 1 (TRPV1) receptor in modulating neuronal activity of the dorsolateral periaqueductal gray (dl-PAG) through excitatory and inhibitory synaptic inputs. First, whole cell voltage-clamp recording was performed to obtain the spontaneous miniature excitatory postsynaptic currents (mEPSCs) and inhibitory postsynaptic currents (mIPSCs) of the dl-PAG neurons. As 1 microM of capsaicin was applied into the perfusion chamber, the frequency of mEPSCs was increased from 3.21 +/- 0.49 to 5.64 +/- 0.64 Hz (P < 0.05, n = 12) without altering the amplitude and the decay time constant of mEPSCs. In contrast, capsaicin had no distinct effect on mIPSCs. A specific TRPV1 receptor antagonist, iodo-resiniferatoxin (i-RTX, 300 nM), decreased the frequency of mEPSCs from 3.51 +/- 0.29 to 2.01 +/- 0.2 Hz (P < 0.05, n = 8) but did not alter the amplitude and decay time. In addition, i-RTX applied into the chamber abolished the effect of capsaicin on mEPSC of the dl-PAG. In another experiment, spontaneous action potential of the dl-PAG neurons was recorded using whole cell current-clamp methods. Capsaicin significantly elevated the discharge rate of the dl-PAG neurons from 3.03 +/- 0.38 to 5.96 +/- 0.87 Hz (n = 8). The increased firing activity was abolished in the presence of glutamate N-methy-D-aspartate (NMDA) and non-NMDA antagonists, 2-amino-5-phosphonopentanoic acid, and 6-cyano-7-nitroquinoxaline-2,3-dione. The results from this study provide the first evidence indicating that activation of TRPV1 receptors increases the neuronal activity of the dl-PAG through selective potentiation of glutamatergic synaptic inputs.

Action Potentials↗