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PubMedDate not supplied

Neurotrophic factors and Alzheimer's disease.

Defects in essential trophic interactions represent one possible explanation for the systems degenerations that occur in Alzheimer's as well as other neurodegenerative diseases. Since a multiplicity of neural pathways are affected in Alzheimer's disease, it is likely that more than one neurotrophic factor may be implicated. Through modern approaches in cell and molecular biology, it may be possible to identify such factors and to more precisely study their role in both sustaining neural connections, and in diseases involving those connections.

Alzheimer Disease↗

PubMed1980

Clinical use of vibratory stimuli to evaluate peripheral nerve injury and compression neuropathy.

The classical approach to evaluating the hand with impaired sensibility is unsatisfactory and frequently incorrect. Since the perception of vibratory stimuli is mediated through the same neural pathways as moving touch, we investigated the clinical use of the tuning fork in 101 patients with peripheral nerve injury and compression neuropathy. In potential nerve lacerations, the preoperative tuning fork evaluations accurately predicted the intraoperative findings: diminished perception of vibratory stimuli correlated with a neural conduction block, due usually to complete nerve division. Furthermore, this study suggests that diminished vibratory perception may be the earliest indication for surgical intervention in the acute compartment syndrome. We concluded that the clinical use of vibratory stimuli to evaluate peripheral nerve injury and compression neuropathy is valid, reliable, expeditious, and a test with high patient acceptability.

Adolescent↗

PubMed1989

Functional electrical stimulation: an overview.

The development of future neural prostheses involves much more than connecting commercially available stimulators to disabled individuals. Safe and effective operation of prostheses requires fundamental studies of the electrode-tissue interface. The electrochemistry of the interface must be controlled to prevent toxic byproducts. Histopathological studies of stimulated tissue are necessary to establish safe limits of stimulation and to determine mechanisms of neural damage when it does occur. Electrophysiological studies elucidate which neural pathways are excited and help in the design of more selective electrode arrays. Biomaterials are required that protect the implant from the hostile environment of the body. Presently available materials are being improved and totally new materials are being developed. One of the goals of neural prostheses developers is a nonhermetic packaging material that can be applied to miniature implants without appreciably increasing their size. The techniques used to make integrated circuits on silicone substrates are ideally suited to making ultraminiature electrodes with self-contained electronic signal processing. Both integrated circuit stimulating and recording electrodes are being designed and fabricated.

Biocompatible Materials↗

PubMed2001

The contribution of the vagus nerve in interleukin-1beta-induced fever is dependent on dose.

It has been suggested that proinflammatory cytokines communicate to the brain via a neural pathway involving activation of vagal afferents by interleukin-1beta (IL-1beta), in addition to blood-borne routes. In support, subdiaphragmatic vagotomy blocks IL-1beta-induced, brain-mediated responses such as fever. However, vagotomy has also been reported to be ineffective. Neural signaling would be expected to be especially important at low doses of cytokine, when local actions could occur, but only very small quantities of cytokine would become systemic. Here, we examined core body temperature after intraperitoneal injections of three doses of recombinat human IL-1beta (rh-IL-1beta). Subdiaphragmatic vagotomy completely blocked the fever produced by 0.1 microg/kg, only partially blocked the fever produced by 0.5 microg/kg, and had no effect at all on the fever that followed 1.0 microg/kg rh-IL-1beta. Blood levels of rh-IL-1beta did not become greater than normal basal levels of endogenous rat IL-beta until the 0.5-microg/kg dose nor was IL-1beta induced in the pituitary until this dose. These results suggest that low doses of intraperitoneal IL-1beta induce fever via a vagal route and that dose may account for some of the discrepancies in the literature.

Animals↗

PubMed2006

The function of proprioceptors in bone organization: a possible explanation for neurogenic heterotopic ossification in patients with neurological damage.

Neurogenic heterotopic ossification is characterized by the formation of extra osseous bone in soft tissue surrounding peripheral joints in neurological patients. It occurs in 25% of spinal cord injury patients, and in 20% of these the pathologic process is severe enough to cause limitations in joint motion. Vascular and metabolic changes resulting from autonomic nervous system impairment may play a role in the etiology of heterotopic ossification. Repetitive vigorous passive manipulation of the joint to preserve range of motion, in the presence of reduced defense mechanisms, may also traumatize soft tissue, thereby initiating the pathological process. Nerve terminals within ligaments and capsules that allow for proprioception have a determinant role in triggering on and off muscle contraction, permitting acceleration and deceleration during gait. The Sarah Network of Rehabilitation Hospitals has treated over 20,000 patients with spinal cord and brain injury in the past 20 years. Based on the observation of heterotopic ossification development in some of these patients, and its tendency to relapse, this present article speculates whether, after an interruption in the neural pathways: (1) altered proprioception can forge a different relationship between tissues; and (2) chaotic new bone formation can occur. We postulate that heterotopic ossification in patients with injury to the central nervous system (CNS) may be related to a dysfunction of proprioception. With interruption of the neural tract of a given limb, ligaments lose control and coordination of their proprioceptive function and begin to react to direct stimulus in an independent, isolated and haphazard way. Free of CNS control and directly stimulated by such independent signals, mesenchymal osteoprogenitor cells located in soft tissues begin to occasion tissue maturation and differentiation into bone: heterotopic bone.

Bone and Bones↗

PubMed2003

Anatomical and functional evidence for a stress-responsive, monoamine-accumulating area in the dorsomedial hypothalamus of adult rat brain.

The dorsomedial hypothalamus (DMH) plays an important role in relaying information to neural pathways mediating neuroendocrine, autonomic, and behavioral responses to stress. Evidence suggests that the DMH is a structurally and functionally diverse integrative structure that contributes to both facilitation and inhibition of the hypothalamo-pituitary-adrenal axis, depending on the nature of the stimulus and the specific neural circuits involved. Previous studies have determined that stress or stress-related stimuli elevate tissue concentrations of serotonin (5-hydroxytryptamine; 5-HT), 5-hydroxyindoleacetic acid (5-HIAA), dopamine, and noradrenaline selectively within the DMH. In order to determine the specific region of the rat DMH involved, we used high-performance liquid chromatography with electrochemical detection to measure tissue concentrations of 5-HT, 5-HIAA, dopamine, and noradrenaline within five different subregions of the DMH in adult female Lewis and Fischer rats immediately or 4 h following a 30-min period of restraint stress. Compared to unrestrained control rats, restrained rats had elevated concentrations of 5-HT, 5-HIAA, dopamine, and noradrenaline immediately after a 30-min period of restraint and had elevated concentrations of 5-HT 4 h following the onset of a 30-min period of restraint stress. These effects were confined to a specific region that included medial portions of the dorsal hypothalamic area and dorsal ependymal, subependymal, and neuronal components of the periventricular nucleus. Furthermore, these effects were observed in Lewis rats, but not Fischer rats, two closely related rat strains with well-documented differences in neurochemical, neuroendocrine, autonomic, and behavioral responses to stress. These data provide support for the existence of a stress-responsive, amine-accumulating area in the DMH that may play an important role in the differential stress responsiveness of Lewis and Fischer rats.

Age Factors↗

PubMed1986

Pharmacological and anatomical analysis of fear conditioning using the fear-potentiated startle paradigm.

Pharmacological and anatomical analysis of fear conditioning using the fear-potentiated startle paradigm are reviewed. This test 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 a shock. This paradigm offers a number of advantages as an alternative to most animal tests of fear or anxiety because it involves no operant and is reflected by an enhancement rather than a suppression of ongoing behavior. Fear-potentiated startle is selectively decreased by drugs such as diazepam, morphine, and buspirone that reduce fear or anxiety clinically. Electrical stimulation techniques suggest that a visual conditioned stimulus ultimately alters acoustic startle at a specific point along the acoustic startle pathway. Relevant visual structures implicated in potentiated startle include the lateral geniculate nucleus, visual cortex, and deep and intermediate layers of the superior colliculus. The central nucleus of the amygdala and the caudal branch of the ventral amygdalofugal pathway projecting to or through the substantia nigra are also necessary for potentiated startle to occur. Electrical stimulation of the central nucleus of the amygdala markedly increases acoustic startle. By combining these behavioral, anatomical, physiological, and pharmacological approaches, it should soon be possible to determine each neural pathway that is required for a stimulus signaling fear to alter startle 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 so as to affect behavior.

Animals↗

PubMed2001

Sensory pathways and cyclooxygenase regulate mucus gel thickness in rat duodenum.

We previously showed that the duodenal hyperemic response to acid occurs through activation of capsaicin-sensitive afferent nerves with subsequent release of vasodilatory substances such as calcitonin gene-related peptide (CGRP) and nitric oxide. We then tested the hypothesis that similar factors regulate duodenal mucus gel thickness. Gel thickness was optically measured using in vivo microscopy in anesthetized rats. Duodenal mucosae were superfused with pH 7.0 buffer with vanilloid receptor agonist capsaicin, bradykinin, or PGE(2) injection or were challenged with pH 2.2 solution, with or without the vanilloid antagonist capsazepine, human CGRP-(8-37), N(G)-nitro-L-arginine methyl ester, and indomethacin. Other rats underwent sensory ablation with high-dose capsaicin pretreatment. Acid, bradykinin, capsaicin, and PGE(2) all quickly thickened the gel. Antagonism of vanilloid and CGRP receptors, inhibition of nitric oxide synthase, and sensory deafferentation delayed gel thickening, suggesting that the capsaicin pathway mediated the initial burst of mucus secretion that thickened the gel. Indomethacin abolished gel thickening due to acid, bradykinin, and capsaicin. Inhibition of gel thickening by indomethacin in response to multiple agonists suggests that cyclooxygenase activity is essential for duodenal gel thickness regulation. Duodenal afferent neural pathways play an important role in the modulation of cyclooxygenase-mediated physiological control of gel thickness.

Animals↗

PubMed1989

The effect on motion sickness and oculomotor function of GR 38032F, a 5-HT3-receptor antagonist with anti-emetic properties.

1. The 5-hydroxytryptamine (5-HT3) receptor antagonist, GR 38032F, which possesses potent anti-emetic properties in vomiting induced by cancer chemotherapeutic drugs, has been tested to determine its value in the prophylaxis of motion sickness induced by cross-coupled stimulation. The double-blind trial compared GR 38032F with both a placebo (lactose) and with hyoscine. In addition, studies of ocular pursuit and saccadic eye movements were carried out following the administration of each drug. 2. The prophylactic effect of GR 38032F on motion-induced nausea was indistinguishable from that of placebo, whereas following hyoscine subjects showed a highly significant (P less than 0.001) increase in tolerance to cross-coupled stimulation. Tests of oculomotor function showed no effect on saccadic eye movement from either drug. However, both drugs produced a significant (P less than 0.05) though small reduction in eye velocity gain during pursuit eye movement. 3. These findings suggest that the 5-HT3 receptor is not involved in the neural pathways that bring about motion sickness, but that it may have a role in the control of ocular pursuit. The absence of an anti-motion sickness effect from a drug that is effective in the treatment of vomiting induced by cancer chemotherapy serves to emphasize that different neural mechanisms are involved in the generation of motion sickness.

Adolescent↗

PubMed2003

Comparative analysis of neurogenesis in the myriapod Glomeris marginata (Diplopoda) suggests more similarities to chelicerates than to insects.

Molecular data suggest that myriapods are a basal arthropod group and may even be the sister group of chelicerates. To find morphological indications for this relationship we have analysed neurogenesis in the myriapod Glomeris marginata (Diplopoda). We show here that groups of neural precursors, rather than single cells as in insects, invaginate from the ventral neuroectoderm in a manner similar to that in the spider: invaginating cell groups arise sequentially and at stereotyped positions in the ventral neuroectoderm of Glomeris, and all cells of the neurogenic region seem to enter the neural pathway. Furthermore, we have identified an achaete-scute, a Delta and a Notch homologue in GLOMERIS: The genes are expressed in a pattern similar to the spider homologues and show more sequence similarity to the chelicerates than to the insects. We conclude that the myriapod pattern of neural precursor formation is compatible with the possibility of a chelicerate-myriapod sister group relationship.

Amino Acid Sequence↗

PubMed1993

Cellular responses to chronic treatment with drugs of abuse.

This review focuses on the long-term adaptations opiates and cocaine induce in specific regions of the nervous system that underlie the additive actions of the drugs, and the mechanisms by which such adaptations are achieved. To date, opiate and cocaine regulation of post-receptor, intracellular messenger pathways has shed considerable light on the mechanisms underlying chronic drug action. Of particular interest is the up-regulation of the cyclic AMP pathway observed in the locus coeruleus (LC), a brain region involved in physical opiate addition, in response to chronic opiate administration. Up-regulation of the cyclic AMP pathway has been shown to contribute to the opiate tolerance, dependence, and withdrawal exhibited by these neurons electrophysiologically. A similar up-regulation of the cyclic AMP pathway in response to chronic opiate and chronic cocaine treatments has been observed in the mesolimbic dopamine system, which is implicated in the psychological aspects of drug addiction. Several lines of evidence suggest the possibility that these biochemical adaptations may contribute to opiate and cocaine regulation of this neural pathway. Related studies in inbred rat strains raise the additional possibility that similar adaptations may contribute to individual genetic vulnerability to drug addition. Current studies are aimed at investigating opiate and cocaine regulation of transcription factors in these discrete brain regions to identify the molecular mechanisms involved in drug action. The investigations have focused on the Fos-Jun family of immediate early gene transcription factors, and the CREB family of transcription factors, as possible mediators of the effects of chronic opiate and cocaine exposure on regulation of neuronal gene expression. Ultimately, more direct analyses are needed that make use of methods for detecting changes in target gene expression in vivo. Together, these studies of opiate and cocaine action will help define the precise mechanisms, at the molecular level, by which these drugs of abuse alter the expression of specific genes in particular neuronal cell types and thereby produce physical and psychological aspects of drug addition.

Adaptation, Physiological↗

PubMed1981

Mechanism of histamine-induced excitation of the cat pylorus.

Intravenous histamine causes high amplitude repetitive phasic contractions of the in vivo cat pylorus but has little effect on the antrum and duodenum. The genesis of this phasic response was studied using a pinned perfused catheter with openings at the pylorus, antrum, and duodenum. 2-Pyridylethylamine, an H1 agonist, produced phasic contractions similar to histamine whereas dimaprit, an H2 agonist, did not. Conversely, histamine-induced excitation is competitively antagonized by the H1 inhibitor diphenhydramine but not by the H2 inhibitor cimetidine. Thus histamine excitation is mediated through H1 receptor stimulation. Tetrodotoxin caused inhibition of the histamine response indicating that pyloric excitation is partly mediated through a neural pathway. To identify the nature of this pathway adrenergic and cholinergic blockers were used. Atropine, hexamethonium, and propranolol had no effect on the histamine response. Phentolamine and reserpine increased the magnitude of the histamine response. Conversely, phenylephrine blocked the histamine response. We conclude: histamine induces high phasic contractions in the pylorus; this effect is mediated through neural (nonadrenergic noncholinergic) and myogenic H1 receptors; alpha adrenergic stimulation inhibits the histamine response and alpha adrenergic blockade and catecholamine depletion increase it.

Animals↗

PubMed1994

The role of pineal gland in circadian rhythms regulation.

In the presented article we try to find a synthesis of the current knowledge on circadian rhythms. We pick up the most prominent oscillations in human physiology and review the current knowledge of their regulation. Circadian oscillations in the parameters of internal environment are driven by the pineal gland. A biochemical pathway in the pineal transforms tryptophan through serotonin to the final product--the indolamine melatonin. Its plasma level is high at night and low during the day. Melatonin, easily penetrating through biological barriers, thus carries phase of day information to all peripheral tissues. Light exposure of retina alters (via neural pathways connecting retina to pineal gland) the amount of serotonin metabolized to melatonin. This physiological mechanism of adjustment of the endogenous clock to the solar day can be altered in some circumstances, leading to pathologic symptoms. The best known diseases caused by breakdown in circadian regulation are seasonal affective disorders and jet-lag syndrome. (Fig. 2, Ref. 71.)

Circadian Rhythm↗

PubMed1976

Inhibition and facilitation of antidromically identified tubero-infundibular neurones following stimulation of the median eminence in the rat.

1. Stimulation of the median eminence of female rats inhibited the spontaneous firing of antidromically identified tubero-infundibular units. Some units could be inhibited by stimuli subthreshold for the antidromic spike. A conditioning stimulus of subthreshold intensity for the antidromic spike also delayed or abolished the invasion of the soma and dendrites of the same unit by antidromic action potentials evoked by a suprathreshold stimulus given 2-10 msec later. 2. Although strychnine (0-2 mg/kg, i.v.) did not significantly alter the inhibition evoked by stimulation of the median eminence, it was abolished by picrotoxin (2-6 mg/kg, iv.). 3. In seven of the fifty-seven identified units examined stimulation of the median eminence facilitated the spontaneous firing. However, after an i.v. injection of picrotoxin the facilitory response was observed in thirty-seven of the forty-six units tested. Post-stimulus time histograms obtained from the same unit before and after an injection of picrotoxin demonstrated that the latency and duration of the facilitation did not always coincide with that of the inhibition. 4. After an injection of picrotoxin the field potential evoked by antidromic stimulation of the median eminence consisted of a small positive wave followed by a negative wave. Frequently the negative wave of the field potential was accompanied by a convulsive discharge. The latency of the negative wave appears to be identical to that of the facilitation seen in nearby single units. 5. The facilitation evoked by antidromic stimulation in the presence of picrotoxin was blocked by an i.v. injection of alpha-methyl-p-tyrosine (250 or 375 mg/kg). None of the nine units sampled from rats pre-treated with alpha-methyl-p-tyrosine injected twice I.P. (250 mg/kg for each) were facilitated by stimulation of the median eminence following I.V. picrotoxin, while eight of the eleven units sampled from control rats pre-treated with L-tyrosine could be facilitated by antidromic stimulation. 6. These results suggest that tuber-infundibular neurosecretory neurones are inhibited and facilitated by neural pathways which could involve the axon collaterals of the neruosecretory neurones which project to the external layer of the median eminence. It is also suggested that GABA-releasing neurones mediate the inhibition and catecholaminergic neurones are involved in the facilitory pathways. Presumably the facilitation is normally masked by the activity of the GABA-releasing neurones.

Animals↗

PubMed1977

The role of local cholinergic pathways in the motor response to cholecystokinin and gastrin in isolated guinea-pig fundus and antrum.

Both cholecystokinin (CCK-PZ) and gastrin stimulated antral rhythmic activity and raised fundal basal pressure. The antral motor effects were significantly blocked by pretreatment with atropine or tetrodotoxin. The fundal motor responses were almost unaffected. It is concluded that CCK-PZ and gastrin exert their antral motor effects essentially through local cholinergic neural pathways, while the motor responses in the fundus are almost entirely independent of these pathways.

Animals↗

PubMed2006

Arousing properties of the vulvar epithelium.

PURPOSE: The initiation of genital tactile stimulation is regarded as a precursor to sexual arousal and perhaps in women it is the most easily recognized initiator of central nervous system arousal. Unfortunately little published material details the specific mechanisms preceding arousal, beginning at the epithelial level, which are the sensory precursors to arousal. Little is known about its cutaneous receptors, nerves and the other histochemical properties of this epithelial tissue that contribute to sexual arousal. Sexual sensitivity evaluations target female genital somatosensory pathways for cutaneous sensation by testing evoked potentials of nerves, hot/cold and vibratory sensory discrimination. The anatomical bases of these several sensibilities form a subject for future investigation. We reviewed the known influences and mechanisms responsible for the arousing properties of the epithelium in the female external genitalia as well neural pathways associated with sexual arousal originating from the vulvar epithelium. MATERIALS AND METHODS: A comprehensive review was done of published, relevant clinical and histological material in human and nonhuman vertebrate studies. RESULTS: Tactile stimulation of the vulvar epithelium initiates changes suggesting complex integrative mechanisms. Influences of skin temperature, hormonal environment, mechanical tissue compliance and inflammation as well as the large number of transmitters and neuropeptides involved in peripheral pathways serving female sexual arousal speak of a direct sensory role. CONCLUSIONS: Genital epithelial cells may actively participate in sensory function to initiate sexual arousal by expressing receptors and releasing neurotransmitters in response to stimuli, resulting in epithelial-neuronal interactions.

Animals↗

PubMed2002

Fluid and electrolyte transport in the small intestine.

The small intestine is in a dynamic state of secretion and absorption, the sum of which results in net absorption. Secretion is principally the result of chloride and bicarbonate extrusion through apical chloride channels after the activation of the second messengers cAMP, cGMP, and calcium. In addition to the cystic fibrosis transmembrane conductance regulator, several other candidate chloride channels have been identified and proposed to play a role in intestinal secretion, including the calcium-dependent chloride channel hCLCA1. Pathways leading to the negative control of secretion have been described that use cellular messengers, including inositol (3,4,5,6) tetrakisphosphate and phosphatidylinositol 3-kinase, which may act via basolateral potassium channels. The control of ion transport can also be viewed in terms of the enteric nervous system. The reflex neural pathways involved in enterotoxin-induced secretion have been substantiated and shown to involve 5-hydroxytryptamine, substance P, and the neurokinin 1 and 2 receptors in the sensory arm, and vasoactive intestinal peptide in the secretomotor efferents. Absorption of glucose in addition to active cotransport with sodium via the Na/glucose cotransporter protein has also been shown to occur passively through a carrier-mediated mechanism, using the membrane protein glucose transporter protein 2.

Journal Article↗

PubMed1982

Optokinetic nystagmus: a review of pathways, techniques and selected diagnostic applications.

There are a myriad of conditions producing abnormal OKN responses. In most of these conditions the diagnosis can be made without recourse to OKN. However, in the five conditions described in this paper (suspected poor visual acuity in infants and young children, parietal lesions, subclinical internuclear ophthalmoplegia, Parinaud's syndrome, and aberrant regeneration of the third nerve) OKN can greatly facilitate the diagnosis. A review of the neural pathways of the OKN response and an explanation of the various equipment and techniques used to assess OKN are included.

Brain Diseases↗