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At least 379 records · Page 21Linked to original sources

PubMed1979

Effect of bilateral cervical vagotomy on balloon-induced lower esophageal sphincter relaxation in the dog.

A study was performed in dogs to determine whether balloon distension within the striated muscle esophagus induces lower esophageal sphincter relaxation via a local intramural pathway or a central neural pathway. Bilateral vagosympathetic nerve blockade was produced by cooling the nerve trunks isolated in skin loops on either side of the neck. Sphincter pressure was measured before and during intraesophageal balloon distension, with and without nerve blockade. With the vagosympathetic nerves intact, balloon distension produced sphincter relaxation, sphincter shortening, and orad movement of the sphincter. The threshold for these responses increased progressively as distension was applied at more proximal levels. Bilateral vagosympathetic nerve blockade abolished all the lower esophageal sphincter responses to distension at any level within the esophagus, whether or not sphincter pressure was raised by pentagastrin infusion. Therefore, lower esophageal sphincter relaxation induced by distension of the dog striated muscle esophagus requires a central nervous system connection via the vagosympathetic nerve trunks. There is no direct intramural pathway for this responses in the dog.

Animals↗

PubMed1990

Spontaneous visual phenomena with visual loss: 104 patients with lesions of retinal and neural afferent pathways.

Fifty-seven percent of 104 consecutive patients with retinal or neural visual loss reported spontaneous visual phenomena (SVP). Elementary SVP occurred more commonly (51% of patients) than complex SVP (21%). SVP occur with lesions of any portion of the visual pathways. Unlike irritative hallucinations, they do not aid in localization of the lesion. SVP occur significantly more frequently with visual acuity of 20/50 or less in both eyes. These purely visual hallucinations are unlikely to herald psychiatric disease and may be release phenomena stemming from loss of inhibitory visual input.

Adolescent↗

PubMed1990

Pharmacological and anatomical analysis of fear conditioning.

The potentiated startle paradigm measures conditioned fear by an increase in the amplitude of a simple reflex (the acoustic startle reflex) in the presence of a cue previously paired with shock. This paradigm offers a number of advantages as an alternative to most animal tests of fear or anxiety, since it involves no operant and is reflected by an enhancement rather than a suppression of ongoing behavior. Lesion and electrical stimulation studies on fear-potentiated startle and startle increased by electrical stimulation of the amygdala are being used to define the neural pathways necessary for a visual conditioned stimulus to alter the acoustic startle reflex. The current working hypothesis is that the conditioned stimulus activates the central nucleus of the amygdala through a pathway involving the lateral geniculate nucleus and insular cortex. The central nucleus of the amygdala may then project directly to the acoustic startle pathway, modulating the startle response. More work has to be done to define conclusively the relevant neural pathways involved in fear-potentiated startle. Nonetheless, by combining behavioral, anatomical, physiological, and pharmacological approaches, it will be possible to determine each step along the pathway that mediates the ability of a stimulus signaling fear to alter behavior. Once the exact structures are delineated, it should be possible to determine the neurotransmitters that are released during a state of fear and how this chemical information is relayed along these pathways to affect behavior. Eventually, this approach should help to determine where plastic changes take place along these pathways to mediate the conditioned effects that are being measured and the biochemical processes that are involved.

Amygdala↗

PubMed2003

Endogenous CCK depresses contractile activity within the ascending myenteric reflex pathway of rat ileum.

The ascending excitatory reflex is an important part of the myenteric reflex. In order to study the ascending neural pathways, isolated segments of rat ileum were stimulated by electrical stimulation of the gut wall (20 V, 3 pulses per second, 1 ms) using platinum electrodes. The excitatory contractile response was recorded using perfused manometric side-hole tubing located 2 and 4 cm orally to the stimulation site. The contractile response to electrical stimulation was abolished by atropine (10(-6) M) or hexamethonium (10(-4) M). The excitatory response increased after administration of the cholecystokinin A (CCK(A)) receptor antagonists lorglumide (3x10(-6) M: +44.1%), devazepide (10(-8) M: +19.4%; 10(-7) M: +30.0%) and SR-27897 (10(-10) M: +21.8%, 10(-8) M: +47.0%, P<0.05, n=8). However, the CCK(B) receptor antagonist L-365,260 also caused a significant increase in the oral excitation (10(-6) M: +27.4%). sCCK-8 caused a significant reduction in the ascending response (10(-8) M: -11.5%) and induced spontaneously occurring contractions at doses ranging from 10(-10)-10(-6) M. CCK-9 significantly increased the ascending response (10(-7) M: +10.9%, P<0.05). However, caerulein (10(-10) M: -25.9%, 10(-8) M: -26.8%; P<0.01) and pentagastrin (10(-10) M: -20.2%, P<0.05; 10(-8) M: -23.7%, P<0.01; 10(-6) M: -28.3%, P<0.001) reduced the ascending contractile response significantly. These data, obtained with potent and highly specific CCK receptor antagonists, demonstrate an inhibitory role of endogenously released CCK within the ascending neural pathway. The data further suggest that exogenously applied CCK-related peptides have different effects on the myenteric reflex which might be due to excitation of the different involved neurons (short and long ascending inter- and motorneurons) in an unphysiological order. Thus in experiments investigating more complex neuronal circuits, experiments with antagonists should be regarded as more specific.

Animals↗

PubMed2002

Variations on the Notch pathway in neural development.

Notch signaling allows cells in contact to adopt different fates. Regulation of the Notch pathway allows for the same signaling mechanism to be used in a wide variety of contexts during development. Intracellular activities of the E3 ubiquitin ligases Sel-10 and Neuralized involve proteasome-dependent degradation in the regulation of Notch pathway activity. Extracellular manipulations of Notch by Fringe and Scabrous regulate the pathway by changing Notch interactions outside the cell. These regulatory mechanisms, along with many others, affect how Notch signaling activity influences cell fate determination.

Animals↗

PubMed1997

Central control mechanisms in hypertension.

There is substantial evidence for an activation of the sympathetic nervous system in man as well as in genetic models of hypertension, such as the spontaneously hypertensive rat (SHR), but we are only beginning to understand the central mechanisms that generate changes in sympathetic activity and elevate blood pressure (BP). Significant recent advances have been made in defining the neural pathways involved in BP regulation and in identifying the neurotransmitters these neurones utilise. In this overview, we describe the neural pathways within the medulla oblongata and spinal cord that participate in BP control and examine the role of amino acid neurotransmitters within these pathways. We demonstrate how alterations in these pathways explain the sympathetic activation observed in the SHR and contribute to hypertension in this model. Lastly, we examine the application of modern molecular biological approaches to further our understanding of the neural regulation of the circulation. In these studies, we used the administration of antisense oligonucleotides to interrupt gene expression.

Animals↗

PubMed1993

The parabrachial nucleus: a brain stem substrate critical for mediating the aversive motivational effects of morphine.

Bilateral ibotenic acid lesions of the lateral, but not the medial, parabrachial nucleus (PBN) blocked conditioned taste aversion (CTA) induced by morphine but not conditioned place preference induced by morphine. The same lateral PBN lesions also blocked conditioned place aversion produced by low intraperitoneal doses of morphine (shown to produce aversion, instead of preference, due to a restricted action on gut opiate receptors). Lateral PBN lesions did not block CTA produced by LiCl. Cerebral peduncle lesions that destroyed the direct descending projections from the visceral cortex to the PBN did not block CTA induced by morphine, nor did ibotenic acid lesions of the tegmental pedunculopontine nuclei (shown to block place preference produced by even high morphine doses). It is suggested that the lateral PBN is a critical link in the neural pathway carrying the aversive motivational effects of opiates from the gut into the central nervous system, independent of the neural pathway carrying the rewarding motivational effects of morphine.

Animals↗

PubMed1998

Centrally-mediated opioid-induced immunosuppression. Elucidation of sympathetic nervous system involvement.

Opioid-induced modulation of the immune system is a complex phenomenon involving opioid receptors, central and sympathetic neural pathways, catecholamine receptors, and other regulatory mechanisms. The precise neural pathways involved in centrally-mediated immune modulation are not currently defined. In addition, the physiological purpose for endogenous opioid modulation of the immune system is not well understood. Perhaps this modulation phenomenon represents an integral feedback loop within a much larger homeostatic control system. Indeed, the role of the HPA axis in immune regulation can not be discarded, and in fact, probably serves to balance immune function, in concert with multiple feedback systems, around some undiscovered parameter of efficiency. Perhaps the physiological role of endogenous opioid control is to act as a monitor poised to subvert chronic inflammatory processes and autoimmune disorders. Regardless of the evolutionary heritage of this and despite the overwhelming complexity of immune regulation, important work substantiating a bidirectional communication link between the brain and the immune system has created a foundation for further elucidation of the intricacies of immunoregulation.

Animals↗

PubMed1990

Topographical features of the substratum for growth of pioneering neurons in the Manduca wing disc.

The sensory neurons of the Manduca wing form a planar network nestled between the wing's upper and lower monolayers. The pioneering axons of this network grow in a distal-to-proximal direction over the basal surface of the upper epithelial monolayer. The basal surface of this monolayer has been examined ultrastructurally during the period of axonal outgrowth. The cellular terrain traversed by axons shows a graded distribution of epithelial processes, with the number of processes increasing in a proximal direction. Growth cones of axons, therefore, encounter increasing surface areas for contact with their substratum as they move toward the base of the wing. Because a basal lamina is laid down over these epithelial processes after axons have pioneered the neural pathways of the wing, axonal guidance cues apparently lie on surfaces of these basal processes. At branch points of the neural pathway examined in this study, axons avoid pathways in which the basal surfaces of cells in the upper wing monolayer interdigitate with basal surfaces of underlying tracheal cells. This interaction between wing epithelial cells and tracheal epithelial cells could act as a physical barrier to axonal outgrowth.

Animals↗

PubMed1981

Effects on breathing of putative neurotransmitters in the rostral hypothalamus of the rat.

The putative neurotransmitters norepinephrine (NE) and thyrotropin releasing hormone (TRH) are normally present in the rostral hypothalamic region (RHT) of the rat, and our aim was to evaluate possible effects of these agents on ventilatory regulations associated with this region. Using haloperidol-tranquilized Sprague-Dawley rats, microinfusions of both NE and TRH into the RHT resulted in an increase in rate, but not depth, of breathing. Control infusions and control infusion sites, mainly in the posterior hypothalamus, yielded no significant effect on breathing rate. Since NE and TRH can inhibit the discharge of some cells in the RHT, it was possible that the observed effects on breathing were due to depression of an inhibitory neural pathway. This idea was further tested by performing microinfusions using lidocaine. Evidence suggests that lidocaine can inhibit discharge in the central nervous system and that inhibitory pathways may be preferentially affected. Lidocaine produced effects on breathing comparable to NE and TRH, thereby supporting the proposition that inhibition of neural pathways in the RHT can stimulate breathing.

Animals↗

PubMed1998

Assessment of afferent gut--brain function using cerebral evoked responses to esophageal stimulation.

Increasing awareness is attributed to altered sensory perception in the pathogenesis of gastrointestinal disorders. Evoked potentials (EP), which represent the brain's electrical response to peripheral stimulation, have recently been used to investigate where and how (GI) afferent information is processed along the brain-gut axis. EP can be obtained with electrical stimulation or balloon distention in the esophagus in humans. Stimulation of afferent neural pathways in the esophagus produces cerebral evoked responses allowing assessment of the peripheral afferent neural pathways involved, and of the function of integrative neural centers within the brain. Recent studies using esophageal EP indicate that the cerebral response to either mode of stimulation depends on the perception of the stimuli. Using electrical stimulation, a clear dose-response relationship is found. The EP response obtained with electrical stimulation is in keeping with those recorded using direct cervical stimulation of the vagus nerve, supporting evidence that esophageal EP are produced by activation of afferent vagal pathways. From the conduction velocity of the autonomic (vagal) nerves conveying information from esophagus to brain, it was concluded that non-painful electrical stimuli predominantly activate fast conducting myelinated afferent sensory fibers (A-fibers), while EP to balloon distention are largely due to activation of unmyelinated C-fibers. Techniques, however, vary widely amongst different investigators, and some electrophysiological parameters remain controversial, as there is no standard approach. Using balloon distention, EP waveforms vary widely between laboratories, suggesting that EP are substantially influenced by the stimulator devices (pump, respirator). EP to balloon distention are hampered by a relatively low signal-to-noise ratio (SNR), which is probably due to long inflation-deflation time (> 200 ms). With electrical stimulation, there is much less variability between different groups, and SNR is distinctly higher. This method appears to be most attractive for studies of afferent esophageal function. Standardization of the techniques is important, before esophageal EP can be regarded as a useful diagnostic approach in patient groups.

Afferent Pathways↗

PubMed1995

The role of dopamine in drug abuse viewed from the perspective of its role in motivation.

Drugs of abuse share with conventional reinforcers the activation of specific neural pathways in the CNS that are the substrate of their motivational properties. Dopamine is recognized as the transmitter of one such neural pathway, being involved in at least three major aspects of motivation: modulation of motivational state, acquisition (incentive learning) and expression of incentive properties by motivational stimuli. Drugs of abuse of different pharmacological classes stimulate in the low dose range dopamine transmission particularly in the ventral striatum. Apart from psychostimulants, the evidence that stimulation of dopamine transmission by drugs of abuse provides the primary motivational stimulus for drug self-administration is either unconvincing or negative. However, stimulation of dopamine transmission is essential for the activational properties of drugs of abuse and might be instrumental for the acquisition of responding to drug-related incentive stimuli (incentive learning). Dopamine is involved in the induction and in the expression of behavioural sensitization by repeated exposure to various drugs of abuse. Sensitization to the dopamine-stimulant properties of specific drug classes leading to facilitation of incentive learning of drug-related stimuli might account for the strong control over behaviour exerted by these stimuli in the addiction state. Withdrawal from drugs of abuse results in a reduction in basal dopamine transmission in vivo and in reduced responding for conventional reinforcers. Although these changes are likely to be the expression of a state of dependence of the dopamine system their contribution to the motivational state of drug addiction is unclear.

Animals↗

PubMed2000

Neurogenic pathways mediating ascending and descending reflexes at the porcine ileocolonic junction.

We studied the pharmacology of the neural pathways mediating the responses of ileo- and coloileo-colonic junction (ICJ) to regional distension in ten anaesthetized pigs. Using manometric pullthroughs and a sleeve sensor, we found the ICJ demonstrated sustained tone that was resistant to tetrodotoxin. Ileal distension decreased ICJ pressure by 22.2 ¿ 10.1% (11.9 ¿ 2.7-10.1 ¿ 2.6 mmHg; P=0.002) and colonic distension augmented ICJ pressure by 23.5 ¿ 8.6% (12.8 ¿ 1.5-15.6 ¿ 2.1 mmHg; P=0.02). Bethanecol and Nw-nitro-L-arginine methyl ester (L-NAME) increased ICJ pressure (P=0.002, P=0.01, respectively). Sodium nitroprusside and isoproterenol reduced ICJ pressure (P=0.004, P=0.02, respectively). In the presence of L-NAME, the early inhibitory ileo-ICJ response was abolished, while early and late inhibitory responses were abolished by further addition of propranolol but not by the addition of hexamethonium, atropine, prazosin or yohimbine. The excitatory colo-ICJ response was replaced by inhibition in the presence of L-NAME. We concluded that: (1) the porcine ICJ displays myogenic tone which is influenced by excitatory muscarinic and inhibitory nitrergic and beta adrenergic pathways (2) an inhibitory ileo-sphincteric reflex mediated by nitrergic and beta adrenergic postganglionic neural pathways (3) both excitatory and inhibitory neurogenic colo-sphincteric reflexes exist, and the excitatory pathway involves nitrergic neurotransmission.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Update on the neuropathogenesis of delirium.

Delirium has been considered a syndrome of generalized dysfunction of higher cortical functions due to its breadth of symptoms and associated diffuse slowing on electroencephalogram. Advances in neuropsychiatry have revealed differences between brain regions, including the hemispheres, which may underlie the constellation of symptoms among different psychiatric disorders. For example, different neural pathways are involved in major depression and obsessive-compulsive disorder, including lateralization to one or the other hemisphere. In this article the author proposes that delirium, too, involves particular neural pathways and that lateralization to the right may be relevant. Structural and functional neuroimaging reports and recent neuropsychological studies support this lateralization. Prefrontal cortices, anterior and right thalamus, and right basilar mesial temporoparietal cortex may play a significant role in subserving delirium symptoms and may be the 'final common pathway' for delirium from a variety of etiologies. The final common pathway may be responsible for certain 'core symptoms' (disorientation, cognitive deficits, sleep-wake cycle disturbance, disorganized thinking, and language abnormalities), while other symptoms (delusions, hallucinations, illusions, and affective lability) may occur depending on the etiology causing delirium. An imbalance in the cholinergic and dopaminergic neurotransmitter systems is most commonly implicated in causing delirium, and could both account for delirium symptoms and be consistent with the neuroanatomical pathways being implicated.

Attention↗

PubMed1996

Physiological actions of angiotensin II mediated by AT1 and AT2 receptors in the brain.

1. Autoradiographic binding studies have shown that the AT1 receptor is the predominant angiotensin II (AngII) receptor subtype in the central nervous system (CNS). Major sites of AT1 receptors are the lamina terminalis, hypothalamic paraventricular nucleus, the lateral parabrachial nucleus, rostral and caudal ventrolateral medulla, nucleus of the solitary tract and the intermediolateral cell column of the thoraco-lumbar spinal cord. 2. While there are differences between species, AT2 receptors are found mainly in the cerebellum, inferior olive and locus coeruleus of the rat. 3. Circulating AngII acts on AT1 receptors in the subfornical organ and organum vasculosum of the lamina terminalis (OVLT) to stimulate neurons that may have a role in initiating water drinking. 4. Centrally administered AngII may act on AT1 receptors in the median preoptic nucleus and elsewhere to induce drinking, sodium appetite, a sympathetic vasoconstrictor response and vasopressin secretion. 5. Recent evidence shows that centrally administered AT1 antagonists inhibit dipsogenic, natriuretic, pressor and vasopressin secretory responses to intracerebroventricular infusion of hypertonic saline. This suggests that n angiotensinergic neural pathway has a role in osmoregulatory responses. 6. Central angiotensinergic pathways which include neural inputs to the rostral ventrolateral medulla may use AT1 receptors and play a role in the function of sympathetic pathways maintaining arterial pressure.

Angiotensin II↗

PubMed1998

Three neural tubes in mouse embryos with mutations in the T-box gene Tbx6.

Somites, segmented mesodermal units of the vertebrate embryo, are the precursors of adult skeletal muscle, bone and cartilage. During embryogenesis, somite progenitor cells ingress through the primitive streak, move laterally to a paraxial position (alongside the body axis) and segment into epithelial somites. Little is known about how this paraxial mesoderm tissue is specified. We have previously described a mouse T-box gene, Tbx6, which codes for a putative DNA-binding protein. The embryonic pattern of expression of Tbx6 in somite precursor cells suggests that this gene may be involved in the specification of paraxial mesoderm. We now report the creation of a mutation in Tbx6 that profoundly affects the differentiation of paraxial mesoderm. Irregular somites form in the neck region of mutant embryos, whereas more posterior paraxial tissue does not form somites but instead differentiates along a neural pathway, forming neural-tube-like structures that flank the axial neural tube. These paraxial tubes show dorsal/ventral patterning that is characteristic of the neural tube, and have differentiated motor neurons. These results indicate that Tbx6 is needed for cells to choose between a mesodermal and a neuronal differentiation pathway during gastrulation; Tbx6 is essential for the specification of posterior paraxial mesoderm, and in its absence cells destined to form posterior somites differentiate along a neuronal pathway.

Animals↗

PubMed1976

Neuroanatomic projections related to biting attack elicited from ventral midbrain in cats.

A single electrode was implanted in each of ten cats at a point in the ventral midbrain from which nonaffective biting attack on a rat could be elicited by electrical stimulation. A lesion was then made which was just large enough to eliminate the elicitation of attack at suprathreshold intensities from that electrode. After post-lesion survival times of 3-14 days the cats were sacrificed, and the degeneration resulting from the lesions was followed with the use of modified Nauta silver stains. Four additional cats were used as anatomic controls. Degenerating fibers were observed to descend bilaterally through the midbrain, pontine, and medullary tegmentum to the vicinity of the principal sensory and motor nuclei of the trigeminal nerve. There was, in addition, evidence of degenerating terminals within the nucleus of the facial nerve and the spinal nucleus of the trigeminal nerve. Of particular note was the observation that the degenerating fibers in the region of the nucleus of the spinal tract of the trigeminal nerve terminated in glomeruli in the rostral portion of the nucleus. Degenerating fibers ascending from the lesion were found to course along the medial forebrain bundle into the hypothalamus and the midline thalamus in a pattern very similar to that previously demonstrated after lesions of biting attack sites in the hypothalamus. The role that the neural pathways associated with ventral midbrain attack sites might play in the mediation of behavior patterns which are elicited during attack stimulation was discussed and it was concluded that the demonstrated neural pathway could provide a cogent explanation for some of the properties of centrally elicited attack behavior.

Affect↗

PubMed2001

Pitfalls in thoracoscopic sympathectomy: mechanisms for failure.

The technical ease of thoracoscopic sympathectomy has established this as the procedure of choice for upper-limb sympathectomy. Notwithstanding the invariable success of this procedure, those rare instances of unsuccessful sympathectomy are disconcerting to the surgeon. Unsuccessful sympathectomy manifests as persistent or recurrent sympathetic activity after a seemingly successful procedure. The causes of this phenomenon include misinterpretation of the sympathetic chain at thoracoscopy, regeneration of the sympathetic chain, and alternate neural pathways via the nerve of Kuntz. With the large numbers of sympathectomies being undertaken, the few instances of unsuccessful sympathectomy have prompted a review of this subject. Although alternate neural pathways may have little significance when a T2 ganglionectomy is undertaken, anatomic misinterpretation of the sympathetic chain is an important yet under-recognized cause of an unsuccessful sympathectomy. Sympathetic nerve regeneration remains extremely uncommon. Persistent and recurrent sympathetic activity may be successfully managed by resympathectomy performed thoracoscopically.

Adolescent↗