bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enteric motor and interneuronal circuits controlling motility
Authors: Bornstein J. C. , Costa M. , Grider J. R. 
Published: April 2004

AbstractThe enteric nervous system regulates intestinal motility. It contains intrinsic sensory neurones, several types of interneurones and excitatory and inhibitory motor neurones. This review summarizes our knowledge of motor neurones and interneurones in simple motility reflex pathways (ascending and descending excitation, descending inhibition) and it focuses on guinea‐pig ileum. Excitatory circular muscle motor neurones contain choline acetyltransferase (ChAT) and tachykinins and project orally 0.5–10 mm. They transmit via muscarinic acetylcholine receptors and tachykinins acting at NK1 and NK2 receptors. Inhibitory circular muscle motor neurones contain nitric oxide synthase (NOS), vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase activating peptide (PACAP), project anally up to 25 mm and transmit via ATP, nitric oxide and/or VIP. Ascending interneurones project up to 10 mm orally and contain ChAT and tachykinins. They transmit to each other via ACh at nicotinic receptors (nAChR), but to excitatory motor neurones via both nAChR and NK3 receptors. There are at least three types of descending interneurones and one transmits to inhibitory motor neurones via ATP acting at P2X receptors. NOS‐containing descending interneurones receive input via P2Y receptors from other interneurones. Transmission to and from the other descending interneurones (ChAT/5‐HT, ChAT/somatostatin) is yet to be characterized.
Submucosal secretomotor and vasodilator reflexes
Authors: Vanner S. , Macnaughton W. K. 
Published: April 2004

AbstractThe presence of neuronal reflexes within the intestine that modulate mucosal ion secretion and blood flow have been recognized for many years, but the organization of these reflexes was unclear. This review highlights important findings from recent in vitro guinea‐pig studies which have shown that both intrinsic primary afferent neurones (IPANs) and extrinsic primary afferent neurones (EPANs) can respond to chemical and/or mechanical stimuli to activate pathways, the afferent and efferent elements of which are confined to the walls of the intestine. Enteric neuronal pathways involve both myenteric and submucosal plexus neurones whereas capsaicin‐sensitive afferent nerves evoke secretion by stimulating submucosal secretomotor neurones and vasodilation by direct actions on the submucosal arterioles. In this review, the cellular mechanisms involved in these pathways are described and the implications of these findings are discussed.
Lessons from the porcine enteric nervous system
Authors: Brown D. R. , Timmermans J.‐P. 
Published: April 2004

AbstractThe porcine intestinal tract possesses functional and pathological similarities to the human digestive tract and the organization of the porcine enteric nervous system, like that of the human, appears to be more complex than that of commonly investigated guinea‐pig intestine. Intrinsic primary afferent neurones appear to differ in the intestines of large and small animals in terms of their chemical coding, distribution over enteric neural networks, electrophysiological behaviour and synaptic properties. Opioid receptors on afferent and motor neurones in the porcine small intestine are predominately of the delta type, whereas those in guinea‐pig ileum are mu. Moreover, delta‐opioid receptors associated with the myenteric and submucosal plexuses of porcine ileum that, respectively, modulate neurogenic smooth muscle contractions and mucosal ion transport appear to differ in their pharmacological characteristics. These profound interspecies and interregional differences underscore the complexity of the enteric nervous system, and the development of new drugs designed to treat human neurogastrointestinal disorders should be based on the results of investigations in homologous animal models, such as the pig.
Role of interstitial cells of Cajal in neural control of gastrointestinal smooth muscles
Authors: Ward S. M. , Sanders K. M. , Hirst* G. D. S. 
Published: April 2004

AbstractSpecialized cells known as interstitial cells of Cajal (ICC) are distributed in specific locations within the tunica muscularis of the gastrointestinal tract and serve as electrical pacemakers, active propagation pathways for slow waves, and mediators of enteric motor neurotransmission. Recent morphological studies have provided evidence that motor neurotransmission in the gut does not occur through loosely defined synaptic structures between nerves and smooth muscle, but rather via synaptic‐like contacts that exist between varicose nerve terminals and intramuscular ICC (ICC‐IM). ICC‐IM are coupled to smooth muscle cells via gap junctions and electrical responses elicited in ICC are conducted to muscle cells. Electrophysiological studies of the stomach of wild‐type and mutant animals that lack ICC‐IM have provided functional evidence for the importance of ICC in cholinergic and nitrergic motor neurotransmission. The synaptic‐like contacts between nerve terminals and ICC‐IM facilitate rapid diffusion of transmitters to specific receptors on ICC. ICC‐IM also play a role in generating unitary potentials in the stomach that contribute to the excitability of the gastric fundus and antrum.
Communication between interstitial cells of Cajal and gastrointestinal muscle
Authors: Daniel E. E. 
Published: April 2004

AbstractInterstitial cells of Cajal (ICC) pace gastrointestinal muscle by initiating slow waves in both muscle layers and appear to be preferred sites for reception of neurotransmitters. ICC of the myenteric plexus (ICC‐MP) pace stomach and small intestine, while intramuscular ICC (ICC‐IM) receive nerve messages. Recently, ICC‐IM have been found to provide regenerative responses to and amplification of pacing messages from ICC‐MP, at least in some systems. This review will examine the assumption that gap junctions provide low‐resistance contacts for pacing. Structural and functional evidence will be evaluated. Structural, theoretical and experimental difficulties with the gap junctions hypothesis for pacing will be considered. So far little direct evidence about the role of gap junctions in neurotransmission exists, although a structural basis exists. Alternate possibilities for transmission of ICC pacing and neural messages will be examined and suggestions for future research made.
Gastric enteric neurones that respond to luminal injury
Authors: Schicho R. , Holzer P. , Lippe I. TH. 
Published: April 2004

AbstractChallenge of the rat gastric mucosa with HCl stimulates intrinsic neurones in the myenteric plexus of the stomach as demonstrated by immunohistochemical detection of c‐Fos. In multiple labelling experiments of whole‐mounts and sections of the gastric corpus we determined the chemical code of the stimulated neurones and investigated further whether neural pathways involving capsaicin‐sensitive afferents, cholinergic neurones or the vagal system contribute to the stimulation of these neurones. Intragastric (IG) administration of 0.5 m HCl caused c‐Fos expression in 12% of myenteric neurones, whereas IG saline failed to induce c‐Fos. All stimulated neurones stained for nitric oxide synthase (NOS), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY), but not for choline acetyltransferase (ChAT). Fibres coexpressing NOS/VIP/NPY were found predominantly in the external muscle layer and the muscularis mucosae of the stomach wall. Pretreatment with capsaicin or hexamethonium, combination of both pretreatments or vagotomy reduced HCl‐induced c‐Fos expression by 54%, 66%, 63% and 68%, respectively. The data indicate that mucosal acid challenge of the stomach stimulates inhibitory motor neurones in the myenteric plexus and that capsaicin‐sensitive afferents as well as cholinergic neurones participate in the neuronal stimulation probably via a vago–vagal reflex.
Role of peripheral CRF signalling pathways in stress‐related alterations of gut motility and mucosal function
Authors: Taché Y. , Perdue M. H. 
Published: April 2004

AbstractCentral corticotrophin releasing‐factor (CRF) signalling pathways are involved in the endocrine, behavioural and visceral responses to stress. Recent studies indicate that peripheral CRF‐related mechanisms also contribute to stress‐induced changes in gut motility and intestinal mucosal function. Peripheral injection of CRF or urocortin inhibits gastric emptying and motility through interaction with CRF2 receptors and stimulates colonic transit, motility, Fos expression in myenteric neurones and defecation through activation of CRF1 receptors. With regard to intestinal epithelial cell function, intraperitoneal CRF increases ion secretion and mucosal permeability to macromolecules. The motility and mucosal changes induced by peripheral CRF mimic those induced by acute stress. In addition, CRF receptor antagonists given peripherally prevent acute restraint and water avoidance stress‐induced delayed gastric emptying, stimulation of colonic motor function and mucosal permeability. Similarly, early trauma enhanced intestinal mucosal dysfunction to an acute stressor in adult rats and the response is prevented by peripheral injection of CRF antagonist. Chronic psychological stress results in reduced host defence and initiates intestinal inflammation through mast cell‐dependent mechanisms. These findings provide convergent evidence that activation of peripheral CRF receptors and mast cells are important mechanisms involved in stress‐related alterations of gut physiology.
New insights into human enteric neuropathies
Authors: De Giorgio R. , Guerrini S. , Barbara G. , Cremon C. , Stanghellini V. , Corinaldesi R. 
Published: April 2004

AbstractThe functioning of enteric neuronal circuitries has been elucidated in the recent past. Evidence is now gathering to explain how dysfunction of the enteric nervous system (ENS) may lead to human gastrointestinal motor disorders. These conditions include achalasia, congenital hypertrophic pyloric stenosis, chronic intestinal pseudo‐obstruction, Hirschsprung's disease, chronic idiopathic constipation, and probably irritable bowel syndrome. Degenerative, inflammatory and genetic mechanisms exert a critical role in ENS dysfunction underlying gut dysmotility. The study of the ENS abnormalities in gut dysmotility provides a framework to better understand the mechanisms involved in degeneration and neuronal loss and fosters the development of targeted therapeutic options.
Lack of Complement Factor C3, but Not Factor B, Increases Hyperlipidemia and Atherosclerosis in Apolipoprotein E−/− Low-Density Lipoprotein Receptor−/− Mice
Authors: Persson Linda , Borén Jan , Robertson Anna-Karin L. , Wallenius Ville , Hansson Göran K. , Pekna Marcela 
Published: April 2004

Objective—To investigate the effect of complement deficiency on atherogenesis and lipidemia, we used mice deficient in the third complement component (C3−/−) or factor B (FB−/−).Methods and Results—Complement-deficient mice were crossed with mice deficient in both apolipoprotein E and the low-density lipoprotein receptor (Apoe−/−LDLR−/−). The percent lesion area in the aorta at 16 weeks, determined byen faceanalysis, was 84% higher inC3−/− mice than in controls (11.8%±0.4% versus 6.4%±0.8%, mean±SEM,P<0.00005). TheC3−/− mice also had 58% higher serum triglyceride levels (P<0.05) and a more proatherogenic lipoprotein profile, with significantly more low-density lipoprotein cholesterol and very-low-density lipoprotein triglycerides than control mice. TheC3−/− mice weighed 13% less (P<0.01) and had a lower body fat content (3.5%±1.0% versus 13.1%±3.0%,P<0.01). There were no differences betweenFB−/− mice and controls.Conclusions—Complement activation by the classical or lectin pathway exerts atheroprotective effects, possibly through the regulation of lipid metabolism.
More Accurate Identification of Reversible Ischemic Injury in Human Stroke by Cerebrospinal Fluid Suppressed Diffusion-Weighted Imaging
Authors: Bykowski Julie L. , Latour Lawrence L. , Warach Steven 
Published: April 2004

Background and Purpose—The apparent diffusion coefficient (ADC) derived from diffusion-weighted (DWI) MRI has been used to differentiate reversible from irreversible ischemic injury. However, the ADC can be falsely elevated by partial volume averaging of cerebrospinal fluid (CSF) with parenchyma, limiting the accuracy of this approach. This study tested the hypothesis that the accuracy of differentiating reversible from irreversible ischemic injury could be improved by CSF suppression at image acquisition.Methods—Sixteen patients presenting within 6 hours from symptoms, and having partial reversal of the acute lesion on DWI were studied using conventional CSF-suppressed DWI. Lesions were segmented from coregistered acute DWI and follow-up fluid-attenuated inversion recovery (FLAIR) series. The segmented volumes were applied to conventional (ADCC) and CSF-suppressed ADC (ADCFLIPD) maps to classify each voxel as progressed to infarct or reversed. Individual voxel ADC values were pooled across all patients. Sensitivity to predict reversal, specificity, and accuracy were calculated for both methods.Results—A total of 25 313 voxels were classified as progressed and 31 952 voxels reversed. Across all lesion voxels, ADCFLIPDvalues more accurately depicted tissue fate compared with ADCCvalues (P<0.0001). The largest difference in the two methods was in voxels with <75% parenchyma, where the accuracy of ADCCwas only 50% compared with 62% for ADCFLIPD.Conclusion—CSF-suppressed ADC measurements gave a more accurate identification of reversible ischemic injury in this sample. We predict that multimodal MRI models of tissue viability in ischemic stroke will be more accurate if CSF-suppressed ADC measurements are used.
Effects of Left Inferior Prefrontal Stimulation on Episodic Memory Formation: A Two-Stage fMRI—rTMS Study
Authors: Köhler Stefan , Paus Tomáš; , Buckner Randy L. , Milner Brenda 
Published: April 2004

Abstract
Successful recovery of words from episodic memory relies strongly on semantic processes at the time of encoding. Evidence from several functional magnetic resonance imaging (fMRI) studies has shown that changes in neural activity in the left inferior prefrontal cortex (LIPFC) during semantic encoding predict subsequent memory performance. This evidence has been taken to suggest that LIPFC plays a critical role in memory formation. Functional neuroimaging findings, however, do not establish a causal brain-behavior relationship. To determine whether there is a causal link between LIPFC involvement at encoding and subsequent success in memory performance, we conducted a two-part study in which we first used fMRI to localize encoding-related activation in LIPFC and then employed repetitive transcranial magnetic stimulation (rTMS) to manipulate neural processes in LIPFC during semantic encoding. To demonstrate the neuroanatomical specificity of any observed effect and to control for nonspecific rTMS side effects, we also stimulated neural processes in two control sites. Using frameless stereotaxy, we positioned the stimulation coil to target (1) the LIPF region that was activated during fMRI (mean xyz = −48 35 5); (2) the homologous righthemisphere region; and (3) an additional left parietal control site. At each site, “stimulated” items (600 msec of 7-Hz rTMS with Cadwell Round Coil) were intermixed with items presented without concurrent stimulation. Subsequently, subjects performed a recognition memory task for the words encountered. We found support for the predicted causal brain-behavior relationship, which was specific to LIPFC. When comparing recognition scores for stimulated items, normalized for variations in performance on nonstimulated trials, we found that words encoded under LIPFC stimulation were subsequently recognized with higher accuracy than words encoded under stimulation in the two cortical control sites. By contrast, no performance difference emerged when the two control sites were compared with each other. Based on additional analyses of the rTMS effects observed directly at the time of encoding (i.e., on semantic-decision performance), we suggest that LIPFC stimulation may have produced its effect on recognition memory, at least in part, through the triggering of more extensive processing of the stimulated items and an ensuing gain in item distinctiveness. Physiological processes of facilitation probably also contributed to the observed memory benefit. Together, these findings suggest that LIPFC does play a causal role in episodic memory formation.
Is the Fusiform Face Area Specialized for Faces, Individuation, or Expert Individuation?
Authors: Rhodes Gillian , Byatt Graham , Michie Patricia T. , Puce Aina 
Published: April 2004

Abstract
Several brain imaging studies have identified a region of fusiform gyrus (FG) that responds more strongly to faces than common objects. The precise functional role of this fusiform face area (FFA) is, however, a matter of dispute. We sought to distinguish among three hypotheses concerning FFA function: face specificity, individuation, and expert individuation. According to the face-specificity hypothesis, the FFA is specialized for face processing. Alternatively, the FFA may be specialized for individuating visually similar items within a category (the individuation hypothesis) or for individuating within categories with which a person has expertise (the expert-individuation hypothesis). Our results from two experiments supported the face-specificity hypothesis. Greater FFA activation to faces than Lepidoptera, another homogeneous object class, occurred during both free viewing and individuation, with similar FFA activation to Lepidoptera and common objects (Experiment 1). Furthermore, during individuation of Lepidoptera, 83% of activated FG voxels were outside the face FG region and only 15% of face FG voxels were activated. This pattern of results suggests that distinct areas may individuate faces and Lepidoptera. In Experiment 2, we tested Lepidoptera experts using the same experimental design. Again, the results supported the face-specificity hypothesis. Activation to faces in the FFA was greater than to both Lepidoptera and objects with little overlap between FG areas activated by faces and Lepidoptera. Our results suggest that distinct populations of neurons in human FG may be tuned to the features needed to individuate the members of different object classes, as has been reported in monkey inferotemporal cortex, and that the FFA contains neurons tuned for individuating faces.
The Role of Spared Calcarine Cortex and Lateral Occipital Cortex in the Responses of Human Hemianopes to Visual Motion
Authors: Morland Antony B. , Lê Sandra , Carroll Erin , Hoffmann Michael B. , Pambakian Alidz 
Published: April 2004

Abstract
Some patients, who are rendered perimetrically blind in one hemifield by cortical lesions, nevertheless exhibit residual visual capacities within their field defects. The neural mechanism that mediates the residual visual responses has remained the topic of considerable debate. One explanation posits the subcortical visual pathways that bypass the primary visual cortex and innervate the extrastriate visual areas as the substrate that underlies the residual vision. The other explanation is that small islands of the primary visual cortex remain intact and provide the signals for residual vision. We have performed behavioral and functional magnetic resonance imaging experiments to investigate the validity of the two explanations of residual vision. Our behavioral experiments indicated that of the seven hemianopes tested, two had the ability to discriminate the direction of a drifting grating. This residual visual response was shown with fMRI to be the result of spared islands of calcarine cortical activity in one of the hemianopes, whereas only lateral occipital activity was documented in the other patient. These results indicate that the underlying neural correlates of residual vision can vary between patients. Moreover, our study emphasizes the necessity of ruling out the presence of islands of preserved function and primary visual cortex before assigning residual visual capacities to the properties of visual pathways that bypass the primary visual cortex.
A Feedback Model of Visual Attention
Authors: Spratling M. W. , Johnson M. H. 
Published: April 2004

Abstract
Feedback connections are a prominent feature of cortical anatomy and are likely to have a significant functional role in neural information processing. We present a neural network model of cortical feedback that successfully simulates neurophysiological data associated with attention. In this domain, our model can be considered a more detailed, and biologically plausible, implementation of the biased competition model of attention. However, our model is more general as it can also explain a variety of other top-down processes in vision, such as figure/ground segmentation and contextual cueing. This model thus suggests that a common mechanism, involving cortical feedback pathways, is responsible for a range of phenomena and provides a unified account of currently disparate areas of research.
Grammaticality Judgment in Aphasia: Deficits Are Not Specific to Syntactic Structures, Aphasic Syndromes, or Lesion Sites
Authors: Wilson Stephen M. , Saygın Ayşe Pınar 
Published: April 2004

Abstract
We examined the abilities of aphasic patients to make grammaticality judgments on English sentences instantiating a variety of syntactic structures. Previous studies employing this metalinguistic task have suggested that aphasic patients typically perform better on grammaticality judgment tasks than they do on sentence comprehension tasks, a finding that has informed the current view that grammatical knowledge is relatively preserved in agrammatic aphasia. However, not all syntactic structures are judged equally accurately, and several researchers have attempted to provide explanatory principles to predict which structures will pose problems to agrammatic patients. One such proposal is Grodzinsky and Finkel's (1998) claim that agrammatic aphasics are selectively impaired in their ability to process structures involving traces of maximal projections. In this study, we tested this claim by presenting patients with sentences with or without such traces, but also varying the level of difficulty of both kinds of structures, assessed with reference to the performance of age-matched and young controls. We found no evidence that agrammatic aphasics, or any other subgroup, are selectively impaired on structures involving traces: Some judgments involving traces were made quite accurately, whereas other judgments not involving traces were made very poorly. Subgroup analyses revealed that patient groups and agematched controls had remarkably similar profiles of performance across sentence types, regardless of whether the patients were grouped based on Western Aphasia Battery classification, an independent screening test for agrammatic comprehension, or lesion site. This implies that the pattern of performance across sentence types does not result from any particular component of the grammar, or any particular brain region, being selectively compromised. Lesion analysis revealed that posterior temporal areas were more reliably implicated in poor grammaticality judgment performance than anterior areas, but poor performance was also observed with some anterior lesions, suggesting that areas important for syntactic processing are distributed throughout the left peri-sylvian region.