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At least 973 records · Page 54Linked to original sources

PubMed1996

A neural precursor cell line derived from murine teratocarcinoma.

A cell line NT with phenotypic features of neural precursor cells has been established from an embryo-derived teratocarcinoma in Swiss mouse where, on serial transplantation, the developmental potential becomes restricted to neural pathway. All the cells are positive for nestin (a marker of neuroepithelial stem cells). Many of them are also positive for NFP and/or GFAP. Moreover there is a gradual decrease from 75% to 50% in reactivity for alkaline phosphatase, a marker for EC cells with repeated passages. The bipotential nature, and the probable decline of EC cells suggest that NT is a neural precursor cell line. The cells have doubling time of 12 h with a plating efficiency of 50%. The cells form colonies in soft agar within 7 days and tumorigenicity in syngeneic mice is lost after 70th passage. However, after 70 passages cells do form tumors in nude mice within 5 days and these tumors exhibit better differentiated morphology than the tumors in syngeneic mice. All the other characteristics remain stable. The myc and ras family of oncogenes do not show any alterations in early or late passages. This cell line may therefore be considered as a differentiated cell line derived from teratocarcinoma.

Alkaline Phosphatase↗

PubMed2005

The control of voluntary eye movements: new perspectives.

Primates use two types of voluntary eye movements to track objects of interest: pursuit and saccades. Traditionally, these two eye movements have been viewed as distinct systems that are driven automatically by low-level visual inputs. However, two sets of findings argue for a new perspective on the control of voluntary eye movements. First, recent experiments have shown that pursuit and saccades are not controlled by entirely different neural pathways but are controlled by similar networks of cortical and subcortical regions and, in some cases, by the same neurons. Second, pursuit and saccades are not automatic responses to retinal inputs but are regulated by a process of target selection that involves a basic form of decision making. The selection process itself is guided by a variety of complex processes, including attention, perception, memory, and expectation. Together, these findings indicate that pursuit and saccades share a similar functional architecture. These points of similarity may hold the key for understanding how neural circuits negotiate the links between the many higher order functions that can influence behavior and the singular and coordinated motor actions that follow.

Animals↗

PubMed1998

Regeneration in the central nervous system: pharmacological intervention, xenotransplantation, and stem cell transplantation.

The factors inhibiting regeneration in the central nervous system (CNS) have been elaborated, debated, and studied for the past 70 years. Recent work has pointed to the fine balance that exists between repair and regeneration following CNS injury. Growth factors have featured prominently in this debate. In attempts to tip the scales toward regeneration and functional reconnection to damaged neurons, pharmacological intervention has come to the fore. However, a perennial concern has been that much of regeneration may be aberrant, although there is now evidence to suggest that this fear may have been exaggerated. In searching for additional avenues for achieving therapeutic reconstruction of damaged neural pathways, transplantation studies occupy a prominent place in the literature. Various principles have become established, and these have proved relevant for all approaches utilizing grafts. Xenotransplantation and stem cell transplantation are approaches with exciting potential. Circuitry can be effectively restored by xenotransplantation, including early indications of integration of pig dopaminergic neurons in Parkinson's disease. The considerable possibilities offered by the differentiation of neural stem cells into progenitor cells and then into neurons and glia are explored.

Animals↗

PubMed1994

Olfactory ensheathing glia and platelet-derived growth factor B-chain reactivity in the transplanted rat olfactory bulb.

Using a monoclonal antibody against the B-chain of platelet-derived growth factor as a marker, we have examined the behavior of olfactory ensheathing glia in the normal and transplanted rat olfactory bulb. In the normal postnatal olfactory bulb, these glia are found to ensheath the bundles of incoming primary olfactory nerve fibers as well as those in the olfactory nerve layer. Olfactory marker protein antibody was used to identify the olfactory nerve proper. Within the transplant, the same glia: (1) ensheath bundles of both primary olfactory and non-primary olfactory axons, (2) ensheath axonal bundles deep within the donor tissue, and (3) eventually permit radiation of individual axons from bundles to surrounding neuropil. We believe that ensheathing glia (being rich in growth-related factors and extracellular matrix molecules) may be useful in providing trophic support and guidance for the reconstruction of developmentally or traumatically damaged neuronal pathways not directly related to the olfactory system. The evidence presented here indicates that ensheathing glia are capable of existing in deep brain areas and ensheathing other than primary olfactory axons. The special molecular characteristics of these glia along with the morphological findings presented here provide a foundation for further studies of these unique glia and their potential utility in the restoration of damaged neural pathways.

Animals↗

PubMed2006

Potent in vivo antinociception and opioid receptor preference of the novel analogue [Dmt1]endomorphin-1.

[Dmt1]Endomorphin-1 is a novel analogue of the potent mu-opioid agonist endomorphin-1. Given the physiological role of endomorphin-1 in vivo, this compound was investigated to determine if the antinociception occurred through systemic, supraspinal or in a combination of both neuronal pathways. This compound exhibited a potent dose-dependent effect intracerebroventricularly in both spinal and supraspinal regions, and was blocked by opioid antagonist naloxone, which verified the involvement of opioid receptors. Specific opioid antagonists characterized the apparent receptor type: beta-funaltrexamine (mu1/mu2-irreversible antagonist) equally inhibited spinal- and central-mediated antinociception; on the other hand, naloxonazine (mu1-subtype) was ineffective in both neural pathways and naltrindole (delta-selective antagonist) partially (26%), though not significantly, blocked only the spinal-mediated antinociception. Therefore, spinal antinociception was primarily triggered by mu2-subtypes without involvement of mu1-opioid receptors; however, although a slight enhancement of antinociception by delta-receptors cannot be completely ruled out since functional bioactivity indicated mixed mu-agonism/delta-antagonism. In terms of the CNS action, [Dmt1]endomorphin-1 appears to act through mu2-opioid receptor subtypes.

Analgesia↗

PubMed2001

Anisocoria and middle cerebral artery saccular (berry) aneurysm in a rhesus macaque (Macaca mulatta).

A 27-year-old female rhesus macaque (Macaca mulatta) developed anisocoria. The left pupil was dilated and unresponsive to light. The macaque was euthanized because of unrelated reasons and the body was submitted for necropsy. On gross examination, a berry aneurysm of the right middle cerebral artery causing marked compression of the right optic tract was found. Arteriosclerotic changes were observed microscopically in the right middle cerebral and in the internal carotid arteries. The left iris was markedly degenerated, with atrophy of the constrictor muscle. Compression of the right optic tract may cause homonimus hemianopsia. A dilated and unresponsive left pupil indicated a lesion in the ipsilateral parasympathetic efferent pathway. In the absence of appreciable lesions of the left oculomotor nerve, the most likely cause of mydriasis was the iridic lesion. Intracranial aneurysms are common in humans (2 to 5%), but not in other species. Only about 10% of unruptured aneurysms are associated with neurologic deficits related to mechanical compression, such as visual deficits or anisocoria. Meticulous investigation of the ocular vascular and neural pathways led us to conclude that the anisocoria was unrelated to the aneurysm. To our knowledge, this report represents the first documented case of a naturally occurring intracranial aneurysm in nonhuman primates.

Animals↗

PubMed1989

The stress response to surgery: release mechanisms and the modifying effect of pain relief.

This short review updates information on the release mechanisms of the systemic response to surgical injury and the modifying effect of pain relief. Initiation of the response is primarily due to afferent nerve impulses combined with release of humoral substances (such as prostaglandins, kinins, leukotrienes, interleukin-1, and tumor necrosis factor), while amplification factors include semi-starvation, infection, and hemorrhage. The relative role of the various signals in producing the complex injury response has not been finally determined, but the neural pathway is probably most important in releasing the classical endocrine catabolic response, while humoral factors are important for the hyperthermic response, changes in coagulation and fibrinolysis immunofunction, and capillary permeability. The modifying effect of pain relief on the surgical stress response is dependent upon the technique of analgesia. However, the effect on humoral-mediated responses is small, regardless of the technique used. Afferent neural blockade with local anesthetics is the most effective technique for reducing the endocrine-metabolic response, but only in operations in the lower part of the abdomen, probably because of insufficient afferent blockade during thoracic epidural analgesia. Systemic opiate administration, as well as non-steroidal antiinflammatory drugs, exert only a small modifying effect on the response. Low-dose combined analgesic regimens may provide total pain relief, but exert no important effect on the stress response. In summary, pain alleviation itself may not necessarily lead to an important modification of the stress response, and a combined approach with inhibition of the neural and humoral release mechanisms is necessary for a pronounced inhibition or prevention of the response to surgical injury.

Analgesia↗

PubMed1999

Animal models of neuroimmune interactions in inflammatory diseases.

Animal models have been used successfully to study various aspects of neural-immune interactions. Although different approaches carry certain advantages and disadvantages, current high sensitivity screening and manipulation methods coupled with molecular and genetic approaches can be successfully used to tease out the neural pathways that regulate inflammatory disease and the effects of immune molecules, such as interleukins, on neuronal function and pathology. Newer methodologies that measure gene expression of thousands of genes will in the future add to the ability to evaluate complex systems interactions in whole animal models. This review addresses the advantages and disadvantages of some of these approaches in the context of application to neural-immune interactions.

Animals↗

PubMed2004

Anion size does not compromise sodium recognition by rats after acute sodium depletion.

Amiloride-insensitive sodium taste transduction is severely limited by large anions (i.e., gluconate). We found that in a brief-access taste test, sodium-depleted rats exhibited similar levels of increased licking to several sodium salts regardless of anion but did not increase licking to nonsodium salts compared with water. The enhanced licking of sodium salts was abolished in the presence of amiloride. These results suggest that the amiloride-sensitive taste transduction pathway is not only necessary but that it is also sufficient for sodium identification in rats. Sodium-depleted rats tested with amiloride initiated significantly more trials than nondepleted rats; hence, appetitive behavior was mildly potentiated by depletion, even in the absence of a sodium taste cue. Overall, these findings provide compelling support for the primacy of the amiloride-sensitive taste transduction mechanism and its associated neural pathway in the recognition of the sodium cation.

Animals↗

PubMed1998

Neuropeptides and asthma.

Although asthma is considered to be an inflammatory disease of the airways, neural mechanisms remain very important. Neural control of airways is far more complex than has been previously recognized. In addition to the classic neural pathways, the nonadrenergic, noncholinergic pathway has been described in the airways of animals and humans. Neuropeptides are present in sensory, parasympathetic, and sympathetic neurons in airways, and have been shown to have proinflammatory effects, such as increased mucus production, microvascular leakage, and smooth muscle contraction. Neuropeptides released from sensory nerves (eg, neurokinin A and substance P) mediate excitatory nonadrenergic, noncholinergic transmission, which causes bronchoconstriction and, possibly, bronchial hyperresponsiveness. Better understanding of neural mechanisms might provide a useful therapeutic approach in the future.

Animals↗

PubMed1999

Nitric oxide and target-organ control in the autonomic nervous system: anatomical distribution, spatiotemporal signaling, and neuroeffector maintenance.

Recent neuroanatomical studies, neurochemical coding and physiological findings of multiple cotransmitter actions and/or receptor patterns, and the characterization of synaptic molecules and nitrergic (NOergic) signaling mechanisms may help for a better understanding of target-organ control in the autonomic nervous system. Thus, nitric oxide (NO) synthase, which generates the freely diffusible and short-lived messenger NO and expression of neurotrophic proteins (e.g., neurotrophins, glial cell-line-derived neurotrophic factor, fibroblast growth factors) in autonomic neural pathways or target organs suggest unique actions in autonomic neurotransmission. In central NOergic pathways, NO may serve as spatial (volume) messenger within hierarchically ordered autonomic neuron pools and convergent/divergent pathways for synchronized autonomic outflow. Likewise, NO modulates intraganglionic and interaxonal transmission and postganglionic activity including long-term potentiation. In the visceral targets, NO appears to be a spatial modulator in local intrinsic networks or at varicose terminals. In endocrine glands, NO possibly acts as synaptic coactivator or inhibitor, as a cotransmitter affecting stimulus-coupled exocytosis, or as a local vasoactive signal. The short-term neural messenger NO may also induce diffusible target-derived long-term neurotrophic signals, thereby supporting neuroeffector maintenance and plasticity, if not synaptic efficacy, in autonomic target-organ control.

Animals↗

PubMed1996

Neuroeffector mechanisms: the interface between inflammation and neuronal responses.

There is a complex relation between inflammation and neural control of the airways. Cholinergic neurotransmission may be enhanced by inflammatory mediators; cholinergic nerves are the dominant neural pathway for bronchoconstriction in humans. Anticholinergic drugs are more effective in acute severe asthma than in chronic asthma, suggesting that cholinergic mechanisms may be important in exacerbations. Several possible abnormalities in adrenergic control in asthma have been proposed and may be caused by the inflammatory process. Adrenergic nerves do not have direct control of airway smooth muscle but may influence bronchomotor tone in several ways, such as adrenergic neural control of the bronchial vasculature or a secondary effect on cholinergic neurotransmission. Nonadrenergic noncholinergic (NANC) mechanisms mediate both bronchoconstriction and bronchodilation, and a defect in NANC bronchodilatation has been suggested to operate in severe asthma. Relatively little is known about the properties of airway sensory (afferent) nerves in human beings. They are thought to be involved in symptoms of cough and chest tightness, and the threshold for their activation is lowered in conditions of chronic inflammation. In addition, retrograde activation of sensory nerves by a local axon reflex, resulting in the release of peptides, may contribute to inflammation of the airways. Neurogenic inflammation is probably not relevant to mild asthma, however, but it may be more important in severe disease such as brittle asthma.

Animals↗

PubMed1988

Muscarinic M1 receptors stimulate a nonadrenergic noncholinergic inhibitory pathway in the isolated rat duodenum.

We examined the effect of the muscarinic agonist McN-A-343 (4-m-chlorophenylcarbamoyloxy-2-butynyl trimethyl ammonium) on in vitro preparations of rat small intestine. McN-A-343 (0.1-10 microM) induced a concentration-dependent relaxation of duodenum, jejunum and ileum. This effect was due to activation of muscarinic receptors of the M1 subtype, inasmuch as it was antagonized by atropine (pA2, 8.93) and by the selective M1 antagonists pirenzepine and dicyclomine with high affinity (pA2, 8.09 and 8.14, respectively). Tetrodotoxin, but not hexamethonium, abolished McN-A-343 relaxation indicating involvement of neural pathways and absence of nicotinic transmission. Moreover, in the presence of apamin (0.1 microM) McN-A-343 induced a contractile response. Unlike McN-A-343, acetylcholine contracted the rat duodenum; its concentration-response curve was significantly potentiated by tetrodotoxin, suggesting stimulation of the McN-A-343 sensitive receptor by acetylcholine (P less than .01). Prior treatment of animals with reserpine reduced the potency of McN-A-343 only by 2.5-fold. The gamma-aminobutyric acid (GABA) antagonist bicuculline inhibited McN-A-343 with an affinity comparable to that found for GABA(A) receptors (pA2, 5.52), indicating involvement of GABAergic fibers. ATP is also likely to play a role, as desensitization experiments showed that alpha-beta-methylene ATP induced a comparable decrease of both McN-A-343 and its own response. In contrast, desensitization induced by GABA occurred to a minor extent. Thus, in the rat duodenum, activation of an M1 muscarinic receptor induces relaxation by releasing GABA, and possibly ATP, from myenteric neurons.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed2001

Inhibition of gastric emptying and small intestinal transit by ethanol is mediated by capsaicin-sensitive afferent nerves.

The neural mechanisms involved in mediation of the inhibitory effects of ethanol on the gastric emptying and the small intestinal transit were studied in adult male rats. The gastrointestinal transit was determined by measuring the amount of phenol red recovered from the stomach and small intestine after intragastric administration. Spinal and/or vagal peptidergic afferent nerves were subjected to selective denervation by chemodenervation techniques using capsaicin, a potent and specific sensory neurotoxin. Intragastric administration of a 2.5 g/kg body weight dose of ethanol resulted in inhibition of the gastric emptying and the small intestinal transit. Prior systemic treatment with capsaicin, which defunctionalizes both spinal and vagal capsaicin-sensitive afferent nerves, abolished the inhibitory effect of ethanol on the gastrointestinal transit. Similarly, selective chemodenervation of the vagal afferents by perineural capsaicin treatment completely blocked the effect of ethanol. These observations furnish evidence indicative of the involvement of capsaicin-sensitive neural pathways, and in particular vagal afferent nerves, in the mediation of the inhibitory effect of large doses of ethanol on the gastrointestinal motility.

Animals↗

PubMedDate not supplied

Biogenic amines in the brain of the honeybee: cellular distribution, development, and behavioral functions.

This review provides a summary of the cellular distribution of amine-containing neurons and the organization of aminergic pathways in the brain and suboesophageal ganglion of the honeybee. Neurons synthesizing the biogenic amines serotonin, dopamine, octopamine, and histamine are stained with well-defined polyclonal antisera. Since some of these aminergic neurons are uniquely identifiable, it is possible to follow their morphogenesis during brain development. Pharmacological studies show that aminergic mechanisms are involved in various behavioral modifications including associative learning. The immunocytochemical approach resolves at a single cell level the neural pathways that mediate adaptive behavioral changes.

Adaptation, Physiological↗

PubMedDate not supplied

[Neurons that encode sound direction].

INTRODUCTION: In the auditory system, the inner ear breaks down complex signals into their spectral components, and encodes the amplitude and phase of each. In order to infer sound direction in space, a computation on each frequency component of the sound must be performed. DEVELOPMENT: Space specific neurons in the owl s inferior colliculus respond only to sounds coming from a particular direction and represent the results of this computation. The interaural time difference (ITD) and interaural level difference (ILD define the auditory space for the owl and are processed in separate neural pathways. The parallel pathways that process these cues merge in the external nucleus of the inferior colliculus where the space specific neurons are selective to combinations of ITD and ILD. How do inputs from the two sources interact to produce combination selectivity to ITD ILD pairs? A multiplication of postsynaptic potentials tuned to ITD and ILD can account for the subthreshold responses of these neurons to ITD ILD pairs. Examples of multiplication by neurons or neural circuits are scarce, but many computational models assume the existence of this basic operation. The owl s auditory system uses such operation to create a 2 dimensional map of auditory space. The map of space in the owl s auditory system shows important similarities with representations of space in the cerebral cortex and other sensory systems. In encoding space or other stimulus features, individual neurons appear to possess analogous functional properties related to the synthesis of high order receptive fields.

Auditory Perception↗

PubMed1975

Separate lateral hypothalamic pathways for extracellular and intracellular thirst.

Small lesions of the midlateral zone of the lateral hypothalamus in rats attentuated water intake elicted by the central microinjection angiotensin or by the peripheral injection of isoproterenol or renin without attenuating drinking to peripherally administered hypertonic saline. Lesions placed further lateral in the hypothalamus, which destroyed the medial aspects of the internal capsule and globus pallidus, produced a marked decrease in water intake induced by hypertonic saline. Abaltion of the ventromedial nucleus of the hypothalamus increased drinking elicited by angiotension, isoproterenol, or renin. These results suggest that extracellular and intracellular thirst stimuli are mediated by separate neural pathways at the level of the lateral hypothalamus.

Angiotensin II↗

PubMed1997

Neuronal activity in monkey superior colliculus related to the initiation of saccadic eye movements.

The introduction of a temporal gap between the disappearance of an initially fixated target and the appearance of an eccentric saccadic target results in a general reduction of saccadic reaction times (SRTs)-the gap effect-and often in the production of express saccades, the latencies of which approach the conduction time of the shortest neural pathways from the retina to the eye muscles. We investigated saccade initiation by recording neuronal activity in the superior colliculus in monkeys performing the gap paradigm. Fixation-related neurons reduced their discharge rate during the gap period, regardless of the SRT. This reduction in activity is consistent with the hypothesized release of ocular fixation that facilitates premotor processes and may contribute to the gap effect. In addition to saccade-related discharges, many saccade-related neurons displayed phasic target-related responses and/or low-frequency preparatory activity during the gap period. The level of this preparatory activity correlated with both SRT and express saccade occurrence when the saccade was made into the response field of the neuron. Evidence indicates that advanced motor preparation is required for express saccade generation, which may be subserved by specific increases in the preparatory activity of saccade-related neurons. Increased preparatory activity may allow the target-related responses to trigger short-latency express saccades directly. This study provides insights into the functional mechanism of saccade initiation and may be relevant to the generation of all voluntary motor responses.

Animals↗