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At least 19 recordsLinked to original sources
PubMed1979

Autonomic pathways responsible for bradycardia on facial immersion.

The autonomic pathways mediating the bradycardia response to facial immersion (FI) have not been fully elaborated in man. By means of parasympathetic and sympathetic blockade we studied the heart rate response to FI in nine highly trained young swimmers, at rest and during dynamic cycle exercise. With no blockade, heart rate at rest declined with FI 36 +/- 18%. Under beta-blockade with propranolol or alpha-blockade with phentolamine FI produced a similar decrement. Atropine reduced the response. During exercise FI produced 48 +/- 9% decline without blockade. The response was similar with beta-blockade, but was completely abolished with atropine. Systolic blood pressure responses to FI measured by cuff in three subjects were small and bore no relation to the heart rate response. The results are compatible with parasympathetic efferent mediation of the heart rate response to FI. They are incompatible with a role for sympathetic mediation except as a complex interaction between parasympathetic and sympathetic influences. Hypertension and other sympathetic responses to FI do not play a role in production of bradycardia, but are apparently incidental effects. The heart rate decrement produced by FI increases with greater steady-state heart rate.

Adolescent↗
PubMed1997

Nitric oxide and fibroblast growth factor in autonomic nervous system: short- and long-term messengers in autonomic pathway and target-organ control.

The freely diffusible messenger nitric oxide (NO), generated by NO synthase (NOS)-containing "nitroxergic" (NO-ergic) neurons, is unique among classical synaptic chemical transmitters because of its "non-specificity", molecular "NO-receptors" (e.g. guanylyl cyclase, iron complexes, nitrosylated proteins or DNA) in target cells, intracellular targeting, regulated biosynthesis, and growth factor/cytokine-dependence. In the nervous system, expression of NOS is particularly intriguing in central and peripheral autonomic pathways and their targets. Here, anatomical and functional links appear to exist between NOS, its associated catalytic NADPH-diaphorase enzyme activity (NOSaD) and fibroblast growth factor-2 (FGF-2), a pleiotropic cytokine with mitogenic actions, suggesting mutual "short- and long-term" actions. Several recent studies performed in the rat sympathoadrenal system, an anatomically and neurochemically well-defined autonomic pathway with target-specific functional units of sympathetic preganglionic neurons (SPNs) in the spinal cord, provide evidence for this hypothesis. The NO and cytokine signals may interact at the level of gene expression, transcription factors, post-transcriptional control or second messenger cross-talk. Thus, unique biological roles of FGF-2 and the NO system are likely to exist in neuroendocrine actions, vasomotory perfusion control as well as in neurotrophic actions in sympathetic innervation of the adrenal gland. In view of their anatomical co-existence, functional interplay and synchronizing effects on neuronal networks, multiple roles are suggested for both "short- and long-term" signalling molecules in neuroendocrine functions and integrated autonomic target organ control.

Animals↗
PubMed1991

Ultrastructural evidence for an olfactory-autonomic pathway through the rat central amygdaloid nucleus.

The innervation of medullary projection neurons in the central amygdaloid nucleus (Ce) by afferents from the ventral taenia tecta (VTT) was investigated using combined lesion-induced axonal degeneration and retrograde transport of horseradish peroxidase-conjugated wheat germ agglutinin (HRP-WGA). Injections of HRP-WGA into the nucleus tractus solitarii resulted in retrograde labeling of neurons in the medial Ce. Ultrastructurally HRP-WGA reaction product was identifiable in the perikarya and proximal dendrites of Ce neurons. Degenerating terminals, probably due to damage at the HRP-WGA injection site, were few and confined to the ventral Ce. Electrolytic coagulation of the VTT resulted in approximately 9% of terminals in medial Ce showing signs of degeneration at 5 days post-lesion. Of the terminals sampled, slightly more than 40% were in contact with the dendrites of retrogradely labeled neurons. Where evident, these terminals formed exclusively symmetrical synaptic contacts. These data provide evidence for an oligosynaptic olfactory-autonomic pathway in the rat that may mediate olfactory influences on gastric and cardiovascular aspects of autonomic function.

Amygdala↗
PubMed2000

Effects of testosterone on pelvic autonomic pathways: progress and pitfalls.

Testosterone has potent effects on reproductive behavior, many of which are due to actions on brain nuclei and spinal motoneurons controlling perineal muscles. The autonomic circuits involved in penile erection, ejaculation and emission, have been less commonly considered as targets for circulating androgens. This review demonstrates that many components of pelvic autonomic reflex pathways, including preganglionic neurons, autonomic ganglion cells and primary afferent neurons, are likely to be influenced by testosterone. The steroid appears to play an important role in maintaining neuronal morphology, transmitter synthesis and receptor expression throughout adulthood. Surprisingly, the effects of testosterone are not limited to neurons involved in reproductive reflexes. The challenge is now to determine the range of neuronal features influenced by androgens, and the mechanisms by which these occur. Studies of androgen receptor location indicate that in many autonomic neurons gene expression may be directly influenced by androgens, but a mismatch between receptor distribution and androgen action shows that in some cells other mechanisms must exist. It is also possible that androgens are metabolised to estrogens by some peripheral neurons. Irrespective of the mechanism, it is time to acknowledge that testosterone is an important "maintenance factor" for autonomic neurons.

Animals↗
PubMed1998

Contribution of C-fiber afferent nerves and autonomic pathways in the urinary bladder to spinal c-fos expression induced by bladder irritation.

Previous studies have revealed that chemical irritation of the urinary bladder and urethral mucosa increases the expression of the immediate-early gene, c-fos, in the lumbosacral spinal cord of the rat. The present experiments were undertaken to determine whether drugs known to suppress bladder reflex pathways or spinal nociceptive mechanisms would influence c-fos expression induced by chemical irritation of the lower urinary tract (LUT). Capsaicin (100 mg/kg subcutaneous (s.c.), 7 days prior to the experiment) which does not block bladder reflexes but does desensitize C-fiber afferents, reduced (89%) the number of Fos-positive cells in the lumbosacral spinal cord induced by acetic acid-induced irritation of the LUT. Morphine (2.5 mg/kg, intravenous (i.v.)) or a low dose of baclofen, a GABA(B) agonist, both of which markedly suppressed reflex bladder activity, did not alter spinal c-fos expression induced by LUT irritation. However, a larger dose of baclofen (10 mg/kg, i.v.) reduced by 45% the number of Fos-positive cells. Clonidine (200 microg/kg, i.v.), an alpha2 adrenergic agonist, depressed bladder reflexes but produced only a small decrease (25%) in c-fos expression in lateral laminae V-VII of the cord. The ganglionic blocking agent, hexamethonium, which blocks autonomic but not afferent pathways to the LUT, decreased c-fos expression by 50%. The results indicate that certain drugs can differentially affect reflex bladder activity and c-fos expression and that analgesic drugs which suppress somatic nociceptive pathways do not necessarily affect the c-fos expression induced by visceral nociceptive input.

Acetic Acid↗
PubMed1998

Assessment of the visceral afferent and autonomic pathways in response to esophageal stimulation in control subjects and in patients with diabetes.

OBJECTIVE: To examine the effects of esophageal stimulation on vagal afferent and efferent pathways in volunteers without diabetes and patients with diabetes. DESIGN: Prospective physiological study. PARTICIPANTS: Fourteen control subjects without diabetes and 6 patients with diabetes. INTERVENTIONS: Electrical and mechanical stimulation of the esophagus. OUTCOME MEASURES: Cortical evoked potentials and the power spectra of heart rate variability. RESULTS: For the control subjects, there was a significant decrease in the ratio of the low frequency to high frequency (LF:HF) power (i.e., increased vagal efferent modulation) during stimulation. Reproducible cortical evoked potentials were obtained from all control subjects. In the 6 patients with diabetes, who had viscerosensory and autonomic neuropathy, the cortical evoked potentials showed an erratic non-reproducible response to electrical esophageal stimulation; however, the LF:HF ratio decreased in these patients during stimulation, suggesting an intact subcortical reflex circuit. CONCLUSIONS: Vago-afferent fibres can be studied using minimally invasive techniques, and the power spectral analysis of heart rate variability permits study of autonomic vago-efferent pathways.

Adolescent↗
PubMed1983

A pharmacological analysis of autonomic pathways mediating myocardial disturbances originating in a lateral hypothalamic area of the cat.

A study was made of the mechanisms mediating autonomic changes resulting from stimulation of a site in the lateral hypothalamic area (LHA). This site, when stimulated, induced angina-like ECG disturbances similar to those observed in some cases of brain traumas. These ECG changes were often associated with other autonomic changes, such as pressor response, tachycardia (in some cases bradycardia), nictitating membrane (NM) contraction and pupillary dilatation. Most symptoms were sympathetic: they were largely abolished by spinal cord section between C1 and C2, but were not affected by vagotomy, except that bradycardia was converted to tachycardia. Adrenal catecholamines were not involved since adrenal vein ligation was without effect. Hexamethonium (5-10 mg/kg) prevented pressor response and tachycardia in most cats but only partly protected against ECG changes and NM contractions. Atropine methyl nitrate (0.2 mg/kg) abolished the remaining ECG abnormalities and NM tension. The beta-receptor antagonists, propranolol and practolol (50 micrograms/kg) completely prevented the ECG changes induced either by isoprenaline or LHA stimulation. It is concluded that the symptoms induced by LHA stimulation result from noradrenaline release in the target organs.

Angina Pectoris↗
PubMed1989

Autonomic pathways in the orbit of the human fetus and the rhesus monkey.

In order to study the three-dimensional topography of the intra-orbital autonomic nerve plexuses and the input for these systems, human fetuses and adult rhesus monkeys were investigated. Specimens of the orbits were processed according to the histochemical acetylcholinesterase methods for staining of peripheral nerves. The nerve fibers enter the orbit along the following pathways: 1. bundles of nerve fibers from the pterygopalatine ganglion (mainly parasympathetic) by penetrating the orbital muscle (Müller); 2. perivascularly along the ophthalmic artery (sympathetic). In the orbit the nerve fibers intermingle. The pathways of the nerve fibers from this interwoven nerve plexus towards the target organs are: 1. perivascularly along branches of the ophthalmic artery; 2. perineurally along and in the branches of the ophthalmic and maxillary nerves; 3. independently of blood vessels and cranial nerve branches in Tenon's capsule. Moreover, bundles of nerve fibers from the ciliary ganglion contribute to the innervation of extraocular structures, e.g. the eyelids. It can be concluded that, as far as the autonomic innervation of the orbit is concerned, the monkey is a good animal model for neuroanatomical studies.

Acetylcholinesterase↗
PubMed1996

Ventromedial preoptic prostaglandin E2 activates fever-producing autonomic pathways.

Fever is thought to be initiated by pyrogenic cytokines inducing the production of prostaglandin E2 (PGE2) in the preoptic area (POA); PGE2 may act as a paracrine mediator that stimulates the neural pathways that raise body temperature. This essential role for prostaglandins in fever first was proposed 25 years ago, but the specific preoptic cell groups at which PGE2 acts and the pathways through which fever is produced remain poorly understood. To better define the role of preoptic PGE2 in fever, we developed a new method for combining acute brain injections with Fos immunohistochemistry. We microinjected a threshold dose of PGE2 to construct an anatomically detailed map of fever-producing preoptic sites. The most pyrogenic preoptic sites were clustered along the ventromedial aspect of the POA, surrounding and just anterior to the organum vasculosum of the lamina terminalis. We then used Fos immunohistochemistry to identify the pattern of neural activation induced by fever-producing preoptic injections of PGE2 and compared it with the Fos pattern seen after systemic immune stimulation. PGE2 fever was accompanied by Fos induction in the ventromedial POA and the parvicellular subnuclei of the paraventricular nucleus of the hypothalamus (PVH). In contrast to the Fos pattern seen after intravenous lipopolysaccharide administration, PGE2 injection did not induce Fos in the circumventricular organs or the magnocellular subnuclei of the PVH. These observations establish a potential site of PGE2 action during fever and help define candidate pathways through which fever occurs.

Animals↗
PubMed1999

Interactions between limbic, thalamo-striatal-cortical, and central autonomic pathways during epileptic seizure progression.

We used immunocytochemistry to determine the regional and temporal distribution of Fos protein expression in awake and unrestrained rats after a unilateral stereotaxic microinjection of a cholinergic agonist, carbachol, in the thalamic ventroposterolateral and reticular nuclei, previously shown to cause limbic and generalized convulsive seizures. The microinjection of carbachol elicits behavioral alterations including immobilization, staring, facial and jaw clonus, rearing, and falling, followed by recurrent generalized convulsive seizures, and a pattern of c-fos expression throughout the brain. In addition to the hypothalamic paraventricular and supraoptic nuclei, the initial induction of c-fos expression was observed as early as 15 minutes after the carbachol microinjection, in the piriform and entorhinal cortices, the thalamic paraventricular, the supramammilary, the lateral parabrachial nuclei, and the central gray. From 30 minutes to 2 hours, corresponding to the occurrence of motor expression of limbic and recurrent generalized convulsive seizures, Fos immunoreactivity was seen in a number of functionally related brain regions including the hippocampus, the amygdala, and the anterior thalamic nucleus (limbic system); the thalamus, the basal ganglia, and the cortex (thalamo-striatal-cortical system); and the hypothalamus, the central nucleus of the amygdala, the pons, and the medulla (central autonomic system). On the basis of the present results showing regional and temporal c-fos expression and well known neuroanatomical connections, we have constructed a neural network relating the limbic, thalamo-striatal-cortical, and central autonomic systems. This analysis provides, for the first time, neuronal circuits and pathways relating epilepsy-elicited behavioral expression of convulsive seizures and adaptive homeostatic responses and could serve as a basis for studying central autonomic regulation during epileptic disorders.

Acetylcholine↗
PubMed1994

Autonomic pathways in development of neural stimulation-induced gastric mucosal damage.

Gastric mucosal erosions can be induced by electrical stimulation of either vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (PVN) of the hypothalamus (200 microA, 60 Hz, 100-microseconds pulse width). We have utilized various pharmacological and surgical interventions to determine the contributions of different components of the autonomic nervous system to the development of this neurally induced gastric damage in urethan-anesthetized Sprague-Dawley rats. In all experiments damage was assessed macroscopically and scored blindly on a 0 (normal) to 3 (severe) scale with samples sectioned for subsequent histological assessment of damage at the light microscopic level. Animals pretreated with either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstrated reduced gastric damage scores after vagal stimulation compared with untreated control animals (P < 0.05). In contrast animals that underwent cervical cord transection exhibited gastric damage after both vagal and PVN stimulation that was not significantly different compared with animals with an intact cord undergoing similar stimulation (P > 0.05). Such cord transection itself did not cause any significant change to the gastric mucosa in the time period studied. These data emphasize the importance of the autonomic nervous system, in particular the parasympathetic component in the development of vagal stimulation-induced gastric damage. In addition, the present studies suggest that neither vagal nor PVN stimulation-induced gastric damage is dependent on neural projections to sympathetic preganglionic neurons of the intermediolateral cell column of the spinal cord.

Animals↗
PubMed1998

Angiotensin II: a peptidergic neurotransmitter in central autonomic pathways.

Over the past 20 years a growing body of evidence has been directed to establishing the roles of angiotensin II (ANG) within the central nervous system. When this work began in the late 1970s the concept that this circulating hormone may also act as a neurotransmitter within the brain was contrary to the established dogma regarding synaptic transmission. There is now substantial anatomical data describing the distribution of ANG receptors, and the biochemical machinery for the production of this peptide, within the CNS. In addition many studies have described physiological and cellular consequences of activation of these receptors by both exogenous administration and endogenous release of ANG. Data from single cell studies are now also beginning to elucidate both signal transduction pathways and ion channels, influenced as a consequence of peptide actions at these receptors. These observations effectively establish the status of ANG as a chemical messenger (neurotransmitter) used for synaptic communication by specific populations of CNS neurons.

Angiotensin II↗
PubMed1991

[Investigation of the vesical sphincter and genital-sexual autonomic pathways. Techniques, normal values, and application to pathology].

Parasympathetic and sympathetic pathways may be assessed by using different electrophysiologic tests. Sympathetic skin potentials (SSP) are elicited with peripheral electrical stimulation (e.g. median nerve or pudendal nerve). SSP are recorded from the skin of the hand and foot and from the genital skin. Skin responses were always obtained from normal volunteers. Absence of SSP is one of the earliest findings in neurogenic impotence. Electromyography of corpora cavernosa is described with a new method. A new corpora cavernosa response to pudendal nerve stimulation is described. This test appear to have application in the evaluation of neurogenic impotence.

Adult↗