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PubMed1988

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear.

The purpose of the present study was to determine whether lesions of areas projected to by the central amygdaloid nucleus (ACE) would disrupt the classical conditioning of autonomic and/or behavioral emotional responses. The areas studied included 3 projection targets of the ACE: the lateral hypothalamic area (LH), midbrain central gray (CG) region, and bed nucleus of the stria terminalis (BNST). Lesions were made either electrolytically or by microinjection of ibotenic acid, which destroys local neurons without interrupting fibers of passage. Two weeks later, the animals were classically conditioned by pairing an acoustic stimulus with footshock. The next day, conditioned changes in autonomic activity (increases in arterial pressure) and emotional behavior ("freezing," or the arrest of somatomotor activity) evoked by the acoustic conditioned stimulus (CS) were measured during extinction trials. Electrolytic and ibotenic acid lesions of the LH interfered with the conditioned arterial pressure response, but did not affect conditioned freezing. Electrolytic lesions of the rostral CG disrupted conditioned freezing but not conditioned changes in arterial pressure. Ibotenic acid injected into the rostral CG reduced neither the arterial pressure nor the freezing response. Injection of ibotenic acid in the caudal CG, like electrolytic lesions of the rostral CG, disrupted the freezing, but not the arterial pressure response. Injection of ibotenic acid into the BNST had no effect on either response. These data demonstrate that neurons in the LH are involved in the autonomic, but not the behavioral, conditioned response pathway, whereas neurons in the caudal CG are involved in the behavioral, but not the autonomic, pathway. Different efferent projections of the central amygdala thus appear to mediate the behavioral and autonomic concomitants of conditioned fear.

Amygdala↗
PubMed1996

Vestibular nucleus projections to the parabrachial nucleus in rabbits: implications for vestibular influences on the autonomic nervous system.

Acute vestibular dysfunction and motion sickness are characterized by autonomic effects such as pallor, nausea, and vomiting. Previous anatomic and physiologic studies suggest that one potential mediator of these effects may be light, direct vestibular nuclear projections to the nucleus tractus solitarius and the dorsal motor nucleus of the vagus nerve. This study presents evidence for relatively dense, direct projections from the vestibular nuclei to the parabrachial nucleus. Male albino rabbits received injections of Phaseolus vulgaris leucoagglutinin into the vestibular nuclei. The tracer was visualized immunocytochemically with standard techniques. Anterogradely labeled axons were traced bilaterally from the vestibular nuclei to the parabrachial nuclear complex, where they terminated around somata in the Kölliker-Fuse nucleus, external medial parabrachial nucleus, medial parabrachial nucleus, and lateral parabrachial nucleus. Less dense terminations were observed in the ventrolateral aspect of the medullary reticular formation, the subtrigeminal nucleus, lateral tegmental field, and nucleus ambiguus. These findings have several important implications. First, they suggest that vestibular input converges directly at brain stem levels with visceral sensory input in both nucleus of the solitary tract and the parabrachial complex. Second, they suggest that vestibular input influences brain stem autonomic outflow via two parallel pathways: (1) direct, light projections to the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve, and ventrolateral medullary reticular formation; and (2) denser projection to regions of the parabrachial nucleus that project to these brain stem regions. Finally, since the parabrachial nucleus regions that receive vestibular input also project to the hypothalamus and the insular and infralimbic prefrontal cortex, the parabrachial nucleus may serve as an important relay and integrative structure for the cognitive impairment and vegetative symptoms associated with motion sickness, vestibular dysfunction, and responses to altered gravitational environments.

Afferent Pathways↗
PubMed2003

Heart rate variability in athletes.

This review examines the influence on heart rate variability (HRV) indices in athletes from training status, different types of exercise training, sex and ageing, presented from both cross-sectional and longitudinal studies. The predictability of HRV in over-training, athletic condition and athletic performance is also included. Finally, some recommendations concerning the application of HRV methods in athletes are made.The cardiovascular system is mostly controlled by autonomic regulation through the activity of sympathetic and parasympathetic pathways of the autonomic nervous system. Analysis of HRV permits insight in this control mechanism. It can easily be determined from ECG recordings, resulting in time series (RR-intervals) that are usually analysed in time and frequency domains. As a first approach, it can be assumed that power in different frequency bands corresponds to activity of sympathetic (0.04-0.15 Hz) and parasympathetic (0.15-0.4 Hz) nerves. However, other mechanisms (and feedback loops) are also at work, especially in the low frequency band. During dynamic exercise, it is generally assumed that heart rate increases due to both a parasympathetic withdrawal and an augmented sympathetic activity. However, because some authors disagree with the former statement and the fact that during exercise there is also a technical problem related to the non-stationary signals, a critical look at interpretation of results is needed. It is strongly suggested that, when presenting reports on HRV studies related to exercise physiology in general or concerned with athletes, a detailed description should be provided on analysis methods, as well as concerning population, and training schedule, intensity and duration. Most studies concern relatively small numbers of study participants, diminishing the power of statistics. Therefore, multicentre studies would be preferable. In order to further develop this fascinating research field, we advocate prospective, randomised, controlled, long-term studies using validated measurement methods. Finally, there is a strong need for basic research on the nature of the control and regulating mechanism exerted by the autonomic nervous system on cardiovascular function in athletes, preferably with a multidisciplinary approach between cardiologists, exercise physiologists, pulmonary physiologists, coaches and biomedical engineers.

Autonomic Nervous System↗
PubMed1984

Mechanoreceptor pathways from the distal colon to the autonomic nervous system in the guinea-pig.

Electrophysiological and histological techniques were used to trace sensory pathways for stretch mechanoreceptor fibres from the distal colon to dorsal root ganglia. Extracellular and intracellular recording techniques revealed sensory pathways for mechanoreceptors to the prevertebral sympathetic ganglia but no further centrally. Histological studies involving the retrograde transport of horseradish peroxidase revealed sensory pathways from the distal colon to the spinal cord, mainly to the level of the second lumbar vertebra. Few (less than 2000) fibres were involved; their perikarya were small (ca. 25 micron). Sensory perikarya in spinal ganglia in the guinea-pig could be categorized into two populations, F and H cells, after a previously defined nomenclature for murine spinal ganglion cells. F and H cells were distinguished initially by their times to decay by 50% of the action potential. H cells took three times as long to repolarize. F and H cells were distinguished further by their electrical properties including membrane potential, input resistance and amplitude and duration of the after-potential following the action potential. Both F and H cells showed unusual time-dependent rectification following either depolarizing or hyperpolarizing current pulses. Threshold currents to show rectification were different for F and H cells. When taken in conjunction with conduction velocities, the electrophysiological evidence may assist in identifying sensory neurones. For example, H cells appeared to have slow conducting (C fibre) axons. From the lack of electrophysiological evidence and limited histological support for major central sensory pathways, it is concluded that stretch mechanoreceptor information from the colon of the guinea-pig is referred mainly to the prevertebral ganglia with minimal involvement of the spinal cord.

Action Potentials↗
PubMed2002

Maturation of postsynaptic nicotinic structures on autonomic neurons requires innervation but not cholinergic transmission.

Postsynaptic development at the neuromuscular junction depends on nicotinic transmission and secreted components from the presynaptic motor nerve terminal. Similarly, secreted components and synaptic activity are both thought to guide development of glutamatergic synapses in the CNS. Nicotinic synapses on chick ciliary neurons are structurally complex: a large presynaptic calyx engulfs the postsynaptic neuron and overlays a series of discrete mats of receptor-rich somatic spines tightly interwoven and folded against the soma. We used fluorescence imaging of alpha 7-containing nicotinic receptors and the spine constituent drebrin to monitor postsynaptic development. The results show that surgical disruption of the preganglionic input or removal of the ganglionic synaptic target tissue after synapses form in the ganglion does not disrupt the receptor-rich spine mats. Similarly, removal of the target tissue even prior to synapse formation in the ganglion does not prevent subsequent formation of the receptor clusters and associated spine constituents. Postsynaptic development is arrested, however, if normal innervation is prevented by ablating the preganglionic neurons prior to synapse formation. In this case the neurons express reduced levels of nicotinic receptors and cytoskeletal components and organize them only into early-stage clusters. Even low levels of residual innervation, however, can restore much of the normal postsynaptic receptor patterns. Chronic pharmacological blockade of cholinergic synaptic activity fails to replicate the effects of ablating the preganglionic nucleus. The results indicate that ciliary neurons are programmed to express postsynaptic components and can initiate clustering of alpha 7-containing receptors but need presynaptic guidance for maturation of the postsynaptic structure.

Acetylcholine↗
PubMed1998

Effect of sorbitol dehydrogenase inhibition on experimental diabetic autonomic neuropathy.

The polyol pathway and its dependent biochemical pathways are thought to play a role in the pathogenesis of diabetic neuropathy. We have developed an animal model of diabetic autonomic neuropathy characterized by neuroaxonal dystrophy involving ileal mesenteric nerves and prevertebral sympathetic superior mesenteric ganglia (SMG) in chronic streptozocin-diabetic rats. Our previous studies have shown a salutary effect of aldose reductase inhibitors on experimental autonomic neuropathy, suggesting a role for the polyol pathway in its pathogenesis. In the current studies we have examined the effect of the sorbitol dehydrogenase inhibitor (SDI) CP-166,572, which interrupts the conversion of sorbitol to fructose (and reactions dependent on the second step of the polyol pathway) resulting in markedly increased levels of sorbitol in peripheral nerve. Fourteen weeks of treatment with CP-166,572 resulted in a dramatically increased frequency of neuroaxonal dystrophy in ileal mesenteric nerves and SMG. Although lesions developed prematurely and in greater numbers in SDI-treated diabetics than untreated diabetics did, their anatomic distribution and ultrastructural appearance were identical to that previously reported in long-term untreated diabetics. CP-166,572 treatment did not produce neuroaxonal dystrophy in control animals despite the fact that sciatic nerve sorbitol levels were markedly increased, reaching the same levels as untreated diabetic animals. Treatment of diabetic rats for 14 weeks with the aldose reductase inhibitor zopolrestat resulted in a significant decrease in the frequency of neuroaxonal dystrophy compared with untreated diabetics.

Animals↗
PubMed2002

The VERNALIZATION INDEPENDENCE 4 gene encodes a novel regulator of FLOWERING LOCUS C.

The late-flowering, vernalization-responsive habit of many Arabidopsis ecotypes is mediated predominantly through repression of the floral programme by the FLOWERING LOCUS C (FLC) gene. To better understand this repressive mechanism, we have taken a genetic approach to identify novel genes that positively regulate FLC expression. We identified recessive mutations in a gene designated VERNALIZATION INDEPENDENCE 4 (VIP4), that confer early flowering and loss of FLC expression in the absence of cold. We cloned the VIP4 gene and found that it encodes a highly hydrophilic protein with similarity to proteins from yeasts, Drosophila, and Caenorhabditis elegans. Consistent with a proposed role as a direct activator of FLC, VIP4 is expressed throughout the plant in a pattern similar to that of FLC. However, unlike FLC, VIP4 RNA expression is not down-regulated in vernalized plants, suggesting that VIP4 is probably not sufficient to activate FLC, and that VIP4 is probably not directly involved in a vernalization mechanism. Epistasis analysis suggests that VIP4 could act in a separate pathway from previously identified FLC regulators, including FRIGIDA and the autonomous flowering promotion pathway gene LUMINIDEPENDENS. Mutants lacking detectable VIP4 expression flower earlier than FLC null mutants, suggesting that VIP4 regulates flowering-time genes in addition to FLC. Floral morphology is also disrupted in vip4 mutants; thus, VIP4 has multiple roles in development.

Acclimatization↗
PubMed2003

The synergistic activation of FLOWERING LOCUS C by FRIGIDA and a new flowering gene AERIAL ROSETTE 1 underlies a novel morphology in Arabidopsis.

The genetic changes underlying the diversification of plant forms represent a key question in understanding plant macroevolution. To understand the mechanisms leading to novel plant morphologies we investigated the Sy-0 ecotype of Arabidopsis that forms an enlarged basal rosette of leaves, develops aerial rosettes in the axils of cauline leaves, and exhibits inflorescence and floral reversion. Here we show that this heterochronic shift in reproductive development of all shoot meristems requires interaction between dominant alleles at AERIAL ROSETTE 1 (ART1), FRIGIDA (FRI), and FLOWERING LOCUS C (FLC) loci. ART1 is a new flowering gene that maps 14 cM proximal to FLC on chromosome V. ART1 activates FLC expression through a novel flowering pathway that is independent of FRI and independent of the autonomous and vernalization pathways. Synergistic activation of the floral repressor FLC by ART1 and FRI is required for delayed onset of reproductive development of all shoot meristems, leading to the Sy-0 phenotype. These results demonstrate that modulation in flowering-time genes is one of the mechanisms leading to morphological novelties.

Arabidopsis↗
PubMed1981

Central noradrenergic pathways for the integration of hypothalamic neuroendocrine and autonomic responses.

Immunohistochemical and axonal transport methods were used to describe the organization of a series of central noradrenergic pathways that interrelate the nucleus of the solitary tract, which receives primary visceral sensory information, and the paraventricular and supraoptic nuclei of the hypothalamus, which participate in autonomic and neuroendocrine modes of homeostatic control. The results indicate that pathways arising from noradrenergic cells in the dorsal vagal complex, the ventrolateral medulla, and the locus coeruleus end in specific subdivisions of the paraventricular and supraoptic nuclei which are involved in the regulation of responses from the pituitary gland and from both divisions of the autonomic nervous system. This circuitry may play an important role in the integration of hypothalamic responses to visceral stimuli.

Animals↗
PubMed1986

Cortical projections to the nucleus of the tractus solitarius: an HRP study in the cat.

Recent evidence suggests that autonomic reflexes involving sensations such as olfaction and gustation may be cortically mediated via centripetal pathways to brainstem autonomic centers. A study was therefore undertaken to elucidate one of these pathways in greater detail. Lectin conjugated horseradish peroxidase was injected into the nucleus tractus solitarius. Following standard light microscopic histochemical procedures to reveal horseradish peroxidase activity, the distribution of retrogradely labeled neurons in the cortex was recorded. Retrogradely labeled somata were seen bilaterally in layer five of the orbital gyrus, anterior insular cortex and infralimbic cortex. In other cats, the same tracer was injected into the orbital gyrus or anterior insular cortex. Bilateral anterograde labeling was seen in various subnuclei throughout the rostrocaudal extent of the nucleus tractus solitarius, but was heaviest in rostral regions of the nucleus. Labeling was also seen bilaterally in the spinal trigeminal nucleus. The projection to the nucleus tractus solitarius could allow for cortical modulation of gustatory and visceral information which is conveyed to the brainstem via the facial, glossopharyngeal and vagus nerves.

Animals↗
PubMedDate not supplied

Central neurohypophyseal peptide pathways: interactions with endocrine and other autonomic functions.

Electrophysiological and pharmacological studies have been carried out in rats and rabbits to attempt to identify possible functional roles for neurohypophyseal peptides in brain. In anesthetized rats, single unit recordings and antidromic activation criteria were utilized to identify projections of the paraventricular nucleus (PVN) to neurohypophysis and to extrahypothalamic areas (amygdala or nucleus tractus solitarius). None of the cells tested innervated more than one of these areas and, when tested for their responses to haemorrhage, increased body osmolarity, or suckling of pups, only the osmotic stimulus caused increased activity in some cells projecting to amygdala or nucleus tractus solitarius. Indirect evidence as well as direct measurement by radioimmunoassay of arginine vasopressin (AVP) in brain perfusates revealed probable central release of AVP in response to stimuli known to activate pituitary secretion of this peptide. These observations raise the possibility that certain brain and pituitary peptidergic systems may function in a co-ordinated manner.

Animals↗
PubMed2006

Effects of spinal cord injury on synaptic inputs to sympathetic preganglionic neurons.

Spinal cord injuries often lead to disorders in the control of autonomic function, including problems with blood pressure regulation, voiding, defecation and reproduction. The root cause of all these problems is the destruction of brain pathways that control spinal autonomic neurons lying caudal to the lesion. Changes induced by spinal cord injuries have been most extensively studied in sympathetic preganglionic neurons, cholinergic autonomic neurons with cell bodies in the lateral horn of thoracic and upper lumbar spinal cord that are the sources of sympathetic outflow. After an injury, sympathetic preganglionic neurons in mid-thoracic cord show plastic changes in their morphology. There is also extensive loss of synaptic input from the brain, leaving these neurons profoundly denervated in the acute phase of injury. Our recent studies on sympathetic preganglionic neurons in lower thoracic and upper lumbar cord that regulate the pelvic viscera suggest that these neurons are not so severely affected by spinal cord injury. Spinal interneurons appear to contribute most of the synaptic input to these neurons so that injury does not result in extensive denervation. Since intraspinal circuitry remains intact after injury, drug treatments targeting these neurons should help to normalize sympathetically mediated pelvic visceral reflexes. Furthermore, sympathetic pelvic visceral control may be more easily restored after an injury because it is less dependent on the re-establishment of direct synaptic input from regrowing brain axons.

Animals↗
PubMed2004

Control of T cell viability.

The factors affecting T cell viability vary depending on the type and status of the T cell involved. Naive T cells die via a Bcl-2/Bim dependent route. Their deaths are prevented in animals by IL-7 and contact with MHC. Activated T cells die in many different ways. Among these is a pathway involving signals that come from outside the T cell and affect it via surface receptors such as Fas. Activated T cells also die through a pathway driven by signals generated within the T cell itself, a cell autonomous route. This pathway involves members of the Bcl-2 family, in particular Bcl-2, Bcl-xl, Bim, and probably Bak. The viability of CD8+ and CD4+ memory T cells is controlled in different ways. CD8+ memory T cells are maintained by IL-15 and IL-7. The control of CD4+ memory T cells is more mysterious, with roles reported for IL-7 and/or contact via the TCR.

Animals↗
PubMed1999

The C. elegans gene lin-36 acts cell autonomously in the lin-35 Rb pathway.

The Caenorhabditis elegans gene lin-36 acts to antagonize Ras-mediated vulval induction in a pathway that includes genes with products similar to the mammalian retinoblastoma (Rb) protein and the Rb-binding protein p48. We report that lin-36 encodes a novel protein of 962 amino acids. We demonstrate that lin-36 functions in and is expressed in the vulval precursor cells, establishing that the lin-36 pathway is involved in intercellular signaling. We also report that the lin-36 pathway and/or another pathway that is functionally redundant with the lin-36 pathway antagonize a ligand-independent activity of the receptor tyrosine kinase/Ras vulval induction pathway.

Alleles↗
PubMed2006

[Signal pathways of flowering time regulation in plant].

The transition from vegetative to reproductive growth is the major developmental switch in plant life cycle. The timing of flower initiation is critical for a successful reproduction. Flowering is regulated by endogenous and environmental signals. Molecular genetic studies on Arabidopsis thaliana revealed four major flowering pathways: the photoperiod, the vernalization, the autonomous, and the gibberellin pathways. This paper reviews some research progresses in control of flowering time in Arabidopsis.

Arabidopsis↗
PubMed1996

[Orthostatic hypotension and postprandial hypotension].

Both orthostatic hypotension (OH) and postprandial hypotension (PPH) may result from lesions in any part of the baroreflex arc, which comprises central autonomic network, afferent pathways, efferent pathways, and neuro-vascular junction. Nonetheless, most attention has been centered to the efferent pathways to date. In the present report, I discussed on the contribution of neuro-vascular junction and central autonomic network to the development of OH and PPH. I also referred to the essential difference in pathophysiology between OH and PPH. (1) Difference between OH and PPH: Essential difference is in triggers inducing the initial blood pressure fall. The trigger in OH is gravity, while that in PPH is abnormal release of vasodilative gastroenteric peptides; the former is equally delivered to all persons living on earth, but the latter varies from person to person. (2) Neuro-vascular junction: Previous studies, in which catecholamine drip infusion tests were carried out on patients with OH, suggested that all of cardiovascular alpha-, beta 1, and beta 2 adrenoceptors gain denervation supersensitivity in OH. This view does, however, underestimate the blood pressure buffering effect of baroreflex. Because long-standing alteration in blood pressure by drip infusion of catecholamine necessarily provokes baroreflex, it is reasonable that augmented cardiovascular responses in OH are largely due to baroreflex failure. We performed bolus infusion tests of noradrenaline and isoprenaline on patients with OH, and found that alpha-adrenoceptor-mediated rise in blood pressure was comparable to control, beta 1-mediated increase in heart rate was blunted, and beta 2-mediated fall in blood pressure was enhanced in OH. It is, therefore, likely that beta 2-mediated vasodilation exceeds alpha-mediated vasoconstriction in OH. In such condition, noradrenaline may produce a paradoxical hypotensive effect, which contributes to the development of OH or PPH. (3) Central autonomic network (CAN): Clinical symptoms due to lesions within CAN are usually not manifested when the efferent sympathetic pathways are highly impaired, as in multiple system atrophy. Some variants of OH and PPH may result from lesions within CAN, however. For example, we have experienced a case of sympathotonic OH associated with herpes simplex encephalitis, in which the efferent pathways do not seem to be involved.

Eating↗