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PubMed1991

Autonomic responses and efferent pathways from the insular cortex in the rat.

The anatomical distribution of autonomic, particularly cardiovascular, responses originating in the insular cortex was examined by using systematic electrical microstimulation. The localization of these responses to cell bodies in the insular cortex was demonstrated by using microinjection of the excitatory amino acid, D,L-homocysteic acid. The efferents from the cardiovascular responsive sites were traced by iontophoretic injection of the anterograde axonal tracer Phaseoleus vulgaris leucoagglutinin (PHA-L). Two distinct patterns of cardiovascular response were elicited from the insular cortex: an increase in arterial pressure accompanied by tachycardia or a decrease in arterial pressure with bradycardia. The pressor responses were obtained by stimulation of the rostral half of the posterior insular cortex while depressor sites were located in the caudal part of the posterior insular area. Both types of site were primarily located in the dysgranular and agranular insular cortex. Gastric motility changes originated from a separate but adjacent region immediately rostral to the cardiovascular responsive sites in the anterior insular cortex. Tracing of efferents with PHA-L indicated a number of differences in connectivity between the pressor and depressor sites. Pressor sites had substantially more intense connections with other limbic regions including the infralimbic cortex, the amygdala, the bed nucleus of the stria terminalis and the medial dorsal and intralaminar nuclei of the thalamus. Alternatively, the depressor region of the insular cortex more heavily innervated sensory areas of the brain including layer I of the primary somatosensory cortex, a peripheral region of the sensory relay nuclei of the thalamus and the caudal spinal trigeminal nucleus. In addition, there were topographical differences in the projection to the lateral hypothalamic area, the primary site of autonomic outflow for these responses from the insular cortex. These differences in connectivity may provide the anatomic substrate for the specific cardiovascular responses and behaviors integrated in the insular cortex.

Animals↗
PubMed1996

Ventricular rate during atrial fibrillation before and after slow-pathway ablation. Effects of autonomic blockade and beta-adrenergic stimulation.

BACKGROUND: Radiofrequency catheter modification of AV conduction can be used to control the ventricular rate during atrial fibrillation both in the baseline state and during exercise. Slow-pathway ablation has been suggested to be the mechanism for this response. The purpose of this study was to determine the effect of slow-pathway ablation on the ventricular rate in atrial fibrillation during autonomic blockade and sympathetic stimulation in patients with AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Thirty-five patients undergoing slow-pathway radiofrequency ablation for AVNRT were assigned to autonomic blockade (0.2 mg/kg propranolol and 0.04 mg/kg atropine; n = 14) or isoproterenol (2 micrograms/min; n = 21). Atrial fibrillation was induced before and after slow-pathway radiofrequency ablation. During autonomic blockade, the mean ventricular cycle length (448 +/- 34 versus 525 +/- 103 ms, P < .01) and maximum ventricular cycle length (640 +/- 105 versus 798 +/- 226 ms, P = .04) were prolonged after ablation, whereas the minimum ventricular cycle length did not change significantly (361 +/- 42 versus 403 +/- 83 ms, P = .05). During isoproterenol infusion, the mean ventricular cycle length (375 +/- 52 versus 390 +/- 61 ms, P = .2), maximum ventricular cycle length (520 +/- 88 versus 537 +/- 106 ms, P = .3), and minimum ventricular cycle length (307 +/- 59 versus 298 +/- 33 ms, P = .4) did not change significantly after slow-pathway ablation. CONCLUSION: Slow-pathway ablation slows the ventricular rate during atrial fibrillation under conditions of autonomic blockade but not during sympathetic stimulation. Therefore, slow-pathway ablation alone cannot account for the clinical results obtained with radiofrequency modification of AV conduction in patients with atrial fibrillation.

Adult↗
PubMed1985

Vasopressin secretion in progressive autonomic failure: evidence for defective afferent cardiovascular pathways.

Patients with progressive autonomic failure with multiple system atrophy show a severely blunted response of plasma arginine vasopressin to the stimulus of head-up tilt. Whether this could be due to lesions either at one or more sites within ascending neural pathways from cardiovascular stretch receptors in the thorax or, alternatively, to lesions affecting vasopressin secreting cells within the hypothalamus was investigated. The arginine vasopressin response to an intravenous infusion of hypertonic saline was determined in six patients with progressive autonomic failure. The mean plasma concentration of arginine vasopressin rose from 1.0 to 3.7 pmol/l, a change comparable to that observed in normal controls. This demonstrates normal functioning of the efferent connections from the osmoreceptors within the hypothalamus and suggests that the loss of vasopressin response to head-up tilt is due to lesions in ascending pathways from cardiovascular receptors. There was a significant rise in mean blood pressure during the infusions on patients with progressive autonomic failure, a change which was not observed with the controls. This may have been at least partly caused by the rise in circulating arginine vasopressin concentrations, since these patients have been reported to be extremely sensitive to the pressor effects of arginine vasopressin.

Afferent Pathways↗
PubMed2002

Effects of linear ablation at the isthmus between the tricuspid annulus and inferior vena cava for atrial flutter on autonomic nervous activity: analysis of heart rate variability.

Heart rate is largely affected by the autonomic nervous system. However, little is known about the anatomic pathway of autonomic nerve fibers innervating the sinus node. The present study: (1) evaluates the effects of cavotricuspid isthmus ablation for common atrial flutter (AFL) on autonomic nervous function by using heart rate variability analysis, and (2) investigates the distribution of autonomic nerve pathways innervating the sinus node. Twelve patients with paroxysmal common atrial flutter who maintained sinus rhythm both before and after radiofrequency ablation were selected for the study. Holter ambulatory recordings were performed before and after (2.3 +/- 1.0 days) radiofrequency ablation of cavotricuspid isthmus. Heart rate and time domain (SDANN, rMSSD, pNN50) and frequency domain (low frequency (LF), high frequency (HF), LF/HF) analysis of heart rate variability were compared before and after ablation. Mean heart rate did not change significantly after ablation (59 +/- 6 vs 61 +/- 9 beats/min); parasympathetic indices of heart rate variability (SDANN, rMSSD, pNN50, HF) did not change significantly (110 +/- 37 vs 117 +/- 20 ms; 32 +/- 21 vs 28 +/- 9 ms; 4.8 +/- 0.9 vs 4.7 +/- 0.71n(ms2)); and sympathetic indices of heart rate variability (LF/HF) did not change significantly (1.1 +/- 0.2 vs 1.2 +/- 0.1). Cavotricuspid isthmus ablation for atrial flutter did not significantly change heart rate and heart rate variability because parasympathetic and sympathetic fibers innervating the sinus node are scarce in this region.

Aged↗
PubMed2003

Regulation of flowering time by histone acetylation in Arabidopsis.

The Arabidopsis autonomous floral-promotion pathway promotes flowering independently of the photoperiod and vernalization pathways by repressing FLOWERING LOCUS C (FLC), a MADS-box transcription factor that blocks the transition from vegetative to reproductive development. Here, we report that FLOWERING LOCUS D (FLD), one of six genes in the autonomous pathway, encodes a plant homolog of a protein found in histone deacetylase complexes in mammals. Lesions in FLD result in hyperacetylation of histones in FLC chromatin, up-regulation of FLC expression, and extremely delayed flowering. Thus, the autonomous pathway regulates flowering in part by histone deacetylation. However, not all autonomous-pathway mutants exhibit FLC hyperacetylation, indicating that multiple means exist by which this pathway represses FLC expression.

Acetylation↗
PubMed2000

Radical hysterectomy: An anatomic evaluation of parametrial dissection.

OBJECTIVES: This study was designed to demonstrate a reduction in the amount of blood loss for vesicouterine ligament dissection and to investigate the intrapelvic autonomic nerve pathway and its preservation by means of anatomic analysis. METHODS: The anchoring mechanism of the pelvic viscera to the pelvic wall was divided into a supporting system facing laterally and a suspensory system facing dorsoventrally. An operative procedure was designed in which both systems were separated and dissected independently. RESULTS: Between the two systems, an artificial space was developed, which required a new dissection method for the parametrium and revealed a new anatomic pathway for the ureter and autonomic nerve. The amount of blood loss (mean +/- SD) during dissection of the vesicouterine ligament was ultimately 260.1 +/- 114.8 ml. Postoperatively, the maximum capacity of the bladder was 393.9 +/- 40.4 ml, maximum detrusor pressure 6.3 +/- 4.1 cm H(2)O, mean compliance >10 ml/cm H(2)O, residual urine 23.8 +/- 9.4 ml, and maximum flow rate 25. +/- 8 2.2 ml/s, respectively. CONCLUSION: A new classification for the parametrium and its dissection method have been established. Development of this new operative procedure has also contributed to a decrease in blood loss and preservation of bladder function.

Blood Loss, Surgical↗
PubMed2001

Hypothalamic pathways underlying the endocrine, autonomic, and behavioral effects of leptin.

Leptin affects body weight by decreasing food intake, activating the sympathetic nervous system and regulating neuroendocrine function. This type of regulation is a hallmark of hypothalamic control, which typically integrates autonomic, endocrine and behavioral responses. We have performed a series of experiments investigating hypothalamic pathways underlying these actions of leptin. We found that leptin activates neurons that coexpress pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA. These neurons innervate several sites, including sympathetic preganglionic neurons in the spinal cord, neurons in the paraventricular hypothalamic nucleus (PVH), and melanin-concentrating hormone and orexin neurons in the lateral hypothalamic area (LHA). Following leptin administration, POMC neurons express both Fos and suppressor of cytokine signalling-3 (SOCS-3) mRNA. In contrast, leptin induced SOCS-3 expression in neuropeptide Y (NPY) neurons but not Fos, suggesting that leptin acts differentially on NPY and POMC cells. We also investigated potential downstream targets of leptin responsive NPY and POMC neurons by assessing the distribution of the melanocortin 4 receptor (MC4-R) mRNA and Y1 and Y5 NPY receptor mRNA in chemically defined neurons. We found dense MC4-R mRNA expression in several sites including the PVH and LHA. Using dual-label in situ hybridization we found that MC4-R mRNA is coexpressed in PVH cells expressing pro-TRH mRNA. We also found Y1 and Y5 NPY receptor mRNA in the PVH in patterns very similar to that of MC4R, suggesting that these receptors may be coexpressed on at least some PVH neurons. These results provide a neuroanatomic framework explaining the endocrine, autonomic and behavioral effects of leptin.

Animals↗
PubMed2001

Analysis of flowering time control in Arabidopsis by comparison of double and triple mutants.

Three genetic pathways promote flowering of Arabidopsis under long photoperiods. These pathways are represented by the genes CO, FCA, and GA1, which act in the long-day, autonomous, and gibberellin pathways, respectively. To test whether these are the only pathways that promote flowering under long photoperiods, the co-2 fca-1 ga1-3 triple mutant was constructed. These plants never flowered under long- or short-day conditions, indicating that the three pathways impaired by these mutations are absolutely required for flowering under these conditions. The triple mutant background represents a "vegetative ground state" enabling the roles of single pathways to be described in the corresponding double mutants. The phenotypes of plants carrying all eight combinations of wild-type and mutant alleles at the three loci were compared under long- and short-day conditions. This analysis demonstrated that under long photoperiods the long-day pathway promoted flowering most effectively, whereas under short photoperiods the gibberellin pathway had the strongest effect. The autonomous pathway had a weak effect when acting alone under either photoperiod but appeared to play an important role in facilitating the promotion of flowering by the other two pathways. The vegetative phenotype of the triple mutant could be overcome by vernalization, suggesting that a fourth pathway promoted flowering under these conditions. These observations are discussed in light of current models describing the regulation of flowering time in Arabidopsis.

Arabidopsis↗
PubMed1984

Cerebellar autonomic function: direct hypothalamocerebellar pathway.

A direct hypothalamocerebellar projection in the cat was revealed by means of retrograde transport of wheat germ agglutinin--horseradish peroxidase complex. This appears to be the first demonstration of a significant autonomic input to the cerebellum. The projection has a widespread origin and is bilateral with an ipsilateral preponderance.

Animals↗
PubMed2004

Genetic regulation of time to flower in Arabidopsis thaliana.

In Arabidopsis thaliana, the initiation of flowering is carried out by four genetic pathways: gibberellin, autonomous, vernalization, and light-dependent pathways. These processes are integrated by the function of the genes FD, FE, FWA, PDF2, SOC1, and FT at the integration pathway. The integrated signal of the floral induction is transmitted to the floral meristem identity genes LFY and AP1, and floral morphogenesis is performed.

Arabidopsis↗
PubMed1989

Neuroanatomical substrates involved in the control of food intake.

Five neural pathways were reviewed regarding their specific role in the control of food intake in birds. The five pathways included the trigeminal sensorimotor system, the visual system/basal ganglia pathway, the gustatory system, the olfactory pathway, and the autonomic nervous system/parasympathetic pathway. The trigeminal system is the pathway best understood among the five systems associated with feeding. It begins with sensory nerves innervating the upper and lower mandibles and buccal cavity and ends with nerves projecting to jaw muscles. The function of the pathway is to control the grasping and mandibulation of pellets or seeds. The visual system includes both the tectofugal and thalamofugal pathways. Both visual pathways interact with the avian paleostriatal complex. The latter is equivalent to the mammalian basal ganglia. The second pathway is important in food recognition as well as in orienting the body with respect to its position in three-dimensional space. The third neural circuit involves the sense of taste. Approximately 300 taste buds have been identified within the buccal cavity of the chicken, suggesting that the gustatory system is better developed than once thought. The fourth pathway involves the olfactory system; as in the visual system, more than one pathway has been identified. The dominant pathway appears to project to the piriform cortex, a structure that may play a role in monitoring essential amino acid contents of the brain. The fifth pathway involves an interaction of the hypothalamus and the dorsal motor nucleus of the vagus. This pathway is important in activating the parasympathetic nervous system and in preparing an organism to feed. All five pathways play different roles in controlling food intake in birds.

Animals↗