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At least 343 records · Page 19Linked to original sources
PubMed1984

Immunohistochemical demonstration of the serotonin neuron system in the central nervous system of the bullfrog, Rana catesbeiana.

The distribution of serotonin immunoreactivity in the brain of the bullfrog (Rana catesbeiana) was studied, using the peroxidase-antiperoxidase (PAP) immunohistochemical method with serotonin antiserum. The somata of the serotonin neurons were mainly located in the raphe regions of the brain stem from the level of the caudal mesencephalon to that of the spinomedullary junction. A small number of serotonin neurons were also distributed as cerebrospinal-fluid contacting neurons in the preoptic recess organ (PRO), the paraventricular organ (PVO), and the nucleus infundibularis dorsalis (Nid). In the raphe region, these serotonin neurons formed nearly-continuous bilaterally-symmetrical cell columns along the midline of the brain stem, divided into lateral and medial groups. The medial group was further subdivided into rostral and caudal parts. Processes of the serotonin neurons were widely distributed in the central nervous system, forming dense networks in various regions. The greatest concentrations of these fibers were in the nucleus medialis septi, lateral portion of striatum, nucleus corporis geniculi, nucleus entopeduncularis, periventricular gray of ventral hypothalamus, optic tectum, nucleus isthmi, nucleus interpeduncularis, dorsal edge of medulla oblongata, and fasciculus solitarius.

Animals↗
PubMed2001

Neuropeptides are ubiquitous chemical mediators: Using the stomatogastric nervous system as a model system.

The stomatogastric nervous system (STNS) controls the movements of the foregut and the oesophagus of decapod crustaceans and is a good example for demonstrating that peptides are ubiquitously distributed chemical mediators in the nervous system. The stomatogastric ganglion (STG), one of the four ganglia of the STNS, contains the most intensively investigated neuronal circuits. The other ganglia, including the two commissural ganglia (CoGs) and the oesophageal ganglion (OG), are thought to be modulatory control centres. Peptides reach the STNS either as neurohormones or are released as transmitters. Peptide neurohormones can be released either from neurohaemal organs or from local neurohaemal release zones located on the surface of nerves and connectives. There were thought to be no peptidergic neurones with cell bodies in the STG itself. However, some have recently been described in adults of four species, in addition to a transient expression of peptides during development in two species. None of these peptidergic neurones has been investigated physiologically, in contrast to peptidergic neurones that project to the STG and have cell bodies in either the CoGs or the OG. It has been shown that neurones containing the same peptide elicit different motor patterns, that the peptide transmitter and the classical transmitter are not necessarily co-released and that the effect of a peptidergic neurone depends on its firing frequency and on which other modulatory neurones are co-active. The activity of modulatory projection neurones can be elicited by sensory neurones, and their activity can depend on the firing frequency of the sensory neurone. In addition to being found within the neuropile of ganglia, peptides are present in neuropile patches located within the nerves of the STNS, suggesting that these nerves can integrate as well as transfer information. Furthermore, sensory neurones and muscles exhibit peptide-like immunoreactivity and are modulated by peptides. Bath-applied peptides elicit peptide-specific motor patterns within the STG by targeting subsets of neurones. This divergence is contrasted by a convergence at the level of currents: five different peptides modulate a single current. Peptides not only induce motor patterns but can also switch the alliance of neurones from one network to another or are able to fuse different networks. In general, peptides are the most abundant group of modulators within the STNS; they are ubiquitously present, indicating that they play multiple roles in the plasticity of neural networks.

Animals↗
PubMed1989

Phase conjugation model for information transfer in the nervous system.

In the nervous system, dispersion in propagation time sometimes brings delay distortion or phase distortion on the information transmission. Also in the memory retrieval processes in the brain, some parts of images may be retrieved more slowly than others. For smooth control of fast movements as well as for keeping exact thinking, these distortions have to be taken out. To understand the distortion cancelling mechanism, new neural network models for compensating the phase distortion are proposed. The models stand on the concept of "phase conjugate mirror" which is used in optical image processing. Simulation studies based on the model resulted in successful cancellation of the delay dispersion involved in the information transmission in the nervous system.

Computer Simulation↗
PubMed1999

New Ca2+-releasing messengers: are they important in the nervous system?

In the nervous system, Ca2+ signalling is determined primarily by voltage-gated Ca2+-selective channels in the plasma membrane, but there is increasing evidence for involvement of intracellular Ca2+ stores in such signalling. It is generally assumed that neurotransmitter-elicited release of Ca2+ from internal stores is primarily mediated by Ins(1,4,5)P3, as originally discovered in pancreatic acinar cells. The more-recently discovered Ca2+-releasing messenger, cyclic ADP-ribose (cADPR), which activates ryanodine receptors, has so far only been implicated in a few cases, and the possible importance of another Ca2+-releasing molecule, nicotinic acid adenine dinucleotide phosphate (NAADP), has been ignored. Recent investigations of the action of the brain-gut peptide cholecystokinin on pancreatic acinar cells have indicated that NAADP and cADPR receptors are essential for Ca2+ release. Tools are available for testing the possible involvement of NAADP and cADPR in neurotransmitter-elicited intracellular Ca2+ release, and such studies could reveal complex mechanisms that control this release in the nervous system.

Animals↗
PubMed1997

Development of the insect stomatogastric nervous system.

The stomatogastric nervous system (SNS) forms a network of peripheral ganglia associated with the insect gut. The SNS originates from a neuroepithelial placode which dissolves into a population of migrating neural precursors. The formation of the SNS presents many parallels to the development of the vertebrate peripheral nervous system. Recent studies have started to provide answers for pertinent questions in SNS development, in particular, how the SNS placode is specified, how SNS precursors are released in a reproducible pattern from this placode and how different cell types in the SNS are determined.

Animals↗
PubMed1976

Sequence of morphological alterations in the nervous system of metachromatic leucodystrophy. Light- and electronmicroscopic observations in the central and peripheral nervous system in a prenatally diagnosed foetus of 22 weeks.

Light and electronmicroscopic findings are reported in a case of metachromatic leukodystrophy diagnosed prenatally who died after iatrogenic abortion during the 23th week of gestation. The brain of this foetus was not yet myelinated while the spinal cord showed early, and the peripheral nerves advanced myelination. The onset and the degree of myelination were similar as in a normal foetus of the same age. Ultrastructurally there was evidence of sulphatide storage before the beginning of myelination. During myelination lysosomal storage material, staining metachromatically in acid cresyl violet preparations, appeared in oligodendrocytes and Schwann cells. Besides sulphatide storage material, prominent amounts of neutral lipids were found in oligodendrocytes. Myelin breakdown was encountered very seldom.

Central Nervous System↗
PubMed1990

The cellular and molecular events of central nervous system remyelination.

Central nervous system (CNS)* regeneration is a subject of great interest, particularly in diseases causing a dramatic loss of neurons. However, some CNS diseases do not affect neurons but damage other cells, such as the myelin-forming cells--called oligodendrocytes--which are also crucial to the harmonious function of the nervous system. Diseases in which oligodendrocytes and myelin are attacked can cause devastating neurological dysfunction which is sometimes followed by recovery and myelin repair or remyelination. The question of the regeneration potential of oligodendrocytes in experimental and human demyelinating diseases such as multiple sclerosis has been debated for a long time. Present evidence suggests that oligodendrocyte precursor cells persist in the adult CNS and that oligodendrocyte regeneration can occur but may be limited by ongoing disease processes. Here we will briefly review recent advances which have broadened our understanding of the cellular and molecular events of CNS remyelination.

Age Factors↗
PubMed1975

[Effect of beta-phenylethylamine derivatives on the central nervous system. II. Pharmacological effect of the intracerebral administration of metaraminol on the central nervous system].

Six hours after intracerebral administration, the central effects of metaraminol were examined with the following results. 1) Metaraminol in doses of 40 approximately 160 mug decreased spontaneous motor activity in mice as measured by the photo-cell counters method, the wheel cage method or the open-field test. Ptosis and catalepsy induced at these doses. 2) Metaraminol in doses of 40 approximately 80 mug which influenced the spontaneous motor activity in mice, blocked the avoidance behaviour but not escape. 3) Metaraminol in doses of 1.25 approximately 10 mug which did not influence the spontaneous motor activity in mice, markedly blocked the attaching response induced by the electroshock. 4) Ten min after intraventricular administration, metaraminol in a dose of 500 mug induced the arousal pattern of EEG in sensory cortex of cats and this pattern lasted for 30 min. Ninety min after administration, EEG tracings reverted to the drowsy pattern.

Aggression↗
PubMed1989

Metabolic factors and the sympathetic nervous system.

The sympathetic nervous system helps regulate both physiologic and metabolic functions. Norepinephrine usually mediates the physiologic functions, including heart rate, myocardial contractility, vasomotor tone, and blood pressure. Epinephrine produces the metabolic effects--including hyperglycemia, hyperlactacidemia, hyperlipemia, increased oxygen consumption, and serum potassium changes. Many of the metabolic effects are common to hypertension. Understanding the metabolic effects of the catecholamines could lead to understanding their role in disease states and thus to knowing the usefulness and risks of drugs that either mimic or block their action. The data presented were selected for their relevance to the metabolic abnormalities commonly encountered among hypertensive patients. The sympathetic nervous system's effects on glucose homeostasis, lipoprotein metabolism, potassium homeostasis, hyperinsulinemia, and hypertension are discussed.

Adrenal Glands↗
PubMed1998

First evidence of otoprotection against carboplatin-induced hearing loss with a two-compartment system in patients with central nervous system malignancy using sodium thiosulfate.

Sodium thiosulfate (STS) provides protection against carboplatin-induced ototoxicity in an animal model. The purpose of this study was to determine the STS dose required for otoprotection, in patients with malignant brain tumors treated with carboplatin in conjunction with osmotic blood-brain barrier disruption. Twenty-nine patients received STS intravenously 2 hr after carboplatin. Doses were escalated from 4 g/m2 to 8, 12, 16 and 20 g/m2 on consecutive months. Audiologic assessment was performed at baseline and monthly. The audiograms were compared with those of 19 similarly treated historical control patients who did not receive STS. The incidence of ototoxicity in the historical control group of patients was 79% (15/19). This group had an average loss of 20.8 +/- 5.9 dB (n = 19) at 8 kHz after one treatment with carboplatin, whereas the STS treatment group lost only 3.7 +/- 2 dB (n = 15) after one treatment. This difference was statistically significant as assessed by Student's t test (P < .05). Furthermore, patients in the STS treatment group with excellent base-line hearing showed little change in hearing thresholds at 8 kHz after the second treatment (8.0 +/- 8.3 dB) (n = 5) compared with the historical control patients with excellent base-line hearing, (40.5 +/- 8.6 dB) (n = 11). Our data support that doses of 16 or 20 g/m2 of STS decrease carboplatin-induced hearing loss without central nervous system entry. Clinical demonstration of an otoprotective effect with a two-compartment system to prevent drug-induced hearing loss, while preserving central nervous system cytotoxicity, has not been reported previously.

Adolescent↗
PubMed1988

Amino acid receptors and uptake systems in the mammalian central nervous system.

The inhibitory and excitatory amino acid neurotransmitter receptors in the mammalian central nervous system mediate functionally opposite synaptic responses yet appear to share certain structural features. Recent conceptual advances in this field have relied heavily on information obtained by single channel analyses, by the expression of receptors in oocytes, and by autoradiographic studies of receptor distribution among brain receptors. This article reviews the pharmacology, cellular physiology, and regional distribution of these receptors and discusses their role in several well-characterized neurological disease states. Also reviewed are the recent advances made in purifying (in some instances cloning) the receptors and uptake sites involved in synaptic transmission in the brain. Throughout, the emphasis is on synthesis and concept rather than on methodological detail.

Animals↗
PubMed1992

Persistence of a hyperdynamic circulation in cirrhotic rats following removal of the sympathetic nervous system.

The sympathetic nervous system is thought to play a role in the pathogenesis of the hyperdynamic circulation associated with portal hypertension. However, the extent of this role is unknown. After elimination of all neurological control by pithing, systemic and regional hemodynamics were studied in rats with portal hypertension caused by either portal vein stenosis or biliary cirrhosis. In normal rats, pithing induced a two-thirds decrease in mean arterial pressure and cardiac index. Compared with pithed normal rats, pithed portal vein-stenosed rats showed similar values for mean arterial pressure, cardiac index, and portal tributary blood flow. In contrast, pithed cirrhotic rats still showed hyperdynamic circulation with increased cardiac index and portal tributary blood flow. Although pithing dramatically reduced portal pressure in all groups, portal pressure remained significantly higher in portal hypertensive rats than in normal rats. These results indicate that in rats with portal vein stenosis, the sympathetic nervous system plays a major role in hemodynamic alterations, whereas in rats with cirrhosis, nonneurogenic factors participate in the pathogenesis of the hyperdynamic circulation.

Animals↗
PubMed1989

Familial aggregation of multiple myeloma and central nervous system diseases.

Degenerative central nervous system diseases such as Alzheimer's disease and lymphoreticular malignancies such as multiple myeloma occur with increased frequency with advancing age. Relatives of early-onset Alzheimer's disease patients may have an increased risk of lymphoreticular malignancies. This led us to evaluate the family history of central nervous system diseases in a case-control study of multiple myeloma. Thirteen of 439 multiple myeloma cases had one or more first-degree relatives with degenerative or demyelinating central nervous system disease. In comparison, there were nine "positive" family histories in 1,317 matched hospital controls (relative risk = 4.4, 95% confidence interval = 1.9-10.3). Relative risks for the component categories of Parkinson's disease, multiple sclerosis, and miscellaneous degenerative central nervous system diseases were 3.0, 4.0 and 11.9, respectively. Our findings suggest that the degenerative and demyelinating central nervous system diseases and the lymphoreticular malignancies may comprise an etiologically related group of "protean diseases." These diseases may have a shared genetic susceptibility, possibly an immunologic abnormality. The varied disease manifestation in family members suggests a second necessary etiologic step of a variable and possibly environmental nature.

Aged↗