Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Autonomic Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed2006

Seizures and syncope: anatomic basis and diagnostic considerations.

Although pathophysiologically distinct, syncope and seizures share clinical characteristics which may make diagnosis difficult. Adding to diagnostic complexity are the facts that seizures and syncope may coexist in the same patient, syncope may be associated with seizure-like motor manifestations, and seizures may be complicated by cardiac arrhythmia and syncope. Combined EEG/ECG telemetry is sometimes necessary to establish the correct diagnosis. These techniques also provide an opportunity to study the role of certain cortical regions in the modulation of cardiac function. There is an increasing understanding of the central autonomic pathways involved in the genesis of the cardiovascular changes that occur during epileptic seizures. This article reviews the use of EEG/ECG telemetry in the evaluation of syncope and seizures, and the neuroanatomic circuitry involved in the production of the cardiovascular manifestations of seizures.

Aged, 80 and over↗
PubMed2001

[Autonomic nervous system in diabetes].

Hyperglycemia and hyperinsulinemia have a primary role in determining the early functional and later anatomic changes at the level of the autonomic pathways controlling the circulation, and besides in directly influencing cardiac and vascular cellular targets and feed-back baroreceptor system sensitivity to neurohumoral modulation in patients with diabetes mellitus. The basic mechanisms of dysfunction and damage, and the clinical and prognostic value of diabetic cardiovascular dysautonomia are discussed together with the diagnostic apparatus and the possible therapeutic approaches.

Autonomic Nervous System↗
PubMed1990

Is orthostatic hypotension in the elderly due to autonomic failure?

In order to investigate whether orthostatic hypotension in elderly people is due to autonomic nervous system dysfunction or blood vessel abnormalities, we have measured platelet and lymphocyte adrenoceptor numbers and agonist binding in addition to venous plasma catecholamine concentrations. Eight elderly subjects with orthostatic hypotension and six control elderly subjects were studied. None of the subjects had other symptoms of autonomic failure. There was no significant difference between the heart rate or plasma catecholamine responses to standing of the two groups. The orthostatic hypotension subjects had a significant rise of their plasma vasopressin levels whereas the control group had no significant change. The number of alpha 2-adrenoceptor sites in platelets was lower in the orthostatic hypotensive group compared to the controls and the binding affinity was greater than in the controls. There were no significant differences in beta-adrenoceptor binding sites or affinities in isolated lymphocytes between the two groups. The similar changes in heart rate and catecholamines together with the vasopressin changes suggest that, in these elderly patients with an abnormal drop of blood pressure on standing, there is no dysfunction of autonomic pathways concerned with cardiovascular function. The lower numbers of alpha 2-adrenoceptor sites on isolated platelets in subjects with orthostatic hypotension could indicate reduced alpha 2-adrenoceptor numbers on their blood vessels which could contribute to their inability to maintain blood pressure while standing.

Aged↗
PubMed1986

Diabetic autonomic neuropathy.

The incidence of autonomic dysfunction as a complication of diabetes mellitus is reported to be as high as 20% to 40%. Symptoms of diabetic autonomic neuropathy (DAN) are often vague, and signs difficult to detect on routine physical examination. The early diagnosis of DAN is possible by utilizing several simple noninvasive tests, which may also be helpful in localizing the lesion(s) to specific autonomic pathways. DAN may affect multiple organ systems, to include cardiovascular, gastrointestinal, genitourinary and/or neuroendocrine, and may, in fact, be life-threatening. The same metabolic disturbances of somatic peripheral nerve may also be responsible for DAN. Like somatosensory neuropathy, definitive therapy for DAN is not yet satisfactory, although multiple chemotherapeutic agents have been tried and warrant further investigation.

Autonomic Nervous System Diseases↗
PubMed2001

Tracing functionally identified neurones in a multisynaptic pathway in the hamster and rat using herpes simplex virus expressing green fluorescent protein.

Using a genetically modified herpes simplex virus encoding green fluorescent protein we sought to establish if this viral modification could be used in transneuronal tracing studies of the sympathetic nervous system. The herpes simplex virus encoding green fluorescent protein was injected into the adrenal medulla of three hamsters and six rats. After a suitable survival period, neurones in the sympathetic intermediolateral cell column of the thoracolumbar spinal cord, rostral ventral medulla and paraventricular nucleus of the hypothalamus were clearly identified by the presence of a green fluorescence in the cytoplasm of the neurones of both species. Thus, herpes simplex virus encoding green fluorescent protein labelled chains of sympathetic neurones in the hamster and rat and therefore has the potential to be used in transneuronal tracing studies of autonomic pathways in these species.

Animals↗
PubMed2003

Defects in cardiac conduction system lineages and malignant arrhythmias: developmental pathways and disease.

To unravel the complex disease phenotype of heart failure, we are utilizing an integrative approach employing genomics, physiology, and mouse genetics to identify nodal pathways for specific physiological end points such as myocyte stretch activation responses, contractility and electrical conduction. A new class of genetic pathways for cardiac sudden death and associated arrhythmias has been based on transcription factors that control conduction system lineages, including HF1b/SP4 and NKX2.5. Previous studies have established that HF1b plays a critical role in conduction system lineage formation and the loss of HF1b leads to a confused electrophysiological identity in Purkinje and ventricular cell lineages, resulting in cardiac sudden death and marked tachy and brady arrhythmias. Utilizing Hf1b and Nkx2.5 floxed alleles, we now have identified the primary pathways which link these transcription factors with cardiac arrythmogenesis. Mice which harbour a neural crest restricted knockout of HF1b display marked arrhythmogenesis and conduction system defects, implicating neural crest cues in conduction system development and disease. Mice which harbour a ventricular-restricted knockout of Nkx2.5 display completely normal conduction at birth, but a hypoplastic atrioventricular (AV) node. During maturation, progressive complete heart block ensues, associated with a selective dropout of distal AV nodal cell lineages at the boundaries of the penetrating His bundle. Single cell analyses examining individual nodal cells within AV node of ventricular restricted Nkx2.5 knockout mice clearly document a cell autonomous requirement for NKX2.5 within AV nodal lineages per se. Micro-electrophysiological AV nodal mapping indicates a selective conduction defect at the boundary of the distal AV node and His bundle. HF1b and NKX2.5 reflect new cardiac cell non-autonomous and autonomous pathways for conduction system lineage defects and associated cardiac arrythmogenesis.

Animals↗
PubMed1994

Mechanisms of pressor and bradycardic responses to L-glutamate microinjected into the NTS of conscious rats.

Microinjection of increasing doses of L-glutamate (L-Glu, 0.03-5.0 nmol/100 nl) into the nucleus tractus solitarii (NTS) produced a dose-related pressor and bradycardic response. Prazosin virtually abolished the pressor response but produced no changes in the bradycardic response to L-Glu, indicating that bradycardia is not reflex in origin. The bradycardic response was blocked by atropine. In three different groups of rats, excitatory amino acid receptors in the NTS were blocked by increasing doses of kynurenic acid (0.5, 2.0, and 10.0 nmol/100 nl) and the pressor and bradycardic responses to L-Glu (1 nmol/100 nl) were reduced in a dose-related pattern. Reflex bradycardia induced by an increase in pressure caused by phenylephrine (iv) was also blocked by kynurenic acid. These data show that microinjection of L-Glu into the NTS of conscious rats produced pressor and bradycardic responses, which are due to the activation of two independent autonomic pathways. The data also indicate that the activation of both pathways is mediated by excitatory amino acid receptors. Considering that reflex bradycardia was also blocked by kynurenic acid, we suggest that L-Glu and excitatory amino acid receptors are part of the parasympathetic limb of the baroreceptor reflex. The pressor response to L-Glu is also mediated by excitatory amino acid receptors, but its physiological meaning is still unclear.

Animals↗
PubMed2003

A theoretical model of the role of brain stem nuclei in alcohol-mediated arrhythmogenesis in older adults.

Uncertainty about the mechanism of alcohol-mediated arrhythmogenesis and the effect of alcohol use on arrhythmic risk among older adults is an increasing concern in light of population aging and recent reports that moderate alcohol consumption may protect older adults against coronary artery disease. In this review, a theoretical model of the role of brain stem nuclei in alcohol-mediated arrhythmogenesis in older adults is developed. The model is based on the hypothesis that the effects of alcohol on central autonomic pathways of cardiac control may alter the threshold for alcohol-mediated arrhythmogenesis among older adults. Findings from multiple lines of research including cellular, electrophysiological, epidemiological, experimental, and clinical studies in human, animal, and in vitro models were synthesized in developing the model. Suggestions for future research on the topic of alcohol-mediated arrhythmogenesis in older adults are offered.

Aging↗
PubMed1985

Sympathetic preganglionic efferent and afferent neurons mediated by the greater splanchnic nerve in rabbit.

Motion sickness, a multisymptom disorder characterized by abnormal gastrointestinal motility and emesis, can be induced by vestibular effects on the sympathetic portion of the autonomic nervous system. However, the vestibular-autonomic pathways are unknown. As a first step in the analysis, we identified the locus of preganglionic sympathetic neurons (PSNs) and dorsal root afferent ganglionic neurons (DRGs) which supply sympathetic innervation to major portions of the gastrointestinal tract in the rabbit. Retrograde labeling of neurons was obtained by application of horseradish peroxidase (HRP) to the cut end of the greater splanchnic nerve. Labeled PSNs were found, ipsilaterally, within the T1 to T11 spinal cord segments, with the highest density of neurons in T6. Most PSNs were located within the intermediolateral column (IML), but a significant portion also occurred within the lateral funiculus (LF), the intercalated region (IC) and the central autonomic area (CA). The proportion of labeling between the four regions depended on the spinal cord segment. In the midthoracic levels, the distribution of labeled neurons was denser in the IML and LF, and in the caudal thoracic segments, the majority were localized in the IC and CA. Labeled cells in these four areas varied morphologically from large fusiform neurons in the IC to small fusiform neurons in the LF, small stellate neurons in the CA, and medium-size stellate neurons in the IML. The DRGs were labeled in thoracic segments T1 to T12, with the majority between T5 and T11. These labeled DRG somata of the greater splanchnic nerve were smaller in comparison with unlabeled ones.

Animals↗
PubMed2006

Induction of Fos immunoreactivity labeling in rat forebrain metabolic loci by caudal fourth ventricular infusion of the monocarboxylate transporter inhibitor, alpha-cyano-4-hydroxycinnamic acid.

Caudal fourth ventricular (CV4) infusion of the monocarboxylate transporter inhibitor, alpha-cyano-4-hydroxycinnamic acid (4CIN), causes hyperglycemia coincident with Fos expression in the hindbrain nucleus tractus solitarius, a rare central source of metabolic deficit signaling. The present studies examined the hypothesis that hindbrain lactoprivic signaling activates central autonomic pathways that regulate systemic glucostasis by examining the effects of this drug treatment paradigm on patterns of Fos expression in forebrain structures that integrate sensory input from metabolic sensors and coordinate motor responses to energy shortages. Two hours after CV4 infusion of graded doses of 4CIN or vehicle alone, adult female rats were sacrificed by transcardial perfusion and sections through the telencephalic and diencephalic metabolic loci were processed for Fos immunoreactivity (-ir). Fos labeling of the hypothalamic paraventricular (PVH), dorsomedial (DMH), and ventromedial (VMH) nuclei was significantly elevated, relative to the vehicle-treated controls, in response to the lowest dose of 4CIN, e.g. 10 microg/animal. Treatment with higher doses of 4CIN (25 or 50 microg) further augmented numbers of Fos-ir-positive neurons in these structures, and also elicited staining of the bed nuclei of the stria terminalis (BST), medial preoptic (MPN), arcuate (ARH), supraoptic (SO), and anterior hypothalamic nuclei (AHN), and lateral hypothalamic area (LHA). Mean numbers of Fos-immunolabeled neurons in the ARH, DMH, LHA, AHN, MPN, and SO were not different between animals infused with 25 versus 50 microg 4CIN, whereas neuronal labeling in the VMH, BST, and PVH was significantly greater in the high- versus the middle-dose groups. The present data show that pharmacological inhibition of lactate uptake within the caudal hindbrain results in dose-dependent neuronal Fos immunoexpression within characterized forebrain components of the central metabolic circuitry, and that these patterns of neuronal transcriptional activation parallel observed drug effects on blood glucose levels. These results suggest that lactoprivic signaling by metabolic 'sensing' neurons in the caudal hindbrain initiates central neural mechanisms that control systemic energy availability, and that local lactate-'sensitive' neurons are connected neuroanatomically with principal higher-order autonomic metabolic loci that regulate glucostasis.

Analysis of Variance↗
PubMed2001

Neural circuitry of the kidney: NO-containing neurons.

The neurons synthesizing nitric oxide (NO) that are part of the renal sympathetic pathways were located by double-staining for the neuronal isoform of nitric oxide synthase (nNOS) using immunocytochemistry to identify NO-synthesizing neurons and transneuronal tracing following infection of the left kidney with pseudorabies virus (PRV). Following kidney injection with PRV, the animals survived 4-day post-inoculation prior to sacrifice and tissue processing. PRV-infected neurons that double-stained for nNOS were found in the paraventricular hypothalamic nucleus (PVN), the raphe obscurus nucleus (ROb), the ventromedial medulla (VMM), the rostral ventrolateral medulla (rVLM) and the A5 cell group. In the thoracolumbar spinal cord, nNOS neurons co-localized with PRV-infected cells in the dorsal horn in laminae I, III-V ipsilateral to the injected kidney and in lamina X, the intermediolateral cell column, the lateral funiculus, the intercalated nucleus and the central autonomic area. We conclude that NO synthesizing cells may significantly affect renal autonomic pathways in the rat by interacting with the renal sensory and sympathomotor circuitry at multiple sites.

Afferent Pathways↗
PubMed2005

Post-stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea-pig uterine artery in vitro.

Vasodilatation produced by stimulation of preganglionic neurones in lumbar and sacral pathways to pelvic ganglia was studied using an in vitro preparation of guinea-pig uterine artery and associated nerves in a partitioned bath allowing selective drug application to the ganglia or artery. Arterial diameter was monitored using real time video imaging. Vasodilatations produced by hypogastric nerve stimulation (HN; 300 pulses, 10 Hz) were significantly larger and longer in duration than with pelvic nerve stimulation (N = 18). Stimulation of ipsilateral lumbar splanchnic nerves or ipsilateral third lumbar ventral roots also produced prolonged vasodilatations. Blockade of ganglionic nicotinic receptors (0.1-1 mM hexamethonium) delayed the onset and sometimes reduced the peak amplitude of dilatations, but slow dilatations persisted in 16 of 18 preparations. These dilatations were not reduced further by 3 microM capsaicin applied to the artery and ganglia, or ganglionic application of 1 microM hyoscine, 30-100 microM suramin or 10 microM CNQX. Dilatations were reduced slightly by ganglionic application of NK1 and NK3 receptor antagonists (SR140333, SR142801; 1 microM), but were reduced significantly by bathing the ganglia in 0.5 mM Ca2+ and 10 mM Mg2+. Intracellular recordings of paracervical ganglion neurones revealed fast excitatory postsynaptic potentials (EPSPs) in all neurones on HN stimulation (300 pulses, 10 Hz), and slow EPSPs (3-12 mV amplitude) in 25 of 37 neurones. Post-stimulus action potential discharge associated with slow EPSPs occurred in 16 of 37 neurones (firing rate 9.4 +/- 1.5 Hz). Hexamethonium (0.1-1 mM) abolished fast EPSPs. Hexamethonium and hyoscine (1 microM) did not reduce slow EPSPs and associated post-stimulus firing in identified vasodilator neurones (with VIP immunoreactivity) or non-vasodilator paracervical neurones. These results demonstrate a predominantly sympathetic origin of autonomic pathways producing pelvic vasodilatation in females. Non-cholinergic mediators of slow transmission in pelvic ganglia produce prolonged firing of postganglionic neurones and long-lasting dilatations of the uterine artery. This mechanism would facilitate maintenance of pelvic vasodilatation on stimulation of preganglionic neurones during sexual activity.

Animals↗
PubMed1989

Organization of afferent and efferent pathways in the pudendal nerve of the female cat.

Application of horseradish peroxidase to the pudendal nerve in the female cat labelled lumbosacral afferent and efferent neurons and their processes. Afferent axons entered the spinal cord primarily at the S1 and S2 segments and traveled rostrocaudally in Lissauer's tract and the dorsal columns. A distinctive component of the dorsal column projection was located at the lamina I-dorsal column border as a densely labelled, compact bundle that distributed fibers to the dorsal horn at spinal levels near the segments of entry of the afferent axons. Afferent terminal labelling was located in the marginal zone, the intermediate gray matter, and the dorsal gray commissure in the lumbosacral and coccygeal spinal cord. A well-defined terminal field restricted to the S1 and rostral S2 segments was present in the medial third of the nucleus proprius and substantia gelatinosa. Labelled motoneurons in Onuf's nucleus (S1 and S2) exhibited longitudinal dendrites that extended rostrocaudally within the nucleus and three groups of transverse dendrites that emanated periodically from the nucleus and passed to the ventrolateral funiculus, the intermediate gray, and the dorsal gray commissure. Components of the pudendal nerve that innervate the anal and urethral sphincters were also labelled by injecting HRP into the respective sphincter muscles. Motoneurons innervating the anal and urethral sphincters were located in the dorsomedial and ventrolateral divisions, respectively, of Onuf's nucleus. Afferent projections from the two sphincters were similar; the most prominent terminations were present in the marginal zone, intermediate gray, and dorsal gray commissure. These results are discussed with respect to the physiological function of the pudendal nerve and its relationship with sacral autonomic pathways.

Afferent Pathways↗
PubMed1984

Blockade of GABA receptors in periventricular forebrain of anesthetized cats: effects on heart rate, arterial pressure, and hindlimb vascular resistance.

Pharmacologic antagonism of GABAergic inhibition in the periventricular forebrain of anesthetized cats caused dose related sympathetically mediated increases in heart rate and arterial pressure in vagotomized cats, and suppression of reflex vagal activation in vagus-intact preparations where sympathetic effects are prevented by cervical spinal cord transection. In the present study performed in cats with intact autonomic pathways, similar administration of the GABA antagonist bicuculline methiodide (BMI) produced dose-related increases in arterial pressure, heart rate, and, when perfusion pressure in the autoperfused hindlimb was measured, vascular resistance. Furthermore, the relationship between heart rate and hindlimb vascular resistance changes suggested that the effects on heart rate reflected the combined sympathetic and vagal baroreflex effects of BMI. Intraventricular administration of muscimol, a potent GABA agonist, elicited abrupt and parallel reversal of BMI-induced effects on systemic arterial pressure and vascular resistance while attempts to acutely denervate the hindlimb at the height of the BMI response by cutting the femoral and sciatic nerves sharply reversed the increase in hindlimb vascular resistance in most experiments. The results suggest that the cardiovascular changes observed represent an integrated pattern consisting of excitation of sympathetic nerves innervating the heart and vasculature along with suppression of reflex evoked vagal excitability.

Adrenergic Fibers↗
PubMed2003

Evaluation and treatment of autonomic disorders of the urogenital system.

Autonomic pathways are important in the regulation of both lower urinary tract and sexual function, and their interruption in neurological pathologies predictably results in variable urogenital dysfunction, depending mainly on the level of the lesion. A normal neurological examination of a patient with urogenital complaints should exclude an underlying neurological pathology, and the neurologist should become involved in the management of symptoms. Electromyography can be of value in the diagnosis and management of cauda equina lesions and multiple system atrophy, but neurophysiological investigations are of no importance in the diagnosis of neurogenic sexual dysfunction. Urodynamic studies have proven helpful in determining the type and management of lower urinary tract dysfunction. Oral anticholinergics usually combined with clean intermittent catheterizations are the first-line treatment options for neurogenic lower urinary tract dysfunction, with intravesical treatments emerging as the main alternative in intractable incontinence. The availability of effective oral phosphodiesterase inhibitors has revolutionized the management of erectile dysfunction, but treatment of ejaculatory and orgasmic disorders as well as of female sexual dysfunction still remains problematic.

Animals↗
PubMed2004

Suprachiasmatic nucleus input to autonomic circuits identified by retrograde transsynaptic transport of pseudorabies virus from the eye.

Intraocular injection of the Bartha strain of pseudorabies virus (PRV Bartha) results in transsynaptic infection of the hypothalamic suprachiasmatic nucleus (SCN), a retinorecipient circadian oscillator. PRV Bartha infection of a limited number of retinorecipient structures, including the SCN, was initially interpreted as the differential infection of a subpopulation of rat retinal ganglion cells, followed by replication and anterograde transport via the optic nerve. A recent report that used a recombinant strain of PRV Bartha (PRV152) expressing enhanced green fluorescent protein demonstrated that SCN infection actually results from retrograde transneuronal transport of the virus via the autonomic innervation of the eye in the golden hamster. In the present study using the rat, the pattern of infection after intravitreal inoculation with PRV152 was examined to determine if infection of the rat SCN is also restricted to retrograde transsynaptic transport. It was observed that infection in preganglionic autonomic nuclei (i.e., Edinger-Westphal nucleus, superior salivatory nucleus, and intermediolateral nucleus) precedes infection in the SCN. Sympathetic superior cervical ganglionectomy did not abolish label in the SCN after intraocular infection, nor did lesions of parasympathetic preganglionic neurons in the Edinger-Westphal nucleus. However, combined Edinger-Westphal nucleus ablation and superior cervical ganglionectomy eliminated infection of the SCN. This observation allowed a detailed examination of the SCN contribution to descending autonomic circuits afferent to the eye. The results indicate that in the rat, as in the hamster, SCN infection after intraocular PRV152 inoculation is by retrograde transsynaptic transport via autonomic pathways to the eye.

Animals↗
PubMed2002

Role of the central and peripheral nervous system in the ovarian function.

This review attempts to give a comprehensive overview of ovarian innervation, considering the whole nervous system and its different levels that may modify the ovarian function. The connection between the ovary and the central nervous system through the autonomic pathways, including the peripheral ganglia, is highlighted. The evidence obtained over the last years highlights the role of the superior ovarian nerve (SON) in the ovarian phenomena. Besides, the effect on the ovary of conventional neurotransmitters and others such as indolamines and peptides, which have been found in this organ, are discussed. Various reproductive diseases have been studied almost exclusively from the endocrine point of view. It is evident that a better knowledge about the role of the neural factors involved in the ovarian physiology may facilitate the understanding of some of these. A review of the concepts and an update of some experimental designs is made that permits clarifying several aspects of the relationship between the neural system and the ovary. At present, there is no doubt that the innervation of the ovary is involved in several physiological aspects of this gland function. However, the relationship of some levels of the nervous system and the ovary offer a wide avenue for future research.

Animals↗
PubMed1991

Use of peptide probes to study brain regulation of glucose metabolism.

Neuropeptides may be used to stimulate or inhibit neurocircuitry involved in regulation of visceral organ function, including glucose metabolism. Through the use of different peptides with different specificities, it may be possible to characterize the neuroendocrine and autonomic pathways involved in the physiologic regulation of glucose homeostasis.

Animals↗