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At least 217 records · Page 12Linked to original sources
PubMed2000

Dendrite extension by methanol extract of Ashwagandha (roots of Withania somnifera) in SK-N-SH cells.

Extension of dendrites and axons in neurons may compensate for and repair damaged neuronal circuits in the dementia brain. Our aim in the present study was to explore drugs activating neurite outgrowth and regenerating the neuronal network. We found that the methanol extract of Ashwagandha (roots of Withania somnifera; 5 microg/ml) significantly increased the percentage of cells with neurites in human neuroblastoma SK-N-SH cells. The effect of the extract was dose- and time-dependent mRNA levels of the dendritic markers MAP2 and PSD-95 by RT-PCR were found to be markedly increased by treatment with the extract, whereas those of the axonal marker Tau were not. Immunocytochemistry demonstrated the specific expression of MAP2 in neurites extended by the extract. These results suggest that the methanol extract of Ashwagandha promotes the formation of dendrites.

Dendrites↗
PubMed2001

Kappa opioid agonists alter dopamine markers and cocaine-stimulated locomotor activity.

To better understand the influence of kappa-opioid agonists on the effects of cocaine, rats were treated with daily injections of the selective kappa-opioid agonist U-69593 or bremazocine. In combination with 10 mg/kg cocaine, both compounds, at a dose of 0.32 mg/kg, greatly diminished locomotor activity, and these effects were maintained over a period of 5 days. In addition, the response to a challenge injection of 10 mg/kg cocaine several days after the end of kappa-Opioid agonist treatment with or without cocaine was markedly reduced. When naltrexone was given in combination with U-69593, it blocked the reduction in cocaine-induced locomotor activity after U-69593 treatment alone. However, a single injection of either kappa-opioid agonist alone had no effect on cocaine-induced locomotion several days later (i.e. no long-term effects), suggesting that multiple injections of the kappa-opioid agonist are needed to reduce the locomotor activating effects of cocaine other than acutely. In addition, treatment with the kappa-opioid agonist U-69593 (0.32 mg/kg) over a 5-day period decreased dopamine transporter densities in the caudate putamen, and this was also blocked by co-administration of naltrexone.

Analgesics↗
PubMed1997

Mossy fiber reorganization in the epileptic hippocampus.

Reorganization of dentate granule cell axons (mossy fibers) is a prominent aspect of the pathological changes observed in human temporal lobe epilepsy. Although recent work has begun to address the significance of mossy fiber reorganization, the specific and overall functional consequences of these network changes remain poorly understood. New studies are beginning to provide insight into molecular mechanisms underlying this process. Advances in our understanding of the causes and effects of mossy fiber reorganization are likely to provide insight into the pathophysiology of temporal lobe epilepsy, as well as the larger issue of network remodeling following nervous system injury.

Animals↗
PubMed1998

Lesion-induced plasticity as a potential mechanism for recovery and rehabilitative training.

Brain lesions not only cause a functional deficit in the lesion area, but also affect the structurally intact brain network connected to the lesion. In brain areas surrounding the lesion, as well as those remote from it, the structural and functional plasticity of the brain is increased because of an alteration of transmitter receptor expression and membrane properties of neurones. Within the penumbra of brain ischaemia, as well as after trauma, an additional perilesional dysfunctional zone is found that contributes to the neurological deficit. The lesion-induced plasticity can be used for adaptation, which also may restore function in the perilesional zone, if adequate rehabilitative training is performed.

Animals↗
PubMed2004

Basic mechanisms of partial epilepsies.

PURPOSE OF REVIEW: Partial epilepsies are characterized by cell loss with consequences for neuronal organization, excitability, mnestic and cognitive functions and present with pharmaco-resistance and difficulties in clinical management. While mesial temporal lobe epilepsies present frequently with cell loss and neuronal reorganization, neocortical epilepsies frequently involve developmental alterations. RECENT FINDINGS: There is increasing evidence that nerve cells in epileptic tissue become more vulnerable to excitotoxic cell death due to impairment of mitochondrial functions and that free radical formation is critically involved in these processes. Whether and to what extent such alterations contribute to pharmaco-resistance is unclear. However, at least three mechanisms may contribute to pharmaco-resistance: changes in target molecules for antiepileptic drugs, upregulation of drug transporters, and potentially reorganization processes in inhibitory networks. Upregulation of drug transporters also seems to be involved in pharmaco-resistance of developmental alterations underlying focal epilepsies. Recent data from the literature suggest that transgenic models for disturbances of cortical development may be useful models for the study of these variable forms of partial epilepsies. SUMMARY: The data suggest that improvement of therapy could result from free radical scavenging and from manipulation of drug transport into the affected tissue. New models of developmental epilepsies may help us to understand mechanisms underlying increased vulnerability to seizures as well as improving strategies for treatment.

Anticonvulsants↗
PubMed1997

The biochemical basis of synaptic plasticity and neurocomputation: a new theory.

The recent finding that dendritic spines (on which 90% of all excitatory synapses on pyramidal cells are formed) are not permanent structures but are continually being formed and adsorbed has implications for the present theoretical basis of neurocomputation, which is largely based on the concept of fixed nerve nets. This evidence would tend to support the recent theories of Edelman, Freeman, Globus, Pribram and others that neuronal networks in the brain operate mainly as nonlinear dynamic, chaotic systems. This paper presents a hypothesis of a possible neurochemical mechanism underlying this synaptic plasticity based on reactive oxygen species and toxic 0-semiquinones derived from catecholamines (i) by the enzyme prostaglandin H synthetase induced by glutamatergic NMDA receptor activation and (ii) by reactive nitrogen species derived from nitric oxide in a low ascorbate environment. A key factor in this neuromodulation may be the fact that catecholamines are potent antioxidants and free radical scavengers and are thus able to affect the redox mediated balance at the glutamate receptors between synapse formation and synapse removal that may be a key factor in neurocomputational plasticity. But catecholamines are also easily oxidized to neurotoxic 0-semiquinones and this may be relevant to the pathology of several diseases including schizophrenia. The relationship between dopamine release and positive reinforcement is relevant to this hypothesis.

Animals↗
PubMed1993

Patterns of electrical activity in comb plates of feeding Pleurobrachia (Ctenophora).

The electromotor behaviour of ciliary comb plates was studied during prey-stimulated and electrically stimulated feeding by intact Pleurobrachia pileus (Müller). Comb plate electrical activity was recorded by extracellular electrodes attached directly to the cilia; comb plate motility was recorded by high-speed video microscopy. Comb plate electrical activity fell into two distinct classes, identified by waveform and amplitude: (i) excitatory postsynaptic potentials (EPSPS) in the comb plate (polster) cells and (ii) regenerative potentials in the cilia, as described previously (Moss & Tamm 1987). Slow phasic bursts of regenerative potentials (reversal volleys) were observed in comb plates of rows undergoing reversed beating during capture of prey or by rhythmic electrical stimulation of the tentacles. All plates of a given comb row exhibited virtually identical electrical activity. Timing and development of electrical activity in comb plates of the subtentacular (ST) rows were nearly identical even though separated by several centimetres; onset of the reversal volleys of plates of subsagittal (ss) rows were delayed on average by about 0.5 s relative to the ST rows, although individual EPSPS displayed very similar timing. Microsurgery, combined with extracellular recording from comb plates and the tentacle and associated basal structures, revealed the presence of an integrative center in the tentacular bulb. This communicates with the comb plates by means of a diffuse pathway, presumably the nerve net, which itself is maximally sensitive to rhythmic input. The pathway underlying the reversal volley may innervate only the stimulated hemisphere. In addition to the rhythmic pathway, a through-conducting pathway runs from distal regions of the tentacle to the comb plate cells. Yet another excitatory pathway, possibly distinct from the tentacular through-conducting pathway, may mediate certain cases of global postsynaptic activity. The pathway that controls mouth movements during feeding is entirely independent of any comb plate pathway.

Animals↗
PubMed2005

Asymptotic construction of pulses in the discrete Hodgkin-Huxley model for myelinated nerves.

A quantitative description of pulses and wave trains in the spatially discrete Hodgkin-Huxley model for myelinated nerves is given. Predictions of the shape and speed of the waves and the thresholds for propagation failure are obtained. Our asymptotic predictions agree quite well with numerical solutions of the model and describe wave patterns generated by repeated firing at a boundary.

Action Potentials↗
PubMed2004

Connectivities and synchronous firing in cortical neuronal networks.

Network connectivities ((-)k) of cortical neural cultures are studied by synchronized firing and determined from measured correlations between fluorescence intensities of firing neurons. The bursting frequency (f) during synchronized firing of the networks is found to be an increasing function of (-)k. With f taken to be proportional to (-)k, a simple random model with a (-)k dependent connection probability p((-)k).has been constructed to explain our experimental findings successfully.

Action Potentials↗
PubMed1982

Myocardial catecholamines and their biosynthetic enzymes in various human heart diseases.

Myocardial noradrenaline (NA) content, together with the activities of the enzymes tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) was measured in biopsy specimens taken during cardiac surgery from patients with various heart diseases. Fluorescence histochemical studies were also performed on comparable specimens. The mean NA content in patients with symptomatic ischaemic heart disease (IHD) was significantly higher than that in patients with valvular heart disease (VHD), atrial septal defect (ASD) or congestive heart failure (CHF). The lowest mean NA content was found in patients with CHF. The activities of TH and DBH were highest in the IHD group, although the differences between IHD and VHD groups were not significant. Histochemical investigations of adrenergic structures showed less fluorescence intensity in the CHF than in the other 3 groups. On the other hand, the density of the adrenergic nerve net and the size and number of varicosities were greatest in patients suffering from IHD. The significance of these results is discussed in relation to the pathophysiological mechanisms underlying these various disease conditions. In IHD the high myocardial NA content creates local conditions for excessive NA release into the myocardial interstitium at the onset of ischaemia, which is known to result in several adverse local consequences.

Adult↗
PubMed2004

Appetite regulatory neuropeptides are expressed in the sheep hypothalamus before birth.

In the adult, a hypothalamic neural network acts to maintain energy balance in response to nutritional feedback from the periphery. Although there is an immediate requirement for this system to be functional at birth, it is unknown whether the components of this central neural network are expressed in the developing brain before birth. We therefore examined in the fetal sheep hypothalamus during late gestation gene expression for leptin receptor (OB-Rb) and neuropeptides that regulate energy balance in the adult. Brains were collected from fetal sheep at 110 days (n = 12) and 140 days of gestation (n = 5) (term = 150 days) and gene expression was detected in all hypothalami using in situ hybridization with radiolabelled riboprobes for OB-Rb, neuropeptide Y (NPY), agouti-related peptide, pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript (CART). All mRNAs were expressed in the arcuate nucleus of fetuses at both time points. Additional sites of mRNA expression were the dorsomedial hypothalamus (DMH) for NPY, the paraventricular nucleus (PVN), ventromedial hypothalamus (VMH) and lateral hypothalamic area for CART, and the DMH, PVN and VMH for OB-Rb. We have therefore demonstrated that adult-like localization of gene expression for OB-Rb and key appetite regulatory neuropeptides is established in the ovine hypothalamus before birth. Thus, the fetus possesses a central appetite regulatory neural network with the potential to respond to changes in nutrient supply, which could impact on energy balance regulation both before and after birth.

Age Factors↗
PubMed1996

Brain structure and task-specific increase in expression of the gene encoding syntaxin 1B during learning in the rat: a potential molecular marker for learning-induced synaptic plasticity in neural networks.

The mRNAs encoding the synaptic vesicle proteins syntaxin 1B and synapsin I were measured using in situ hybridization in several brain regions--the dentate gyrus, CA3 and CA1 of the hippocampus, the parietal, the motor and prefrontal cortices and the core and shell of the accumbens--of rats that were learning a spatial reference or working memory task on a radial arm maze. The mRNA encoding syntaxin 1B was significantly increased in all hippocampal regions in rats learning the working memory task, whereas it was increased in the prelimbic area of the prefrontal cortex and the shell of the accumbens in rats learning the spatial reference memory task. No change in mRNA encoding syntaxin 1B was observed in the motor and parietal and cortices or the core of the accumbens, and the mRNA encoding synapsin I was not significantly different from that of naive caged controls or rats running the maze for continuous reinforcement in any of the brain structures examined. These results demonstrate that the gene encoding a key member of synaptic vesicle function is up-regulated in a task- and brain-specific manner during learning. They are discussed in terms of the potential role this protein may play in trans-synaptic propagation of plasticity within specific neural networks as a function of the information required in the laying down of different types of memory.

Animals↗
PubMed2006

A context-specific single contingent-reinforcing stimulus boosts intermediate-term memory into long-term memory.

Following operant conditioning of aerial respiration in Lymnaea, memory forms. Depending on the training procedure either intermediate memory (ITM, < 3 h) or long-term memory (LTM, > 6 h) results. ITM is dependent on de novo protein synthesis whilst LTM is dependent on both transcription and de novo protein synthesis. LTM formation requires the soma of RPeD1 (one of the central pattern generator neurons) to be present. Following activation of a memory, it re-enters a labile state and undergoes a reconsolidation process to restabilize it. During reconsolidation, memory may be updated and/or changed. We add here another consequence of memory reactivation: a single contingent-reinforcing stimulus (SCRS), given in the same context as previous ITM training, boosts a residual memory trace to LTM. Separate cohorts of snails first received the ITM training procedure. In the cohort that received the SCRS 24 h after the last ITM training session, LTM was observed on the following day. LTM was not observed in cohorts that were: (i) given a single noncontingent stimulus; (ii) given the SCRS in a context other than the ITM training; (iii) given a 48-h gap between the last ITM training session and the context-specific SCRS; (iv) cooled immediately after the last ITM training session; (v) cooled immediately after the delivery of the context-specific SCRS; (vi) had the soma of RPeD1 ablated before the presentation of the context-specific SCRS; (vii) received a yoked control procedure. These data lead us to conclude that the context-specific SCRS reactivates a residual molecular memory trace in RPeD1 and boosts it into becoming the substrate for LTM.

Animals↗
PubMed1993

A brain-specific protein p25 is localized and associated with oligodendrocytes, neuropil, and fiber-like structures of the CA3 hippocampal region in the rat brain.

Developmental expression and cellular localization of a novel brain-specific 25-kDa protein (p25), a substrate of tau protein kinase II, were investigated in the rat brain using polyclonal antibodies raised against peptides synthesized based on the p25 amino acid sequence. By western immunoblotting, p25 was found to be expressed only slightly in the embryonic period; the expression increased from 11 days up to 5 weeks of age, and continued to increase gradually until 1-2 years of age. Immunohistochemistry revealed distinct staining of glial cells in most regions of the central nervous system in the adult rat brain. These positively immunostained cells were especially abundant in the white matter, such as the corpus callosum, cingulum, external capsule, and internal capsule. The glial cells were identified as oligodendrocytes, and the nuclei of the cells remained unstained. Whereas the neuropil in most parts of the brain was immunostained less intensely than glias, the neuropil in the first and second layers of the cerebral cortex and the dentate gyrus was relatively strongly stained. Fiber-like structures were also stained in the CA3 region of hippocampus.

Aging↗
PubMedDate not supplied

Expression of Pax gene family members in the anthozoan cnidarian, Nematostella vectensis.

Pax genes are a family of homeodomain transcription factors that have been isolated from protostomes (e.g., eight in Drosophilia) and deuterostomes (e.g., nine in vertebrates) as well as outside the Bilateria, from sponges, a placozoan, and several classes of cnidarians. The genome of an anthozoan cnidarian, the starlet sea anemone, Nematostella vectensis, has been surveyed by both degenerate polymerase chain reaction and in silico for the presence of Pax genes. N. vectensis possesses seven Pax genes, which are orthologous to cnidarian Pax genes (A,B,C, and D) previously identified in another anthozoan, a coral, Acropora millepora. Phylogenetic analyses including data from nonchordate deuterostomes indicates that there were five Pax gene classes in the protostome-deuterostome ancestor, but only three in the cnidarian-bilaterian ancestor, with PaxD class genes lost in medusozoan cnidarians. Pax genes play diverse roles in bilaterians, including eye formation (e.g., Pax6), segmentation (e.g., Pax3/7 class genes), and neural patterning (e.g., Pox-neuro, Pax2/5/8). We show the first expression data for members of all four Pax classes in a single species of cnidarian. N. vectensis Pax genes are expressed in both a cell-type and region-specific manner during embryogenesis, and likely play a role in patterning specific components of the cnidarian ectodermal nerve net. The results of these patterns are discussed with respect to Pax gene evolution in the Bilateria.

Amino Acid Sequence↗
PubMed2006

Analysis of two P-element enhancer-trap insertion lines that show expression in the giant fibre neuron of Drosophila melanogaster.

The giant fibre system (GFS) of Drosophila is a simple neural circuit that mediates escape responses in adult flies. Here we report the initial characterization of two genes that are preferentially expressed in the GFS. Two P-element insertion lines, carrying the GAL4 transcriptional activator, were identified that exhibited pronounced expression in elements of the GFS and relatively low levels elsewhere within the adult central nervous system. Genomic DNA flanking the P-element insertion site was recovered from each of these lines, sequenced, and nearby transcripts identified and confirmed to exhibit GFS expression by in situ hybridization. This analysis revealed that these P-elements were in previously characterized genes. Line P[GAL4]-A307 has an insert in the gene short stop for which we have identified a novel transcript, while line P[GAL4]-141 has an insert in the transcription factor ken and barbie. Here we show that ken and barbie mutants have defects in escape behaviour, behavioural responses to visual stimuli and synaptic functions in the GFS. We have therefore revealed a neural role for a transcription factor that previously had no implicated neural function.

Animals↗