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PubMed1977

Sympathetic reflex responses presumably specific for nociceptive stimulation.

1. In superficially anaesthetized and in unanaesthetized decerebrate cats, tetanic stimulation of A or A + C afferent fibres of the tibial nerve evoked in renal and inferior cardiac nerves a three-phasic change of activity, which consisted of a short powerful burst of discharges, followed by an inhibitory pause and then, by a moderate excitation. When such a command appeared in sympathetic nerves, reflex rising of systemic arterial pressure was extremely fast. 2. The latencies of the three-phasic command and of the so-called very late A response are almost the same. The very late A response is evident if the central nervous system is in the same state as when repetitive stimulation of A afferents evokes the three phasic command in sympathetic nerves and a steep rise of systemic arterial pressure. This permits the assumption that the very late A response reflects the excitation of just those central structures that on repetitive stimulation organize the three-phasic command. 3. A command of this kind is shown to ensure the optimal-time-control of the heart and blood vessels. Such a control (three-phasic command) is supposed to be evoked by nociceptive stimulation, i.e., to be specific for the defence reaction.

Action Potentials↗
PubMed1998

[Mediators of the local reflex arc in airways of the rat and guinea pig].

Transmission of neural pulses from afferents to functional module's neurons in rats and guinea pigs can be carried out with the aid of the P substance. Further transmission to a smooth muscle of the trachea occurs through a neuro-muscular junction with acetylcholine as a transmitter. Transmission of inhibitory influences from the tracheo-bronchial receptors to the smooth muscle is carried out via nicotinic cholinoreceptors. Adrenergic mechanisms can modulate neural transmission at the level of intramural ganglia.

Acetylcholine↗
PubMed1997

[Activation of locus coeruleus inhibits vagal inputs in nucleus tractus solitarius].

On pentobarbital anesthetized rabbits, a three-wavelet compound potential to cervical vagal afferent stimulation was recorded in ipsilateral nucleus tractus solitarius (NTS). The latency of the three wavelets (P1, P2 and P3) was 6.8 +/- 0.6 ms (P1), 25.8 +/- 4.2 ms (P2) and 89.1 +/- 2.7 ms (P3) respectively, which might represent postsynaptic activity of different kinds of vagal afferent fibers. Microinjection of glutamate into ipsilateral locus coeruleus (LC) decreased the amplitude of P2 and P3 significantly. Electrical stimulation of LC could activate 111 units in ipsilateral NTS with a mean latency of 6.3 +/- 1.4 ms. Of the 169 units in the NTS to vagal afferent stimulation, 90 units also responded to LC stimulation. 39 (43.3%) of the ninety, units shows similar response to both stimuli, while the rest show different response. Of the 25 units which showed excitatory response to both LC and vagal stimulation, but when LC stimulation was followed by vagus stimulation, the latter's response was either markedly suppressed (14 units) or completely inhibited (11 units). These results showed that activation of LC exerts an inhibitory effect on the responses of the NTS to vagal afferent stimulation.

Afferent Pathways↗
PubMed2004

Projections from the parabrachial nucleus to the vestibular nuclei: potential substrates for autonomic and limbic influences on vestibular responses.

Previous anatomical studies in rabbits and rats have shown that the superior vestibular nucleus (SVN), medial vestibular nucleus (MVN) and inferior vestibular nucleus (IVN) project to the parabrachial nucleus (PBN) and Kölliker-Fuse (KF) nucleus. Adult male albino rabbits and Long-Evans rats received iontophoretic injections of biotinylated dextran amine, Phaseolus vulgaris leucoagglutinin, Fluoro-Gold or tetramethylrhodamine dextran amine into either the vestibular nuclei or the PBN and KF nuclei. The results were similar in both rats and rabbits. Injections of retrograde tracers into the vestibular nuclei produced retrogradely labeled neurons bilaterally in caudal third of the medial, external medial, and external lateral PBN in both species, with more variable labeling in KF. Rats also had consistent bilateral (predominantly contralateral) labeling in the ventrolateral PBN. The most prominent labeling was produced from injections that included the SVN, with fewer labeled neurons observed from injections in the caudal MVN and the IVN. Anterograde transport of BDA from injections into the PBN and KF nuclei of rabbits revealed prominent projections to the SVN, dorsal aspect of the rostral MVN, caudal MVN, pars beta of the LVN and IVN. These connections appear to contain a component that is reciprocal to the vestibulo-parabrachial pathway and a non-reciprocal component to regions connected with the vestibulocerebellum and vestibulo-motor reflex pathways. These connections support the concept that a synthesis of autonomic, vestibular and limbic information is an integral property of pathways related to balance control in both the brain stem and forebrain. It is suggested that these projections may contribute broadly to both performance tradeoffs in vestibular-related pathways during variations in the behavioral context and affective state and the close association between anxiety and balance function.

Afferent Pathways↗
PubMed1999

The autonomic nerve supply of male sex organs--an important target of circulating androgens.

The autonomic nervous system plays a critical role in the regulation of smooth muscle contraction, exocrine secretion and blood flow in the male reproductive organs. Many of the autonomic neurons that supply these targets lie in the pelvic ganglia, which contain both sympathetic and parasympathetic ganglion cells. In rats, removal of circulating androgens by castration before or after puberty has profound effects on the structure, chemistry and function of particular classes of pelvic autonomic neurons. While most of these effects occur in reproductive pathways, some bladder- or bowel-projecting neurons also exhibit androgen-sensitivity. Our studies on these ganglion cells and their spinal preganglionic inputs show that testosterone (or a metabolite) has potent actions both before and after puberty and can be considered essential for the normal maturation and maintenance of some pelvic autonomic reflex pathways. Androgen receptors are distributed widely throughout various components of these circuits, suggesting that testosterone may have direct effects on neuronal gene expression. Together, the studies show that in addition to powerful effects on some central neurons controlling reproductive behaviour, testosterone has similarly important effects on peripheral neurons that trigger and complete copulatory reflexes.

Androgens↗
PubMed1997

Frequency-response characteristics of autonomic nervous system function in conscious rats.

To characterize the efferent pathway from the hypothalamic paraventricular nucleus (PVN) to peripheral autonomic neurons and finally to selected effector organs, we stimulated the PVN in 10 conscious rats at frequencies ranging from 0.05 to 2.0 Hz. Simultaneously, blood pressure, heart rate, splanchnic sympathetic nerve activity, and mesenteric artery blood flow were measured. The sinus node of the heart responded to PVN stimulation via the parasympathetic pathway (during beta 1-adrenergic blockade) up to a stimulation frequency of 2.0 Hz, whereas the sympathetically mediated response (during muscarinic blockade) was limited to stimulation frequencies < 0.5 Hz. The splanchnic nerve responded to PVN stimulation with synchronous discharges up to stimulation frequencies of 2.0 Hz, whereas the oscillatory component of the vasoconstrictor response of the mesenteric artery was negligible beyond stimulation frequencies of 1.0 Hz. We conclude that sympathetic transmission to the heart is at least four times slower than parasympathetic transmission. In addition, the time-limiting step in sympathetic transmission from the hypothalamus to vascular smooth muscle contraction and pacemaker activity of the sinus node may be located at the site of synaptic transmission to the adrenergic receptors.

Animals↗
PubMed1992

NANC nerve pathways controlling mucus glycoconjugate secretion into feline trachea.

We used autonomic-blocking drugs to define nonadrenergic noncholinergic (NANC) vagus nerve pathways regulating tracheal mucus secretion. In anesthetized cats, mucus glycoconjugates, radiolabeled biosynthetically with [35S]sulfate and [3H]glucose, were washed from a tracheal segment in situ and dialyzed before scintillation counting and chemical assay with periodic acid-Schiff (PAS). Without autonomic blockade, vagal stimulation (9.5 Hz, 10 V, 2-ms pulse width, 10-min duration) increased outputs of radiolabeled and PAS-reactive glycoconjugates repeatably over four stimulation periods. In other animals, vagus nerves were stimulated with administration of autonomic blockers between stimulations. The first stimulation (no blockers) increased glycoconjugate output (delta 35S = 221 +/- 43.3%, delta 3H = 58 +/- 13.8%; delta PAS = +299 +/- 82.7%). Atropine, phentolamine, and propranolol reduced these responses (delta 35S = 67 +/- 15.6%; delta 3H = 26 +/- 5.3%; delta PAS = 88 +/- 25.6%). Guanethidine did not significantly lessen them further, although delta 3H was no longer significant. Ganglion blockade with hexamethonium prevented most of the remaining response to vagal stimulation (P less than 0.05 for diminution of delta 35S and delta PAS), but small effects persisted (delta 35S = 17 +/- 5.6%; delta PAS = 20 +/- 6.8%; P less than 0.05). We conclude that the main NANC vagal pathway controlling tracheal glycoconjugate secretion runs orthodromically.

Adrenergic Antagonists↗
PubMed2006

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure.

Multiple system atrophy (MSA) and pure autonomic failure (PAF) represent distinct pathological models of autonomic failure in humans. We have investigated the neuroendocrine, behavioural and autonomic cardiovascular responses to the 35% CO2 challenge. Nine patients with MSA, nine with PAF and five control subjects received a single breath of 35% CO2. Peripheral autonomic failure (i.e., PAF) was associated with significantly lower resting noradrenaline levels. All groups demonstrated a significant pressor response to CO2. In controls, the mean pressor response was +60.2 mm Hg, which was significantly smaller in both the PAF (+26.8 mm Hg, P < 0.01) and MSA (+18.3 mm Hg, P < 0.001) patients. In addition, the onset of the response was significantly delayed in both MSA (140.2 s) and PAF (154.2 s) patients compared with controls (32.4 s, P = 0.04 and P = 0.03, respectively). Noradrenaline levels increased only in controls. Central autonomic impairment (i.e., MSA) was associated with lower cortisol release (+8.8% in MSA compared with +35.2% in control and +23.7% in PAF) and fewer somatic symptoms of emotional arousal. Both MSA and PAF exhibit marked sympathetic autonomic impairment, however, residual (albeit differing) sympathetic pathways can still maintain a partial cardiovascular response. A central autonomic lesion, however, also appears to be associated with blunting of both cortisol and emotional responses to this stress paradigm.

Aged↗
PubMedDate not supplied

[Physiology of the autonomic nervous system].

INTRODUCTION: The autonomic nervous system (ANS) is made up of a complex set of neurons and pathways that control the functioning of the different body systems within the organism. Its overall function is that of maintaining a state of homeostasis in the organism and of performing the adaptation responses when faced with changes in the external and internal environment. METHODS: The ANS is composed of visceral afferent pathways, integration centres at the brain stem, hypothalamus and cerebral cortex levels, as well as sympathetic and parasympathetic efferent pathways. The efferent pathways innerve the cardiac muscle, the smooth muscle and the exocrine and endocrine glands, while the afferent pathways are arranged in two patterns: oligosynaptic circuits, which mediate reflex adaptation responses of the visceral systems, and complex circuits, with projections to nuclei in the brain stem and the brain, where the information is collected and responses are produced that affect numerous systems. The afferent signals activate or inhibit the efferent components of the ANS by means of reflex pathways, independently of the will. These reflex circuits are also modulated by means of signals from central structures, and constitute a central autonomic neuronal network that integrates somatic, autonomic and affective responses. CONCLUSION: Dysfunctions of the ANS are possibly due to increases or decreases in autonomic control activity, which can appear because of lesions to the brain, spinal cord or peripheral nerves.

Autonomic Denervation↗
PubMed1984

Diminished bronchial reactivity to cold air in diabetic patients with autonomic neuropathy.

To investigate the role of neural pathways in the nonasthmatic response to eucapnic hyperventilation with below freezing air five diabetic patients with severe symptomatic autonomic neuropathy were studied. Their responses were compared with those shown by five diabetic patients without autonomic neuropathy and five non-diabetic controls. After bronchial provocation testing with cold air the diabetic patients with autonomic neuropathy did not show a significant fall in specific airways conductance (mean (SE) maximum percentage fall 2.0 (3)%), whereas conductance fell in the diabetic patients without neuropathy by 30.8 (2.0)% (p less than 0.001) and in the non-diabetic controls by 22.7 (4.6)% (p less than 0.02). In subjects who do not have asthma the bronchial response to cold air is mediated largely via neural mechanisms.

Adult↗
PubMed1978

Neural pathways of a cardiogenic hypertensive chemoreflex.

Excitation of a cardiac chemoreceptor with 5-hydroxytryptamine (serotonin) produces a complex autonomic reflex which includes hypertension, changes in heart rate and contractile force, and disturbances of AV conduction. This study examines the afferent and efferent neural pathways of this autonomic reflex in 60 anesthetized dogs. We used cooling and sectioning techniques in 40 of these, and in 20 others recorded afferent neurograms. The most common afferent pathways for the reflex were found in the left and right recurrent cardiac nerves. No preferential efferent routes to the heart were found, although the nature of the reflex cardiac response could be altered by specific nerve interruption. Cyproheptadine (1 mg/kg iv) regularly abolished both the reflex and the chemoreceptor afferent neural traffic, but injection of a 10 times higher concentration of serotonin (1 mg/ml) readily surmounted the blockade and restored the chemoreceptor neural traffic. Thus cyproheptadine interdicts the reflex at the site of its initiation.

Afferent Pathways↗
PubMed2003

Chromosomal integration and homologous gene targeting by replication-incompetent vectors based on the autonomous parvovirus minute virus of mice.

The molecular mechanisms responsible for random integration and gene targeting by recombinant adeno-associated virus (AAV) vectors are largely unknown, and whether vectors derived from autonomous parvoviruses transduce cells by similar pathways has not been investigated. In this report, we constructed vectors based on the autonomous parvovirus minute virus of mice (MVM) that were designed to introduce a neomycin resistance expression cassette (neo) into the X-linked human hypoxanthine phosphoribosyl transferase (HPRT) locus. High-titer, replication-incompetent MVM vector stocks were generated with a two-plasmid transfection system that preserved the wild-type characteristic of packaging only one DNA strand. Vectors with inserts in the forward or reverse orientations packaged noncoding or coding strands, respectively. In human HT-1080 cells, MVM vector random integration frequencies (neo(+) colonies) were comparable to those obtained with AAV vectors, and no difference was observed for noncoding and coding strands. HPRT gene-targeting frequencies (HPRT mutant colonies) were lower with MVM vectors, and the noncoding strand frequency was threefold greater than that of the coding strand. Random integration and gene-targeting events were confirmed by Southern blot analysis of G418- and 6-thioguanine (6TG)-resistant clones. In separate experiments, correction of an alkaline phosphatase (AP) gene by gene targeting was nine times more effective with a coding strand vector. The data suggest that single-stranded parvoviral vector genomes are substrates for gene targeting and possibly for random integration as well.

Animals↗
PubMed2002

Dissociated autonomic regulation during stress and physical complaints.

OBJECTIVE: In order to evaluate the relevance of individual differences in the regulation of autonomic subsystems to psychosomatic processes, reactivity of the autonomic nervous system to an emotional stressor was related to the occurrence of physical complaints. In contrast to most other studies, the measures were related to the degree of actually experienced stress. METHODS: In a large sample (n=111), electrodermal activity (EDA) and heart rate variability (HRV) were obtained at rest and during emotional stress. Physical complaints were assessed by a standardized symptom checklist providing subscales for different physiological systems. RESULTS: Subjects who were actually stressed by the stress induction procedure but showed only weak reactivity of EDA, and subjects who were only slightly stressed but showed a marked EDA response reported a high amount of gastrointestinal complaints. A greater decrease of high-frequency HRV from the rest to the stress condition was associated with reports of relatively more cardiovascular complaints. CONCLUSION: Findings indicate that the link between regulation of EDA and gastrointestinal functions has to be localized in higher brain structures and support the hypothesis that minor autonomic dysregulation may represent one pathway linking negative affect and the development of physical disorders.

Adolescent↗
PubMed1979

Defective cardiovascular reflexes and supersensitivity to sympathomimetic drugs in autonomic failure.

In 10 patients with chronic autonomic failure the clinical features and cardiovascular reflexes were correlated with the pressor responses to intravenous noradrenaline and tyramine. In all patients there was an exaggerated response to noradrenaline but a normal or only mildly exaggerated response to tyramine. Patients with lack of sinus arrhythmia and by implication baroreceptor reflex loss had greater responsiveness to pressor drugs than patients with preservation of this reflex. The responses to tyramine infusions imply that there must be sufficient noradrenaline released at defective sympathetic endings for a pressor response to occur. However, the lack of rise of plasma noradrenaline following tyramine, except in the patients with pure autonomic failure, clearly separates these responses from those of normal subjects. These results can be explained by the presence of lesions of both central and peripheral sympathetic pathways in patients with chronic autonomic failure and multiple system atrophy or Parkinsonism. The peripheral lesion, which is incomplete, may consist of replication of the receptors so causing supersensitivity with a duration of response that is little prolonged. The peripheral defect in the two patients with pure autonomic failure was found to be more complex and the prolonged response in one of these patients suggests the possibility of defective re-uptake or metabolism of noradrenaline. Clearly further study of the defects of sympathetic endings is required, including the use of other techniques such as catecholamine fluorescence. The extreme supersensitive responses underline the need for blood pressure monitoring during pressor drug studies prior to treatment, if the hazards of recumbent hypertension are to be avoided.

Adult↗
PubMed1993

A monosynaptic pathway from an identified vasomotor centre in the medial prefrontal cortex to an autonomic area in the thoracic spinal cord.

Chemical microstimulation (1 mM L-glutamate or 25 mM KCl) of the medial prefrontal cortex of anaesthetized rats produced falls in systolic and diastolic blood pressure of similar magnitude, without a change in heart rate. Application of the lectin Phaseolus vulgaris leucoagglutinin by iontophoresis from an adjacent barrel of the same micropipette revealed a direct projection to the central autonomic area of the thoracic spinal cord from this vasomotor area, which is equivalent to the region called prelimbic cortex by Krettek and Price [J. comp. Neurol. (1977) 171, 157-192] or Cg3 by Paxinos and Watson [The Rat Brain in Stereotaxic Coordinates (1986)]. Labelled axons descended in the dorsal corticospinal tract in the cervical spinal cord, where they displayed a few varicosities. In the thoracic spinal cord, labelled fibres occurred bilaterally in the gray matter, predominantly in the central autonomic area, where they displayed many varicosities. Electron microscope studies revealed that the anterogradely labelled varicosities in the central autonomic area were vesicle-filled boutons that formed asymmetric synaptic contacts. The synaptic targets were small dendrites or dendritic protrusions that were characterized by a high incidence of multivesicular bodies and coated vesicles. We conclude that a monosynaptic pathway that originates from a physiologically-defined vasomotor area in the medial prefrontal cortex terminates on a characteristic type of neuron in the central autonomic area of the thoracic spinal cord.

Animals↗
PubMed2003

Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans.

Ageing is a fundamental, unsolved mystery in biology. DAF-16, a FOXO-family transcription factor, influences the rate of ageing of Caenorhabditis elegans in response to insulin/insulin-like growth factor 1 (IGF-I) signalling. Using DNA microarray analysis, we have found that DAF-16 affects expression of a set of genes during early adulthood, the time at which this pathway is known to control ageing. Here we find that many of these genes influence the ageing process. The insulin/IGF-I pathway functions cell non-autonomously to regulate lifespan, and our findings suggest that it signals other cells, at least in part, by feedback regulation of an insulin/IGF-I homologue. Furthermore, our findings suggest that the insulin/IGF-I pathway ultimately exerts its effect on lifespan by upregulating a wide variety of genes, including cellular stress-response, antimicrobial and metabolic genes, and by downregulating specific life-shortening genes.

Aging↗