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At least 19 recordsLinked to original sources
PubMed1997

Neurosteroids: of the nervous system, by the nervous system, for the nervous system.

Neurosteroids are synthesized in the central and peripheral nervous system, particularly but not exclusively in myelinating glial cells, from cholesterol or steroidal precursors imported from peripheral sources. They include 3 beta-hydroxy-delta 5-compounds, such as pregnenolone (PREG) and dehydroepiandrosterone (DHEA), their sulfates, and reduced metabolites such as the tetrahydroderivative of progesterone 3 alpha-hydroxy-5 alpha-pregnane-20-one (3 alpha,5 alpha-THPROG). These compounds can act as allosteric modulators of neurotransmitter receptors, such as GABAA, NMDA, and sigma receptors. Progesterone (PROG) is also a neurosteroid, and a progesterone receptor (PROG-R) has been identified in peripheral and central glial cells. At different places in the brain, neurosteroid concentrations vary according to environmental and behavioral circumstances, such as stress, sex recognition, or aggressiveness. A physiological function of neurosteroids in the central nervous system is strongly suggested by the role of hippocampal PREGS with respect to memory, observed in aging rats. In the peripheral nervous system, a role for PROG synthesized in Schwann cells has been demonstrated in the repair of myelin after cryolesion of the sciatic nerve in vivo and in cultures of dorsal root ganglia neurites. It may be important to study the effect of abnormal neurosteroid concentrations/metabolism with a view to the possible treatment of functional and trophic disturbances of the nervous system.

Animals↗
PubMed1997

Autonomic nervous dysfunction in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA): possible pathogenic role of autoantibodies to autonomic nervous structures.

Autonomic nervous dysfunction has been previously reported in SLE, RA and systemic sclerosis, but the pathogenesis of such a complication is poorly understood. In the present study, four standard cardiovascular autonomic function tests were performed in 34 female patients with connective tissue diseases and in 25 healthy control subjects, and results expressed as cardiovascular (CV) test scores. Moreover, in each subject the presence of circulating complement-fixing autoantibodies directed against sympathetic and parasympathetic nervous structures, represented by superior cervical ganglia and vagus nerve, respectively, was simultaneously assessed by an indirect immunofluorescent complement-fixation technique, using rabbit tissue as substrate. None of the patients reported autonomic symptoms. However, an abnormal CV test score (> or = 5) was detected in 15% of the patients and in none of the healthy control subjects, approaching statistical significance (P = 0.07). No correlation was found between CV test results and disease duration, type of therapy or presence of conventional autoantibodies. One or two autoantibodies to autonomic nervous structures were detected in six patients (18%) and not in the control subjects (P < 0.05). Values of deep breathing test were significantly lower in autoantibody-positive patients compared with those amongst the control subjects (P < 0.05), and an abnormal CV test score was significantly associated with the presence of autoantibodies to autonomic nervous structures (P < 0.05). In conclusion, we confirm that autonomic nervous function can be impaired in patients with connective tissue diseases, and suggest that autoantibodies directed against autonomic nervous system structures may play a role in the pathogenesis of the autonomic dysfunction.

Adolescent↗
PubMed2002

General pharmacological profile of the novel muscarinic receptor agonist SNI-2011, a drug for xerostomia in Sjögren's syndrome. 2nd communication: effects on somatic nervous system and on autonomic nervous system and smooth muscle.

A novel muscarinic receptor agonist SNI-2011 ((+/-)-cis-2-methylspirol[1,3-oxathiolane-5,3'-quinuclidine] monohydrochloride hemihydrate, cevimeline, CAS 153504-70-2), is a candidate therapeutic drug for xerostomia in Sjögren's syndrome. The general pharmacological properties of this drug on the somatic nervous system and on the autonomic nervous system and smooth muscle were investigated in mice, rats, guinea pigs, rabbits and cats. 1. Somatic nervous system: SNI-2011 had no effect on the neuromuscular junction in rats and no muscle relaxant effect in mice. No surface anesthetic effect was observed in guinea pigs, but infiltration anesthetic effect was found after intracutaneous injection of solution (1% or higher). 2. Autonomic nervous system and smooth muscle: SNI-2011 tended to cause mydriasis at 3 mg/kg i.v. or higher in rabbits and dose-dependently caused mydriasis at 10 mg/kg p.o. or higher in rats. Mydriasis in rats was also observed by ophthalmic instillation, caused via the peripheral muscarinic acetylcholine receptors. SNI-2011 elevated the base line tension of nictitating membrane in cats when it was injected intravenously at 3 mg/kg or higher. In the smooth muscle, SNI-2011 increased the spontaneous movement of isolated rabbit ileum (1 x 10(-6) mol/l or higher), contractions of isolated guinea pig ileum (1 x 10(-6) mol/l or higher) and isolated guinea pig trachea (3 x 10(-6) mol/l or higher). SNI-2011 relaxed the histamine- and noradrenaline-induced contractions of isolated guinea pig aorta and augmented noradrenaline- and phenylephrine-induced contractions of isolated rat vas deferens. These effects were induced by relatively higher concentrations only i.e. 1 x 10(-5) mol/l or higher. From these results, SNI-2011 has muscarinic side effects on the somatic nervous system and on the autonomic nervous system and smooth muscle, however, in the case of oral administration, that is clinical administration route, SNI-2011 caused no muscarinic side effect at the effective doses needed for saliva secretion.

Anesthetics↗
PubMed1995

Increased central nervous system monoamine neurotransmitter turnover and its association with sympathetic nervous activity in treated heart failure patients.

BACKGROUND: Congestive heart failure is a debilitating disease characterized by impaired cardiac function with accompanying activation of a variety of neural and hormonal counter-regulatory systems. Abnormal activity of the sympathetic nervous system and renin-angiotensin-aldosterone axis and a predisposition to the generation of fatal ventricular arrhythmias are often associated with the development of the disease. Although the underlying cause of sudden death in these patients remains to be unequivocally elucidated, abnormally increased cardiac sympathetic nervous activity may be involved. METHODS AND RESULTS: Twenty-two patients with severe congestive heart failure (New York Heart Association functional class III or IV with left ventricular ejection fraction of 18 +/- 1%) and 29 healthy male volunteers participated in this study. By combining direct sampling of internal jugular venous blood via a percutaneously placed catheter with a norepinephrine and epinephrine isotope dilution method for examining neuronal transmitter release, we were able to quantify the release of central nervous system monoamine and indoleamine neurotransmitters and investigate their association with the increased efferent sympathetic outflow that is variably present in treated patients with this condition. Mean cardiac norepinephrine spillover was 145% higher in treated heart failure patients than in healthy subjects (P < .05), with norepinephrine release from the heart in 6 of 22 patients being more than the highest control value. Raised internal jugular venous spillover of epinephrine (26 +/- 12 versus 2 +/- 4 pmol/min, P < .05) and of norepinephrine and its metabolites (2740 +/- 480 versus 875 +/- 338 pmol/min, P < .05), indicative of increased central nervous system turnover of both catecholamines, occurred in cardiac failure and was quantitatively linked to the degree of activation of the cardiac sympathetic nervous outflow, as was the jugular overflow of the principal serotonin metabolite, 5-hydroxyindoleacetic acid. CONCLUSIONS: An association between the degree of activation of central monoaminergic neurons and the level of sympathetic nervous tone in the heart was identified in treated patients with heart failure. Epinephrine neurons in the brain may contribute to the sympathoexcitation that is seen in this condition, with the activation of sympathoexcitatory noradrenergic neurons, most likely those of the forebrain, playing an accessory role.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

[Mutual interaction of vestibular afferent nervous system and vestibular efferent nervous system in vestibular compensation].

OBJECTIVE: To study the mutual interaction of vestibular afferent nervous system and vestibular efferent nervous system in vestibular compensation. METHODS: Build up animal model of vestibular compensation by destroying single side vestibule of wistar rat. In the study the rats were divided into 3 groups: Group A 16 normal rats; Group B 15 rats, after 7 days of left vestibular damage; Group C 7 rats 3 months after left vestibular damage; and Group D 7 rats, after vestibular compensation. Electromyography of the rats was recorded and the expression of calcitonin gene relative peptide (CGRP), choline acetyltransferase (AChT) and Na-K-ATPase were investigated in efferent vestibular nervous system. RESULTS: Electric potential activity of muscles of injury side decreased while that of the opposite side increased. In animals of vestibular compensation electric potential of bilateral musculus longus capitis at quiescent stage recovered symmetrically. CGRP positive cells of efferent vestibular nervous system increased bilaterally, and their activity enhanced, especially obvious at the acute stage. AChT positive cells of injury side of efferent vestibular nervous system decreased, but reaction degree of two sides enhanced. Reaction degree of the opposite side enhanced obviously at the stage of vestibular compensation. Expression of Na-K-ATPase mRNA of the same side was lower, but vestibular signal of the opposite side enhanced, clinically head and neck inclined obliquely by means of medial fasciculus of tractus vestibulospinalis. Months later, vestibular signal of the same side enhanced, and that of the opposite side enhanced also, clinical symptoms improved slightly. At the vestibular compensation stage, expression of Na-K-ATPase mRNA of the same side enhanced, and it was same as that of the opposite side or much higher, clinically it reached vestibular compensation. CONCLUSION: Comprehensive effect of the above results maybe as follows: Efferent vestibular nervous system inhibited afferent signal of the opposite vestibule, and it modulated excitement of vestibular center of the same side, and it worked in the complicated mechanisms of vestibular compensation. CGRP may have facilitation function to the vestibular afferent signal of injury side. While Ach improved vestibule compensation by means of inhibition of vestibule excitement of the healthy side.

Afferent Pathways↗
PubMed2003

Gene transfer to the nervous system: prospects for novel treatments directed at diseases of the aging nervous system.

In the past 3 decades, gene therapy has moved from a theoretical construct to an active field of basic research, animal studies, and clinical trials. In this article, we describe the conceptual basis underlying the use of gene therapy for diseases of the aging nervous system, the principal techniques used for gene delivery, and review preclinical animal studies in 4 different classes of neurologic dysfunction: 1) focal neuronal degeneration in the central nervous system; 2) global neuronal dysfunction in the central nervous system; 3) degenerative disease affecting components of the peripheral nervous system; and 4) intractable focal pain. The full potential of this approach will not be established until the human trials are completed.

Aging↗
PubMed1979

Immunocytochemical localization of rat peripheral nervous system myelin proteins: P2 protein is not a component of all peripheral nervous system myelin sheaths.

Specific antibodies have been developed against P1, P2, and P0 myelin proteins and were used to study the localization of these proteins in the rat peripheral nervous system. Both peripheral and central nervous system myelin sheaths contain P1 protein. P0 and P2 proteins are found exclusively in peripheral nervous system myelin sheaths. Antisera to P1 and P0 proteins stain all peripheral nervous system myelin sheaths uniformly. P2 protein is not a component of all peripheral nervous system myelin sheaths. In sheaths that do contain P2 protein, it is concentrated in the area of the Schmidt-Lanterman incisures.

Animals↗
PubMed1997

Apoptosis in development and disease of the nervous system: 1. Naturally occurring cell death in the developing nervous system.

In recent years, apoptosis, the process by which cells orchestrate their own demise, has been the subject of increasingly intense investigation, both from the stand-point of basic mechanisms of signal transduction and with regard to its role in normal and pathological processes in the nervous system. For the neurologist, an understanding of the mechanisms by which apoptosis determines at a cellular level the normal form of the nervous system, an appreciation of how both unchecked apoptosis and failure of enactment of the apoptotic pathway contribute to nervous system pathology and a sense of how both induction and inhibition of apoptosis can be exploited therapeutically are critical to applying the basic knowledge in this field to human disease. Early studies made it clear that substances produced by the target tissue influenced the survival of developing neurons. More recent investigations have demonstrated that they do so by influencing the production of a series of endogenous mediators and modulators of neuronal survival. Furthermore, it is evident that apoptosis is important for the development of both neuronal and non-neuronal cells in the peripheral and central nervous systems.

Animals↗
PubMed1988

The nervous system of the male Dinophilus gyrociliatus (Polychaeta, Dinophilidae): II. Electron microscopical reconstruction of nervous anatomy and effector cells.

All neuronal cells in the dwarf male of the dimorphic polychaete species Dinophilus gyrociliatus were individually identified by means of serial ultrathin sections. Altogether 68 neural cells--including 40 sensory neurons and 2 glial cells--constitute a small but complex nervous system. Fifty-three neural cells are located in three pairs of ganglia and connected by paired nerve cords. The prominent frontal ganglia, each consisting of a well-developed neuropile and surrounded by 20 or 21 neural cells, represent the animal's brain. The ventral ganglia contain only 2 neurons each. The penis ganglia--four cells each--are associated with the copulatory organ. A conspicuous circumpenial fiber mass surrounds the basal part of the penis. The effector cells--22 multiciliated epidermal cells, 34 muscle cells, and different gland cells (?)--were also reconstructed and their innervation was partly elucidated. Sensory-motor neurons were unambiguously identified. They are discussed in regard to the small body size of the animal. The male's nervous organization resembles a very simple rope ladder and may represent a reduced derivative of a nervous system in normal-sized males of monomorphic species. Similarities, however, also occur with the developing nervous system of a planktotrophic metatrochophore. The neuronal organization, with its two centers (frontal ganglia and ventral ganglia vs. penis ganglia and circumpenial fiber mass), accords well with the bipartite behavioral pattern, which is entirely devoted to locomotion and copulation, respectively.

Animals↗
PubMed1987

The nervous system of Diplostomum pseudospathaceum Niewiadomska, 1984 (Trematoda, Diplostomatidae). III. Structure of the nervous system in the adult stage.

The nervous system of adult Diplostomum pseudospathaceum Niewiadomska, 1984 was studied using Koelle's (1951) method for revealing cholinesterase activity. The nervous system in the fore body grows but its pattern remains the same as in the metacercaria: three pairs of stems connected by numerous commissures and differentiated innervation of various organs in this part of the body. In the elongated hind body the nervous system develops according to another pattern: two pairs of stems connected by a number of commissures form a loose net surrounding the whole segment. The net is more dense at the body end around the genital opening and copulatory organs. A brief discussion of the development of the nervous system of D. pseudospathaceum from cercaria to adult stage is given.

Animals↗
PubMed1988

Immunohistochemical detection of GTP-binding regulatory protein (Go) in the autonomic nervous system including the enteric nervous system, superior cervical ganglion and adrenal medulla.

The localization of a GTP-binding regulatory protein, Go, in the autonomic nervous system including the enteric nervous system, superior cervical ganglion, and adrenal medulla, has been immunohistochemically examined by use of affinity-purified antibody against the alpha-subunit of Go. In the small intestine, dense Go-immunoreactive products were localized on the enteric nervous system, i.e. the myenteric plexus of Auerbach and the submucosal plexus of Meissner. In the superior cervical ganglion, presynaptic terminals were strongly immunoreactive to the Go antibody. The adrenal medulla was stained with this antibody, but the adrenal cortex was not immunoreactive to this antibody. Thus, the present study strongly suggests that Go is localized in the autonomic nervous system and plays its role in transmembrane signal transmission in this system.

Adrenal Medulla↗
PubMed1984

[Effects of ritodrine hydrochloride on motor nervous system and central nervous system].

Pharmacological effects of ritodrine hydrochloride (ritodrine), a beta 2-adrenoceptor agonist, were investigated in comparison with that of isoxsuprine hydrochloride (isoxsuprine) on the motor nervous system and the central nervous system. Ritodrine (1-30 mg/kg, i.v.) suppressed spontaneous movements in mice, rats and dogs. The animals became slightly sedative and immobile. Ritodrine caused an increase of water intake and vomitting in dogs. These fingings were recovered in 3-5 hr. Isoxsuprine showed similar effects on general behaviour, but the depressive action was more potent than that of ritodrine. Ritodrine slightly suppressed exploratory behaviour in high dose, but had little effect on emotional behaviour. Ritodrine had no effects on conditioned avoidance response, tremor, motor coordination, thiopental induced sleeping time and few types of convulsions. Ritodrine showed no analgetic effects or muscle relaxant actions. Isoxsuprine, in high dose, suppressed motor coordination and showed ataxia. Ritodrine slightly raised body temperature and dose-dependently suppressed hypothermia and ptosis induced by reserpine. Ritodrine (1-10 mg/kg, i.v.) caused a slight resting pattern of spontaneous EEG in rabbits. On the other hand, arousal responses evoked by auditory stimulation, photic stimulation or electrical stimulation of mesencephalic reticular formation were unaffected by ritodrine at any doses used. These results suggest that ritodrine shows little effect on the motor nervous system and central nervous system, and its effects may be nonspecific.

Animals↗