PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Neural Pathways”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 505 records · Page 28Linked to original sources
PubMed2003

Acute intracerebroventricular insulin microinjection after nitric oxide synthase inhibition of renal sodium handling in rats.

The role of the central nervous system (CNS) in the control of hydrosaline homeostasis has been strikingly demonstrated by several studies. Recent and growing evidence suggests that insulin or a nonapeptide-derived from the C-terminus of the insulin beta-chain may influence many brain functions. However, there is little information on the insulin-activated neural pathways regulating urinary sodium excretion. Also, we examined the influence of nitric oxide synthase activity by chronic oral administration of N(omega)-nitro-l-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, after previous i.c.v. administration of insulin to unanesthetized, unrestrained rats that were randomly assigned to one of seven separated groups: (a) i.c.v. 0.15 M NaCl-injected (n = 11) and i.c.v. 126 ng (n = 11) insulin-injected rats; (b) i.c.v. insulin-injected in systemic L-NAME-treated (n = 10) and vehicle-treated insulin-injected rats (n = 10); and (c) subcutaneously (SC) insulin-injected rats (n = 5). We showed that centrally administered insulin produced increase in the urinary output of sodium (from 0.15 M NaCl: 855.6 +/- 85.1 Delta%.min(-1) to 126 ng insulin: 2055 +/- 310.6 Delta%.min(-1)) and potassium (126 ng: from 0.15 M NaCl: 460.4 +/- 100 Delta%.min(-1) to 126 ng insulin: 669 +/- 60.8 Delta%.min(-1)). The urinary sodium excretion response to i.c.v. 126 ng insulin microinjection was significantly abolished by previous systemic treatment of animals with 15 mg/kg/day L-NAME (from vehicle + 126 ng insulin: 1935 +/- 258.3 Delta%. min(-1) to L-NAME + 126 ng insulin: 582.3 +/- 69.6 Delta%. min(-1)). In addition, we showed that insulin-induced natriuresis occurred by increasing post-proximal tubule sodium rejection (FEPP(Na)), despite an unchanged glomerular filtration rate (C(Cr)). The current data suggests the novel concept that CNS NO-dependent neural pathways may play an instrumental role on efferent insulin-sensitive nerve activity from periventricular region. Speculatively, it seems interesting to suggest that perhaps one of the efferent signals triggered by insulin in the CNS may be nitrergic in nature, and that defects in this efferent signal could result in insulin central resistance, inability of renal tubules to handle the hydro electrolyte balance and hypertension.

Animals↗
PubMed2003

Effect of 5-hydroxytryptamine on duodenal mucosal bicarbonate secretion in mice.

BACKGROUND & AIMS: 5-hydroxytryptamine (5-HT) is an important neurotransmitter and intercellular messenger that modulates many gastrointestinal functions. Because little is known about the role of 5-HT in the regulation of duodenal bicarbonate secretion, we examined the role of 5-HT on duodenal bicarbonate secretion and define neural pathways involved in the actions of 5-HT. METHODS: Duodenal mucosa from National Institutes of Health Swiss mice was stripped of seromuscular layers and mounted in Ussing chambers. The effect of 5-HT on duodenal bicarbonate secretion was determined by the pH stat technique. Acetylcholine (ACh) release from duodenal mucosa was assessed by preincubating the tissue with [(3)H] choline and measuring 5-HT-evoked release of tritium. RESULTS: 5-HT added to the serosal bath markedly stimulated duodenal bicarbonate secretion and short circuit current (Isc) in a dose-dependent manner (10(-7) mol/L to 10(-3) mol/L; P < 0.0001), whereas mucosally added 5-HT was without effect. 5-HT-stimulated bicarbonate secretion was independent of luminal Cl(-). Pretreatment with tetrodotoxin (TTX) (10(-6) mol/L) or atropine (10(-5) mol/L) markedly reduced 5-HT-stimulated duodenal bicarbonate secretion (by 60% and 65%, respectively; P < 0.001) and Isc (by 45% and 27%, respectively; P < 0.001 and P < 0.05). Pretreatment with N(omega)-nitro-l-arginine methyl ester (l-NAME) (10(-3) mol/L), propranolol (10(-5) mol/L), or phentolamine (10(-5) mol/L) did not significantly alter 5-HT-stimulated duodenal mucosal bicarbonate secretion or Isc. 5-HT concentration-dependently evoked ACh release from duodenal mucosal preparations (P < 0.0001). TTX markedly inhibited 5-HT-evoked ACh release (P < 0.001). CONCLUSIONS: 5-HT is a potent activator of duodenal mucosal bicarbonate secretion in mice. Duodenal bicarbonate secretion induced by 5-HT in vitro occurs principally via a cholinergic neural pathway.

Acetylcholine↗
PubMed1998

Reach to grasp: the response to a simultaneous perturbation of object position and size.

This study assessed the reach to grasp movement and its adaptive response to a simultaneous perturbation of object location and size. The aim was to clarify the means by which integration between the neural pathways modulating transport and manipulation is achieved. Participants (n = 11) were required to reach 30 cm to grasp a central illuminated cylinder of either small (0.7 cm) or large (8 cm) diameter. For a small percentage of trials (20/100) a visual perturbation was introduced unexpectedly at the onset of the reaching action. This consisted of a shift of illumination from the central cylinder to a cylinder of differing diameter (large in session A; small in session B) that was positioned 20 degrees to the left (n = 10 trials) or to the right (n = 10) of the central cylinder. The subject was required to grasp the newly illuminated cylinder. Movement duration for these "double" (position and size) perturbed trials was much longer than those of control trials to the central cylinder (session A: by an average of 250 ms; session B: 180 ms), and the increased values were much greater than those reported previously in "single" perturbation studies where either size or location of the object was perturbed. Initial signs of a response to the "double" perturbation were seen almost simultaneously in the transport parameter of peak arm deceleration and in the manipulation parameter of maximum grip aperture, but these changes were not evident until more than 400 ms after movement onset, a response onset much later than that found in "single" perturbation studies. It is proposed that the visual change resultant from the double perturbation activates integration centres that at first gate the flow of information to the parallel channels of transport and manipulation. Following processing of this information, these centres act to instigate a synchronised and coordinated response in both components. These results add support to the existence of neural centres dedicated to the integration of parallel neural pathways, and which exercise flexibility in the degree to which these components are "coupled" functionally.

Adaptation, Physiological↗
PubMed1995

Biochemical actions of chronic ethanol exposure in the mesolimbic dopamine system.

In previous studies, we have demonstrated that chronic administration of morphine or cocaine produces some common biochemical adaptations in the ventral tegmental area (VTA) and nucleus accumbens (NAc), components of the mesolimbic dopamine system implicated in the reinforcing actions of these and other drugs of abuse. Since this neural pathway is also implicated in the reinforcing actions of ethanol, it was of interest to determine whether chronic ethanol exposure results in similar biochemical adaptations. Indeed, as seen for chronic morphine and cocaine treatments, we show here that chronic ethanol treatment increased levels of tyrosine hydroxylase and glial fibrillary acidic protein immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA. Also like morphine and cocaine, ethanol increases levels of cyclic AMP-dependent protein kinase activity in the NAc. These actions of ethanol required long-term exposure to the drug, and were in most cases not seen in the substantia nigra or caudateputamen, components of the nigrostriatal dopamine system studied for comparison. Altered levels of tyrosine hydroxylase in catecholaminergic cells frequently reflect altered states of activation of the cells. Moreover, increasing evidence indicates that ethanol produces many of its acute effects on the brain by regulating NMDA glutamate and GABAA receptors. We therefore examined the influence of chronic ethanol treatment on levels of expression of specific glutamate and GABA receptor subunits in the VTA. It was found that long-term, but not short-term, ethanol exposure increased levels of immunoreactivity of the NMDAR1 subunit, an obligatory component of NMDA glutamate receptors, and of the GluR1 subunit, a component of many AMPA glutamate receptors; but at the same time, long-term ethanol exposure decreased immunoreactivity levels of the alpha 1 subunit of the GABAA receptor complex. These changes are consistent with an increased state of activation of VTA neurons inferred from the observed increase in tyrosine hydroxylase (TH) expression. These results demonstrate that chronic ethanol exposure results in several biochemical adaptations in the mesolimbic dopamine system, which may underlie prominent changes in the structural and functional properties of this neural pathway related to alcohol abuse and alcoholism.

Adenylyl Cyclases↗
PubMed2004

Comparison between the influence of the systemic and central injection of alcohol on Leydig cell activity.

BACKGROUND: Systemic alcohol exposure lowers plasma testosterone (T) levels in adult males, but the relative role of impaired luteinizing hormone (LH)-releasing hormone synthesis and decreased pituitary LH release versus that of a direct ability of circulating alcohol to inhibit testicular steroidogenesis remains poorly understood. We had reported preliminary evidence that alcohol might stimulate a pituitary-independent, neural pathway between the hypothalamus and the testes whose activation blunts T secretion in response to human chorionic gonadotropin (hCG). The present work was done to further investigate the influence of alcohol on this pathway by comparing the effect of the intragastric (i.g.) and intracerebroventricular (i.c.v.) injection of alcohol on the T response to hCG, to probe the role of LH and corticotropin-releasing factor (CRF) in both models, and to examine potential changes in levels of the cholesterol transfer protein steroidogenic acute regulatory (StAR) protein. METHODS: Male Sprague Dawley rats were implanted with chronic i.c.v., i.g., and/or intravenous cannulae that allowed drug delivery and blood sampling in nonanesthetized, undisturbed animals. T blood levels were measured by radioimmunoassay. The role of LH and of hormones of the hypothalamic-pituitary-adrenal axis such as adrenocorticotropic hormone and corticosterone was investigated in rats pretreated with an LH-releasing hormone antagonist or CRF antibodies. The potential presence of neuronal damage was assessed by Fluoro-Jade methodology. StAR protein levels were measured by Western blot in Leydig cells isolated from rats injected with the vehicle or alcohol. RESULTS: Although it was not accompanied by measurable blood alcohol levels, i.c.v. administered alcohol, at a dose (5 microl of 200 proof, 86 microM) that did not cause neuronal damage and did not lead to detectable levels of the drug in the cerebrospinal fluid of the fourth ventricle of the brain, significantly blunted hCG-induced T release. The ig injection of alcohol, which in contrast induced significant increases in blood alcohol levels, also significantly interfered with the ability of hCG to induce T release. This effect was comparable in 40- and 65-day-old rats. Neither prior blockade of LH-releasing hormone receptors with a potent LH-releasing hormone antagonist nor immunoneutralization of endogenous CRF altered the inhibitory effect of alcohol injected i.c.v. or i.g. on T secretion. Preliminary results suggested that testicular levels of StAR protein may be slightly decreased by both alcohol regimens. CONCLUSIONS: Collectively, our results indicate that alcohol can act within the brain to influence testicular activity independently of LH, independently of hormones of the hypothalamic-pituitary-adrenal axis, and/or independently of the presence of the drug in the circulation. Our present working hypothesis is that the i.c.v. injection of alcohol stimulates an inhibitory neural pathway that connects the hypothalamus to the testes.

Animals↗
PubMed1980

Fibronectin in early avian embryos: synthesis and distribution along the migration pathways of neural crest cells.

Immunoperoxidase labelling for fibronectin (FN) in chick embryos showed FN-positive basement membranes surrounding the neural crest cell population prior to crest-cell migration. At cranial levels, crest cells migrated laterally into a large cell-free space. Initially they moved as a tongue of cells contacting the FN-positive basement membrane of the ectoderm but later the crest cell population expanded into space further from the ectoderm, until eventually the entire cranial cell-free space was occupied by mesenchyme cells. This was accompanied by the appearance of FN among the crest cells. At trunk levels, crest cells entered a relatively small space already containing FN-positive extracellular material. At later stages the migration of trunk crest cells broadly matched the distribution of FN. In vitro, chick and quail embryo ectoderm, endoderm, somites, notochord and neural tube synthesized and organized fibrous FN-matrices, as shown by immunofluorescence. Ectoderm and endoderm deposited this matrix only on the substrate face. The FN content of endoderm and neural tube matrices was transient, the immunofluorescence intensity declining after 1-2 days in culture. Some crest cells of cranial and sacral axial levels synthesized FN. Our data suggests that these were the earliest crest cells to migrate from these levels. This ability may be the first expression of mesenchymal differentiation in these crest cells, and in vivo enable them to occupy a large space. Almost all crest cells from cervico-lumbar axial levels were unable to synthesize FN. In vivo, this inability may magnify the response of these crest cells to FN provided by the neighbouring embryonic tissues.

Animals↗
PubMed2003

Peroxisome proliferator-activated receptor gamma coactivator-1-dependent uncoupling protein-2 expression in pancreatic islets of rats: a novel pathway for neural control of insulin secretion.

AIMS/HYPOTHESIS: Sympathetic inputs inhibit insulin secretion through alpha2-adrenergic receptors coupled with Gi protein. High adrenergic tonus generated by exposure of homeothermic animals to cold reduces insulin secretion. In this study we evaluate the participation of UCP-2 in cold-induced regulation of insulin secretion. METHODS: Static insulin secretion studies, western blotting and immunohistochemistry were used in this investigation. RESULTS: Exposure of rats to cold during 8 days promoted 60% ( n=15, p<0.05) reduction of basal serum insulin levels concentration accompanied by reduction of the area under insulin curve during i.p. GTT (50%, n=15, p<0.05). Isolated islets from cold-exposed rats secreted 57% ( n=6, p<0.05) less insulin following a glucose challenge. Previous sympathectomy, partially prevented the effect of cold exposure upon insulin secretion. Islets isolated from cold-exposed rats expressed 51% ( n=6, p<0.5) more UCP-2 than islets from control rats, while the inhibition of UCP-2 expression by antisense oligonucleotide treatment partially restored insulin secretion of islets obtained from cold-exposed rats. Cold exposure also induced an increase of 69% ( n=6, p<0.05) in PGC-1 protein content in pancreatic islets. Inhibition of islet PGC-1 expression by antisense oligonucleotide abrogated cold-induced UCP-2 expression and partially restored insulin secretion in islets exposed to cold. CONCLUSION/INTERPRETATION: Our data indicate that sympathetic tonus generated by exposure of rats to cold induces the expression of PGC-1, which participates in the control of UCP-2 expression in pancreatic islets. Increased UCP-2 expression under these conditions could reduce the beta-cell ATP/ADP ratio and negatively regulate insulin secretion.

Acclimatization↗
PubMed1995

Impaired proliferative activity of mesenchymal cells affects the migratory pathway for neural crest cells in the developing gut of mutant murine embryos.

The developmental expression of neural and cell proliferation-related antigens in guts from mutant murine embryos (Is, lethal spotted) as a model for Hirschsprung's disease was studied. The expression was examined immunohistochemically using antibodies specific for neural cell adhesion molecule (NCAM), the L1 molecule, and proliferative cell-related nuclear antigen (PCNA). Cells immunoreactive for neural components proceeded from the esophagus to the anorectum showing a one-way migratory wave between embryonal day 10 (E10) and E14 in control specimens (Is/+, +/+). The patterns of NCAM and L1 immunoreactivity in Is/Is mutant specimens was the same as in controls on E10. However, from E10.5 to E13.5, the immunoreactivity in the mutants decreased and remained in the more oral side as compared with controls. No migration of immunoreactivity was found after E14.0. Therefore, the terminal portion of the colon remained aganglionic in Is/Is mutant embryos. PCNA immunoreactivity of mesenchymal cells preceded the migratory wave of the neural specific immunoreactivity, but the PCNA-positive cells were meager and poorly organized in the mutant embryos. Deficient PCNA staining patterns were found in mesenchymal tissue rather than in the migrating cells themselves. This impaired PCNA expression may reflect a deficient microenvironment for migration such that neural crest cells cannot colonize properly.

Animals↗
PubMed2003

Diffusion MRI of complex neural architecture.

While functional brain imaging methods can locate the cortical regions subserving particular cognitive functions, the connectivity between the functional areas of the human brain remains poorly understood. Recently, investigators have proposed a method to image neural connectivity noninvasively using a magnetic resonance imaging method called diffusion tensor imaging (DTI). DTI measures the molecular diffusion of water along neural pathways. Accurate reconstruction of neural connectivity patterns from DTI has been hindered, however, by the inability of DTI to resolve more than a single axon direction within each imaging voxel. Here, we present a novel magnetic resonance imaging technique that can resolve multiple axon directions within a single voxel. The technique, called q-ball imaging, can resolve intravoxel white matter fiber crossing as well as white matter insertions into cortex. The ability of q-ball imaging to resolve complex intravoxel fiber architecture eliminates a key obstacle to mapping neural connectivity in the human brain noninvasively.

Cerebral Cortex↗
PubMed2005

Pathways modulating neural KCNQ/M (Kv7) potassium channels.

K(+) channels play a crucial role in regulating the excitability of neurons. Many K(+) channels are, in turn, regulated by neurotransmitters. One of the first neurotransmitter-regulated channels to be identified, some 25 years ago, was the M channel. This was categorized as such because its activity was inhibited through stimulation of muscarinic acetylcholine receptors. M channels are now known to be composed of subunits of the Kv7 (KCNQ) K(+) channel family. However, until recently, the link between the receptors and the channels has remained elusive. Here, we summarize recent developments that have begun to clarify this link and discuss their implications for physiology and medicine.

Animals↗
PubMed2000

Involvement of BMP-4/msx-1 and FGF pathways in neural induction in the Xenopus embryo.

The msx homeodomain protein is a downstream transcription factor of the bone morphogenetic protein (BMP)-4 signal and a key regulator for neural tissue differentiation. Xmsx-1 antagonizes the dorsal expression of noggin and cerberus, as revealed by in situ hybridization and reverse transcription-polymerase chain reaction assays. In animal cap explants, Xmsx-1 and BMP-4 inhibit the neural tissue differentiation induced by noggin or cerberus. A loss-of-function study using the Xmsx-1/VP-16 fusion construct indicated that neural tissue formation was directly induced by the injection of fusion ribonucleic acid, although the expression of neural cell adhesion molecule (N-CAM) in the cap was less than that in the cap injected with tBR or noggin. In contrast to the single cap assay, unexpectedly, both BMP-4 and Xmsx-1 failed to inhibit neurulation in the ectodermal explants to which the organizer mesoderm was attached. The results of cell-lineage tracing experiments indicated that the neural cells were differentiated from the animal pole tissue where the excess RNA of either BMP-4 or Xmsx-1 was injected, whereas notochord was differentiated from the organizer mesoderm. Neural tissue differentiated from BMP-4-injected ectodermal cells strongly expressed posterior neural markers, such as hoxB9 and krox20, suggesting that the posterior neural cells differentiated regardless of the existence of the BMP signal. The introduction of a dominant-negative form of the fibroblast growth factor (FGF) receptor (XFD) into the ectodermal cells drastically reduced the expression of pan and posterior neural markers (N-CAM and hoxB-9) if co-injected with BMP-4 RNA, although XFD alone at the same dose did not shut down the expression of N-CAM in the combination explants. Therefore, it is proposed that an FGF-related molecule was involved in the direct induction of posterior neural tissue in the inducing signals from the organizer mesoderm in vivo.

Animals↗
PubMed1982

The influence of visceral mechanoreceptors on sympathetic efferent discharge in the cat.

1. Recordings have been made from eighty-three single sympathetic efferent units in the hypogastric nerve in two types of preparation. In all animals the baroreceptors were denervated to exclude changes in sympathetic discharge resulting from any variations in arterial pressure, and the spinal cord was sectioned at the 6th lumbar segment to exclude changes in efferent discharge that might have been due to pelvic nerve afferents from the bladder or other viscera. In some animals the afferent pathways were sectioned from all pelvic and lower abdominal viscera other than the bladder, so that the vesical afferent pathway was the only neural pathway that might mediate reflex events from these viscera. The hypogastric nerve afferent pathway was excited by bladder distension or by bladder contractions induced by electrical stimulation of the sacral cord.2. Approximately half the units gave an increase in spike rate during distension or during contraction of the bladder. Three-quarters of the units tested also gave an increase in spike rate during colonic distension. In no units that exhibited convergence of afferent input did colonic and vesical stimuli cause responses of opposite sign.3. Approximately 10% of units showed a reduction in discharge rate when the bladder was distended or caused to contract.4. The estimated intravesical pressure thresholds for these reflexes were in the range 8-56 mmHg which extends beyond that of the mechanoreceptors which form the afferent limb of the reflex.5. These reflex studies indicate that the hypogastric nerve afferents from the bladder can elicit sympathetic reflexes within the physiological range of intravesical pressures, and that vesico-sympathetic reflexes can be elicited in the absence of pelvic nerve afferent inputs.In 75% of sympathetic efferent units that respond to bladder distension or contraction, there is evidence for convergent inputs with similar actions from the colon.

Action Potentials↗
PubMed2004

Beta1 integrins activate a MAPK signalling pathway in neural stem cells that contributes to their maintenance.

The emerging evidence that stem cells develop in specialised niches highlights the potential role of environmental factors in their regulation. Here we examine the role of beta1 integrin/extracellular matrix interactions in neural stem cells. We find high levels of beta1 integrin expression in the stem-cell containing regions of the embryonic CNS, with associated expression of the laminin alpha2 chain. Expression levels of laminin alpha2 are reduced in the postnatal CNS, but a population of cells expressing high levels of beta1 remains. Using neurospheres - aggregate cultures, derived from single stem cells, that have a three-dimensional architecture that results in the localisation of the stem cell population around the edge of the sphere - we show directly that beta1 integrins are expressed at high levels on neural stem cells and can be used for their selection. MAPK, but not PI3K, signalling is required for neural stem cell maintenance, as assessed by neurosphere formation, and inhibition or genetic ablation of beta1 integrin using cre/lox technology reduces the level of MAPK activity. We conclude that integrins are therefore an important part of the signalling mechanisms that control neural stem cell behaviour in specific areas of the CNS.

Animals↗
PubMed1985

Quadriceps strengthening with the DAPRE technique: case studies with neurological implications.

The Daily Adjustable Progressive Resistive Exercise (DAPRE) technique was developed clinically in an effort to provide an objective means of increasing resistance concurrently with strength increases during knee rehabilitation subsequent to injury/surgery. The key to the DAPRE technique is that on the third and fourth sets of exercise the patient performs as many repetitions as possible. The number of repetitions performed during the third and fourth sets is used to determine the amount of weight that is added to (or sometimes removed from) the working weight for the next set and session, respectively. Consequently, patients exercise nearer their optimal capacity during each weight rehabilitation session, and their strength redevelopment occurs at a much faster rate. This report describes the quariceps muscle strength gains by 21 athletes who used the DAPRE technique following knee immobilization for a minimum of 3 wk. These patients averaged an increase of 4.3 +/- 2.2 (SD) kg X d-1 for a period of 6.4 +/- 2.2 d, as measured by a six repetitions maximum test. It seems unlikely that morphological changes were responsible for these strength increases. It is postulated that strength redevelopment following immobilization involves changes in neural pathways and/or overcoming possible neural inhibitors.

Athletic Injuries↗