Dendrites

Intracellular recordings were obtained from pyramidal neurons in layer 5 of rat somatosensory and visual cortical slices maintained in vitro. When directly depolarized, one subclass of pyramidal neurons had the capacity to generate intrinsic burst discharges and another generated regular trains of single spikes. Burst responses were triggered in an all-or-none manner from depolarizing afterpotentials in most bursting neurons. Regular spiking cells responded to electrical stimulation of ascending afferents with a typical EPSP-IPSP sequence, whereas IPSPs were hard to detect in bursting cells. Orthodromic activation of the latter evoked a prominent voltage-dependent depolarization that could trigger a burst response. Intracellularly labelled bursting and regular spiking cells were located in layer 5b, but had distinctly different morphologies. Bursting neurons had a large pyramidal soma, a gradually emerging apical dendrite, and an extensive apical and basal dendritic tree. Their axonal collateral arborization was predominantly limited to layers 5/6. In contrast, regular spiking cells had a more rounded soma with abruptly emerging apical dendrite, a smaller dendritic arborization, and 2 to 8 ascending axonal collaterals that arborized widely in the supragranular layers. Both bursting and regular spiking cells had main axons that entered the subcortical white matter.

This paper presents a spike-based model which employs neurons with functionally distinct dendritic compartments for classifying high dimensional binary patterns. The synaptic inputs arriving on each dendritic subunit are nonlinearly processed before being linearly integrated at the soma, giving the neuron a capacity to perform a large number of input-output mappings. The model utilizes sparse synaptic connectivity; where each synapse takes a binary value. The optimal connection pattern of a neuron is learned by using a simple hardware-friendly, margin enhancing learning algorithm inspired by the mechanism of structural plasticity in biological neurons. The learning algorithm groups correlated synaptic inputs on the same dendritic branch. Since the learning results in modified connection patterns, it can be incorporated into current event-based neuromorphic systems with little overhead. This work also presents a branch-specific spike-based version of this structural plasticity rule. The proposed model is evaluated on benchmark binary classification problems and its performance is compared against that achieved using Support Vector Machine (SVM) and Extreme Learning Machine (ELM) techniques. Our proposed method attains comparable performance while utilizing 10 to 50% less computational resources than the other reported techniques.

The spatial distribution of synaptic inputs on the dendritic tree of a neuron can have significant influence on neuronal function. Consequently, accurate anatomical reconstructions of neuron morphology and synaptic localization are critical when modeling and predicting physiological responses of individual neurons. Historically, generation of three-dimensional (3D) neuronal reconstructions together with comprehensive mapping of synaptic inputs has been an extensive task requiring manual identification of putative synaptic contacts directly from tissue samples or digital images. Recent developments in neuronal tracing software applications have improved the speed and accuracy of 3D reconstructions, but localization of synaptic sites through the use of pre-and/or post-synaptic markers has remained largely a manual process. To address this problem, we have developed an algorithm, based on 3D distance measurements between putative pre-synaptic terminals and the post-synaptic dendrite, to automate synaptic contact detection on dendrites of individually labeled neurons from 3D immunofluorescence image sets. In this study, the algorithm is implemented with custom routines in Matlab, and its effectiveness is evaluated through analysis of primary sensory afferent terminals on motor neurons. Optimization of algorithm parameters enabled automated identification of synaptic contacts that matched those identified by manual inspection with low incidence of error. Substantial time savings and the elimination of variability in contact detection introduced by different users are significant advantages of this method.

Protein synthesis-dependent forms of hippocampal long-term potentiation (late LTP) and long-term depression (late LTD) are prominent cellular mechanisms underlying memory formation. Recent data support the hypothesis that neurons store relevant information in dendritic functional compartments during late LTP and late LTD rather than in single synapses. It has been suggested that processes of "synaptic tagging" are restricted to such functional compartments. Here, we show that in addition to apical CA1 dendrites, synaptic tagging also takes place within basal CA1 dendritic compartments after LTP induction. We present data that tagging in the basal dendrites is restricted to these compartments. Plasticity-related proteins, partially nonspecific to the locally induced process, are synthesized in dendritic compartments and then captured by local, process-specific synaptic tags. We support these findings in two ways: (1) late LTP/LTD, locally induced in apical or basal (late LTP) dendrites of hippocampal CA1 neurons, does not spread to the basal or apical compartment, respectively; (2) the specificity of the synaptic plasticity event is achieved by the activation of process-and compartmentspecific synaptic tag molecules. We have identified calcium/calmodulin-dependent protein kinase II as the first LTP-specific and extracellular signal-regulated kinase 1/2 as LTD-specific tag molecules in apical dendritic CA1 compartments, whereas either protein kinase A or protein kinase M mediates LTP-specific tags in basal dendrites.

öTo elucidate the role of dendritic morphology in signal transfer, the passive propagation of somatic and dendritic potentials was compared in multi-compartment models of three interneuron subpopulations in the CA1 region. Nine calbindin-, 15 calretinin-and 10 parvalbumin-containing cells were modelled incorporating the detailed geometry, the currents of the action potentials in the soma, and the AMPA, N-methyl-D-aspartate and GABA-B receptor-mediated postsynaptic currents in the dendrites. The cable properties show characteristic di¡erences among the subpopulations. The morphotonic length of calbindin and calretinin cell dendrites is larger than of parvalbumin cells. Thus parvalbumin cells are more compact than calbindin or calretinin cells unless the ratio of their axial and membrane resistivities exceeds the ratios of the other two cell types by more than 33%. In calbindin cells, the distal parts of the extremely long dendrites that invade the alveus are virtually isolated from the soma for passively propagating signals. The synaptic potentials evoked at a given morphotonic distance from the soma show larger di¡erences locally on the dendrites than on the soma in all subpopulations. Both the somatic and dendritic amplitude ratios are the smallest in PV cells. In calbindin cells the somatic amplitude of synaptic potentials evoked at the same morphotonic distance from the soma is similar regardless of the number of branchpoints along their path. In calretinin and parvalbumin cells, from dendrites with long primary segments synaptic potentials reach the soma with larger amplitude than from dendrites that are branching close to the soma. The dendrites with the larger impact on somatic membrane potential are usually the dendrites that enter the stratum lacunosum-moleculare. These results indicate that dendritic morphology plays a role in changing the e¡ectiveness of synaptic potentials evoked at di¡erent dendritic locations, and in this way is likely to be an important factor in determining the integrative properties of the di¡erent neuron populations.

Perineuronal nets (PNNs) are dense extracellular matrix (ECM) structures that form around many neuronal cell bodies and dendrites late in development. They contain several chondroitin sulphate proteoglycans (CSPGs), hyaluronan, link proteins and tenascin-R. Their time of appearance correlates with the ending of the critical period for plasticity, and they have been implicated in this process. The distribution of PNNs in the spinal cord was examined using Wisteria floribunda agglutinin lectin and staining for chondroitin sulphate stubs after chondroitinase digestion. Double labelling with the neuronal marker, NeuN, showed that PNNs were present surrounding 30% of motoneurons in the ventral horn, 50% of large interneurons in the intermediate grey and 20% of neurons in the dorsal horn. These PNNs formed in the second week of postnatal development. Immunohistochemical staining demonstrated that the PNNs contain a mixture of CSPGs, hyaluronan, link proteins and tenascin-R. Of the CSPGs, aggrecan was present in all PNNs while neurocan, versican and phosphacan ⁄ RPTPb were present in some but not all PNNs. In situ hybridization showed that aggrecan and cartilage link protein (CRTL 1) and brain link protein-2 (BRAL 2) are produced by neurons. PNN-bearing neurons express hyaluronan synthase, and this enzyme and phosphacan ⁄ RPTPb may attach PNNs to the cell surface. During postnatal development the expression of link protein and aggrecan mRNA is up-regulated at the time of PNN formation, and these molecules may therefore trigger their formation.

Bacopa monniera (BM), a traditional Ayurvedic medicine has been used in treatment for a number of disorders, particularly those involving anxiety, intellect and poor memory. The current study examined the effects of standardized extract of Bacopa monniera on the dendritic morphology in adult rats of hippocampal CA3 neurons, one of the regions concerned with learning and memory. Adult Wistar (2.5-month-old) rats were designated into 2-, 4- and 6-week treatment groups. Rats in each of these groups were divided into 20 mg/kg, 40 mg/kg and 80 mg/kg dose groups (n=8 for each dose). These rats along with age-matched control rats were then subjected to spatial learning (T-maze) and passive avoidance tests. Subsequent to the T-maze and passive avoidance tests, these rats were killed by decapitation, brains were removed and hippocampal neurons were impregnated with silver nitrate (Golgi staining). Hippocampal CA3 neurons were traced using camera lucida. Dendritic branching points (a measure ...

Color coding and directional selectivity (DS) of retinal neurons were studied in the Pseudemys turtle by using similar intracellular recording and staining techniques as in the preceding paper (J. Ammermuller and H. Kolb, 1995, J. Comp. Neurol. 358:l-34). Color-coded responses were elicited by red (621 or 694 nm), green (525 or 514 nm), and blue (455 nm) light flashes. In addition to redigreen and yellow/blue types of chromaticity horizontal cells, in our sample of 305 identified cells we found that 17% of bipolar cells, 6.5% of amacrine cells, and 18% of ganglion cells exhibit color-coded responses. DS responses were found in 37% of the tested ganglion cells and 41% of the tested amacrine cells.

substantially to the neuronal population of the adult dentate gyrus. We report here that the neurons located in the deep aspects of the granule cell layer, near the proliferative zone, have different properties from those located in the superficial layers. The former group of neurons, tentatively designated as young, can be readily identified in a standard hippocampal slice preparation by morphological, immunohistochemical, and electrophysiological criteria. Electrophysiological recordings and imaging with Lucifer yellow from these neurons in the standard hippocampal slice preparation showed one or two main dendrites and conically shaped branches possessing varicose protrusions. These features are in agreement with the appearance of the same population of young neurons immunopositive for TOAD-64, a marker for immature neurons. In disinhibited slices, these putative young neurons are distinguished from the mature neurons, located in the superficial granule cell layer, by showing paired pulse facilitation and having a lower threshold for induction of long-term potentiation. The putative young neurons are completely unaffected by GABA A inhibition and always display robust longterm potentiation. In contrast, the mature neurons never produce long-term potentiation when the GABA A inhibition is intact. We propose that the heterogeneity of the functional properties of the granule neurons is related to the ongoing neurogenesis in the adult animals.

Functional architecture of the striate cortex is known mostly at the tissue level -how neurons of different function distribute across its depth and surface on a scale of millimetres. But explanations for its design -why it is just so -need to be addressed at the synaptic level, a much finer scale where the basic description is still lacking. Functional architecture of the retina is known from the scale of millimetres down to nanometres, so we have sought explanations for various aspects of its design. Here we review several aspects of the retina's functional architecture and find that all seem governed by a single principle: represent the most information for the least cost in space and energy. Specifically: (i) why are OFF ganglion cells more numerous than ON cells? Because natural scenes contain more negative than positive contrasts, and the retina matches its neural resources to represent them equally well; (ii) why do ganglion cells of a given type overlap their dendrites to achieve 3-fold coverage? Because this maximizes total information represented by the array -balancing signal-to-noise improvement against increased redundancy; (iii) why do ganglion cells form multiple arrays? Because this allows most information to be sent at lower rates, decreasing the space and energy costs for sending a given amount of information. This broad principle, operating at higher levels, probably contributes to the brain's immense computational efficiency.

Dendritic structures are one of the most frequent patterns in nature, that appear in crystalline systems (such as metals), advanced ceramics and neural systems of the living organisms. Embedded in the core of many industrially important processes such as casting, there is a strong relationship between the material properties and the solidified dendritic microstructures.

In our proposed study microstructural simulations were performed using MICRESS® code, which implements a multi-phase-field approach and essentially provides a mathematical solution to the coupled partial differential equations of phase-field and diffusion. In the context of the study, MICRESS® was used to simulate the morphological transitions and the solute segregations during directional solidification under a wide spectrum of temperature gradients, solidification rates and chemical compositions. The proposed model is integrated with an in-situ experimental study of solidification in a high-temperature laser-scanning confocal microscope. Such in-situ studies are able to provide an experimental mean to measure some of the crucial physical properties of the studied alloys, resulting in more refined microstructural simulations of such phenomena. For instance we demonstrated a real-time method for the calculation of Gibbs-Thomson coefficient and the solid-liquid interfacial energy of the studied alloys by analysing the shape of the grain-boundary grooves at the solid-liquid interface. The interface mobility parameter was calibrated so to achieve a realistic interface velocity aligned with the regime experimentally observed in real-time in the confocal microscopy.

Altered dendritic spines are characteristic of traumatized or diseased brain. Two general categories of spine pathology can be distinguished: pathologies of distribution and pathologies of ultrastructure. Pathologies of spine distribution affect many spines along the dendrites of a neuron and include altered spine numbers, distorted spine shapes, and abnormal loci of spine origin on the neuron. Pathologies of spine ultrastructure involve distortion of subcellular organelles within dendritic spines. Spine distributions are altered on mature neurons following traumatic lesions, and in progressive neurodegeneration involving substantial neuronal loss such as in Alzheimer's disease and in Creutzfeldt-Jakob disease. Similarly, spine distributions are altered in the developing brain following malnutrition, alcohol or toxin exposure, infection, and in a large number of genetic disorders that result in mental retardation, such as Down's and fragile-X syndromes. An important question is whether altered dendritic spines are the intrinsic cause of the accompanying neurological disturbances. The data suggest that many categories of spine pathology may result not from intrinsic pathologies of the spiny neurons, but from a compensatory response of these neurons to the loss of excitatory input to dendritic spines. More detailed studies are needed to determine the cause of spine pathology in most disorders and relationship between spine pathology and cognitive deficits.

The onset of spontaneous seizures in the pilocarpine model of epilepsy causes a hyperpolarized shift in the voltage-dependent activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel-mediated current (I h ) in CA1 hippocampal pyramidal neuron dendrites, contributing to neuronal hyperexcitability and possibly to epileptogenesis. However, the specific mechanisms by which spontaneous seizures cause downregulation of HCN channel gating are yet unknown. We asked whether the seizure-dependent downregulation of HCN channel gating was due to altered phosphorylation signalling mediated by the phosphatase calcineurin (CaN) or the kinase p38 mitogen-activated protein kinase (p38 MAPK). We first found that CaN inhibition upregulated HCN channel gating and reduced neuronal excitability under normal conditions, showing that CaN is a strong modulator of HCN channels. We then found that an in vitro model of seizures (one hour in 0 Mg 2+ and 50 μM bicuculline at 35 -37 °C) reproduced the HCN channel gating change seen in vivo. Pharmacological inhibition of CaN or activation of p38 MAPK partially reversed the in vitro seizure-induced hyperpolarized shift in HCN channel gating, and the shift was fully reversed by the combination of CaN inhibition and p38 MAPK activation. We then demonstrated enhanced CaN activity as well as reduced p38 MAPK activity in vivo in the CA1 hippocampal area of chronically epileptic animals. Pharmacological reversal of these phosphorylation changes restored HCN channel gating downregulation and neuronal hyperexcitability in epileptic tissue to control levels. Together, these results suggest that alteration of two different phosphorylation pathways in epilepsy contributes to the downregulation of HCN channel gating, which consequently produces neuronal hyperexcitability and thus may be a target for novel antiepileptic therapies.

The larval visual system of Drosophila melanogaster consists of two bilateral clusters of 12 photoreceptors, which express Rhodopsin 5 and 6 (Rh5 and Rh6) in a non-overlapping manner. These neurons send their axons in a fascicle, the larval optic nerve (LON), which terminates in the larval optic neuropil. The LON is required for the development of a serotonergic arborization originating in the central brain and for the development of the dendritic tree of the circadian pacemakers, the small ventral lateral neurons (LNv) Larval optic nerve and adult extra-retinal photoreceptors sequentially associate with clock neurons during Drosophila brain development. Development 129, 1443 -1453; Mukhopadhyay, M., Campos, A.R., 1995. The larval optic nerve is required for the development of an identified serotonergic arborization in Drosophila melanogaster. Dev. Biol., 169, 629 -643]. Here, we show that both Rh5-and Rh6-expressing fibers overlap equally with the 5-HT arborization and that it, in turn, also contacts the dendritic tree of the LNv. The experiments described here aimed at determining whether Rh5-or Rh6-expressing fibers, as well as the LNv, influence the development of this serotonergic arborization. We conclude that Rh6-expressing fibers play a unique role in providing a signal required for the outgrowth and branching of the serotonergic arborization. Moreover, the innervation of the larval optic neuropil by the 5-HT arborization depends on intact Rac function. A possible role for these serotonergic processes in modulating the larval circadian rhythmicity and photoreceptor function is discussed. D

Valeriana officinalis have been used in traditional medicine for its sedative, hypnotic, and anticonvulsant effects. There are several eports in the literature supporting a GABAergic mechanism of action for valerian. The rationale of the present work is based on the concept that by decreasing neuronal network excitability valerian consumption may contribute to neuroprotection. The aim of our investigation was to evaluate the neuroprotective effects ofV. officinalis against the toxicity induced by amyloid beta peptide 25–35 [Aβ(25–35)]. Cultured rat hip-pocampal neurons were exposed to Aβ(25–35)(25 μM) for 24–48 h,after which morphological and biochemical properties were evaluated. The neuronal injury evoked by Aβ, which includes a decrease in cell educing capacity and associated neuronal degeneration, was prevented by valerian extract. Analysis of intracellular free calcium ([Ca2+]i)indicated that the neuroprotective mechanisms may involve the inhibition of excess influx of Ca2+ following neuronal injury. Moreover, membrane peroxidation in rat hippocampal synaptosomes was evaluated, and our data indicate that valerian extract partially inhibited ascorbate/iron-induced peroxidation. In conclusion we show evidence that the signalling pathways involving [Ca2+]i and the redox state of the cells may play a central ole in the neuroprotective properties ofV. officinalis extract against Aβ toxicity. The novelty of the findings of the present work, indicating neuroprotective properties of valerian against Aβ toxicity may, at the long-term, contribute to introduction of a new elevant use of valerian alcoholic extract to prevent neuronal degeneration in aging or neurodegenerative disorders.

Alzheimer's disease (AD) is characterized by progressive dysfunction of memory and higher cognitive functions with abnormal accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles throughout cortical and limbic brain regions. At present no curative treatment is available, and research focuses on drugs for slowing disease progression or providing prophylaxis. Withania somnifera (WS) also known as 'ashwagandha' is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer. However, there is a paucity of data on the potential neuroprotective effects of W.somnifera against β-Amyloid (1-42)-induced neuropathogenesis. In the present study, we have tested the neuroprotective effects of methanol:Chloroform (3:1) extract of ashwagandha against β-amyloid induced toxicity and HIV-1 Ba-L (clade B) infection using a human neuronal SK-N-MC cell line. Our results showed that β-amyloid induced cytotoxic effects in SK-N-MC cells as shown by decreased cell growth when tested individually. Also, confocal microscopic analysis showed decreased spine density, loss of spines and decreased dendrite diameter, total dendrite and spine area in clade B infected SK-N-MC cells compared to uninfected cells. However, when ashwagandha was added to β-amyloid treated and HIV-1 infected samples, the toxic effects were neutralized. Further, the MTT cell viability assays and the peroxisome proliferator-activated receptor-γ (PPARγ) levels supported these observations indicating the neuroprotective effect of WS root extract against β-amyloid and HIV-1 Ba-L (clade B) induced neuro-pathogenesis.

The adult brain is not as hard-wired as traditionally thought. By modifying their small- or large-scale morphology, neurons can make new synaptic connections or break existing ones (structural plasticity). Structural changes accompany memory formation and learning, and are induced by neurogenesis, neurodegeneration and brain injury such as stroke. Exploring the role of structural plasticity in the brain can be greatly assisted by mathematical and computational models, as they enable us to bridge the gap between system-level dynamics and lower level cellular and molecular processes. However, most traditional neural network models have fixed neuronal morphologies and a static connectivity pattern, with plasticity merely arising from changes in the strength of existing synapses (synaptic plasticity). In The Rewiring Brain, the editors bring together, for the first time, contemporary modeling studies that investigate the implications of structural plasticity for brain function and pathology. Starting with an experimental background on structural plasticity in the adult brain, the book covers computational studies on homeostatic structural plasticity, the impact of structural plasticity on cognition and cortical connectivity, the interaction between synaptic and structural plasticity, neurogenesis-related structural plasticity, and structural plasticity in neurological disorders. Structural plasticity adds a whole new dimension to brain plasticity, and The Rewiring Brain shows how computational approaches may help to gain a better understanding of the full adaptive potential of the adult brain. The book is written for both computational and experimental neuroscientists. Key features: • Reviews the current state of knowledge of structural plasticity in the adult brain. • Gives a comprehensive overview of computational studies on structural plasticity. • Provides insights into the potential driving forces of structural plasticity and the functional implications of structural plasticity for learning and memory. • Serves as inspiration for developing novel treatment strategies for stimulating functional repair after brain damage. For a preview and to order the book, go to: https://www.elsevier.com/books/the-rewiring-brain/van-ooyen/978-0-12-803784-3

The rocker mice are hereditary ataxic mutants that carry a point mutation in the gene encoding the Ca V 2.1 (P ⁄ Q-type) Ca 2+ channel a 1 subunit, and show the mildest symptoms among the reported Ca V 2.1 mutant mice. We studied the basic characteristics of the rocker mutant Ca 2+ channel and their impacts on excitatory synaptic transmission in cerebellar Purkinje cells (PCs). In acutely dissociated PC somas, the rocker mutant channel showed a moderate reduction in Ca 2+ channel current density, whereas its kinetics and voltage dependency of gating remained nearly normal. Despite the small changes in channel function, synaptic transmission in the parallel fiber (PF)-PC synapses was severely impaired. The climbing fiber inputs onto PCs showed a moderate impairment but could elicit normal complex spikes. Presynaptic function of the PF-PC synapses, however, was unexpectedly almost normal in terms of paired-pulse facilitation, sensitivity to extracellular Ca 2+ concentration and glutamate concentration in synaptic clefts. Electron microscopic analyses including freeze-fracture replica labeling revealed that both the number and density of postsynaptic a-amino-3hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors substantially decreased without gross structural changes of the PF-PC synapses. We also observed an abnormal arborization of PC dendrites in young adult rocker mice ( 1 month old). These lines of evidence suggest that even a moderate dysfunction of Ca V 2.1 Ca 2+ channel can cause substantial changes in postsynaptic molecular composition of the PF-PC synapses and dendritic structure of PCs.

GPR88, an orphan G protein-coupled receptor, was designated Strg ⁄ GPR88 for striatum-specific G protein-coupled receptor (K. Mizushima et al. (2000) Genomics, 69, 314-321). In this study, we focused on striatal GPR88 protein localization using a polyclonal antibody. We established that the distribution of immunoreactivity in rat brain matched that of GPR88 transcripts and provided evidence for its exclusive neuronal expression. GPR88 protein is abundant throughout the striatum of rat and primate, with expression limited to the two subsets of striatal projection medium spiny neurons (MSNs) expressing preprotachykinin-substance P or preproenkephalin mRNAs. Ultrastructural immunolabelling revealed the GPR88 concentration at post-synaptic sites along the somatodendritic compartments of MSNs, with pronounced preference for dendrites and dendritic spines. The GPR88-rich expression, in both striatal output pathways, designates this receptor as a potential therapeutic target for diseases involving dysfunction of the basal ganglia, such as Parkinson's disease. Hence, we investigated changes of GPR88 expression in a model of Parkinson's disease (unilateral 6-hydroxydopamine-lesioned rats) following repeated L-DOPA treatment. In dopamine-depleted striatum, GPR88 expression was differentially regulated, i.e. decreased in striatopallidal and increased in striatonigral MSNs. L-DOPA treatment led to a normalization of GPR88 levels through dopamine D1 and D2 receptor-mediated mechanisms in striatopallidal and striatonigral MSNs, respectively. Moreover, the removal of corticostriatal inputs, by ibotenate infusion, downregulated GPR88 in striatopallidal MSNs. These findings provide the first evidence that GPR88 is confined to striatal MSNs and indicate that L-DOPA-mediated behavioural effects in hemiparkinsonian rats may involve normalization of striatal GPR88 levels probably through dopamine receptor-mediated mechanisms and modulations of corticostriatal pathway activity.

An investigation was carried out to understand the effect of Mg addition on the dendritic arm spacing and hardness of A356 aluminium alloy. The effect of Mg content was assessed by melting the A356 Al alloy in a muffle furnace with the addition of varying weight percentage Mg (1, 1.5, 2.5, 3.5 % wt) and casting in both permanent metal die and sand mould. It was observed that the secondary dendritic arm spacing reduces with Mg content concluding that Mg addition improves the formation of nucleation sites and thereby results in grain refinement. The Brinell hardness tester was used to measure the hardness of the alloy. It was found that the hardness increased with Mg content and comparatively, die cast samples showed improved hardness when compared with that of sand cast samples.

This paper discusses the possibility of quantum coherent oscillations playing a role in neuronal signaling. Consciousness correlates strongly with coherent neural oscillations, however the mechanisms by which neurons synchronize are not fully elucidated. Recent experimental evidence of quantum beats in light-harvesting complexes of plants (LHCII) and bacteria provided a stimulus for seeking similar effects in important structures found in animal cells, especially in neurons. We argue that microtubules (MTs), which play critical roles in all eukaryotic cells, possess structural and functional characteristics that are consistent with quantum coherent excitations in the aromatic groups of their tryptophan residues. Furthermore we outline the consequences of these findings on neuronal processes including the emergence of consciousness.

Abuse of cough mixture is increasingly prevalent worldwide. Clinical studies showed that chronic consumption of cough mixture at high dosages may lead to psychiatric symptoms, especially affective disturbances, with the underlying mechanisms remain elusive. The present study aims at exploring the effect of repeated, high-dose dextromethorphan (DXM, a common active component of cough mixture) treatment on adult hippocampal neurogenesis, which is associated with pathophysiology of mood disturbances. After treatment with a high-dose of DXM (40 mg/kg/day) for 2 weeks, Sprague-Dawley rats showed increased depression-like behavior when compared to the control animals. Neurogenesis in the hippocampus was suppressed by DXM treatment, which was indicated by decreases in number of proliferative cells and doublecortin (an immature neuron marker)-positive new neurons. Furthermore, the dendritic complexity of the immature neurons was suppressed by DXM treatment. These findings suggest that DXM i...

We measured the S-cone contrast threshold for stimuli of different size modulated along the white j 90 deg direction in the isoluminant plane of DKL color space. The stimuli were presented at eccentricities of 5Y30 deg in the horizontal temporal retinal meridian. Ricco's area of complete spatial summation was estimated using a bilinear fit of the log threshold/log area function. Ricco's area increased towards the retinal periphery to include an increasing number of S-cones while remaining 1.6Y1.8 times larger than the dendritic field area of the small bistratified and parasol retinal ganglion cells. Assuming constant coverage factor by the dendritic field, Ricco's area incorporated a constant number (three to four) of small bistratified cells. It was also found that the threshold contrast for stimuli that matched Ricco's area was constant across the studied eccentricity range, similar to previous findings for achromatic vision. Our data support the point of view that this invariance is the result of a constant number of cells involved in stimulus detection.

In cortical neurones, analogue dendritic potentials are thought to be encoded into patterns of digital spikes. According to this view, neuronal codes and computations are based on the temporal patterns of spikes: spike times, bursts or spike rates. Recently, we proposed an 'action potential waveform code' for cortical pyramidal neurones in which the spike shape carries information. Broader somatic action potentials are reliably produced in response to higher conductance input, allowing for four times more information transfer than spike times alone. This information is preserved during synaptic integration in a single neurone, as back-propagating action potentials of diverse shapes differentially shunt incoming postsynaptic potentials and so participate in the next round of spike generation. An open question has been whether the information in action potential waveforms can also survive axonal conduction and directly influence synaptic transmission to neighbouring neurones. Several new findings have now brought new light to this subject, showing cortical information processing that transcends the classical models.

You might find this additional information useful... 858 articles, 389 of which you can access free at: This article cites https://physrev.physiology.org/cgi/content/full/88/2/769#BIBL 12 other HighWire hosted articles, the first 5 are: This article has been cited by [PDF] [Full Text] [Abstract] , July 24, 2009; 16 (8): 474-478. Learn. Mem. Diversity in long-term synaptic plasticity at inhibitory synapses of striatal spiny neurons [PDF] [Full Text] [Abstract] dyes Wide-field and two-photon imaging of brain activity with voltage-and calcium-sensitive [PDF] [Full Text] [Abstract] , [PDF] [Full Text] [Abstract] , October 28, 2009; 29 (43): 13649-13661.

Pyramidal cells in the electrosensory lateral line lobe (ELL) of weakly electric fish have been observed to produce high-frequency burst discharge with constant depolarizing current . We present a twocompartment model of an ELL pyramidal cell that produces burst discharges similar to those seen in experiments. The burst mechanism involves a slowly changing interaction between the somatic and dendritic action potentials. Burst termination occurs when the trajectory of the system is reinjected in phase space near the "ghost" of a saddlenode bifurcation of fixed points. The burst trajectory reinjection is studied using quasi-static bifurcation theory, that shows a period doubling transition in the fast subsystem as the cause of burst termination. As the applied depolarization is increased, the model exhibits first resting, then tonic firing, and finally chaotic bursting behavior, in contrast with many other burst models. The transition between tonic firing and burst firing is due to a saddle-node bifurcation of limit cycles. Analysis of this bifurcation shows that the route to chaos in these neurons is type I intermittency, and we present experimental analysis of ELL pyramidal cell burst trains that support this model prediction. By varying parameters in a way that changes the positions of both saddle-node bifurcations in parameter space, we produce a wide gallery of burst patterns, which span a significant range of burst time scales.

Mammals rely heavily on olfaction to interact adequately with each other and with their environment 1 . They make use of seventransmembrane G-protein-coupled receptors to identify odorants and pheromones. These receptors are present on dendrites of olfactory sensory neurons located in the main olfactory or vomeronasal sensory epithelia, and pertain to the odorant 2 , trace amineassociated receptor 3 and vomeronasal type 1 (ref. 4) or 2 (refs 5-7) receptor superfamilies. Whether these four sensor classes represent the complete olfactory molecular repertoire used by mammals to make sense of the outside world is unknown. Here we report the expression of formyl peptide receptor-related genes by vomeronasal sensory neurons, in multiple mammalian species. Similar to the four known olfactory receptor gene classes, these genes encode seven-transmembrane proteins, and are characterized by monogenic transcription and a punctate expression pattern in the sensory neuroepithelium. In vitro expression of mouse formyl peptide receptor-like 1, 3, 4, 6 and 7 provides sensitivity to disease/inflammation-related ligands. Establishing an in situ approach that combines whole-mount vomeronasal preparations with dendritic calcium imaging in the intact neuroepithelium, we show neuronal responses to the same molecules, which therefore represent a new class of vomeronasal agonists. Taken together, these results suggest that formyl peptide receptor-like proteins have an olfactory function associated with the identification of pathogens, or of pathogenic states.

The dsRNA-binding protein Staufen was the first RNA-binding protein proven to play a role in RNA localization in Drosophila. A mammalian homolog, Staufen1 (Stau1), has been implicated in dendritic RNA localization in neurons, translational control, and mRNA decay. However, the precise mechanisms by which it fulfills these specific roles are only partially understood. To determine its physiological functions, the murine Stau1 gene was disrupted by homologous recombination. Homozygous stau1 tm1Apa mutant mice express a truncated Stau1 protein lacking the functional RNA-binding domain 3. The level of the truncated protein is significantly reduced. Cultured hippocampal neurons derived from stau1 tm1Apa homozygous mice display deficits in dendritic delivery of Stau1-EYFP and ␤-actin mRNA-containing ribonucleoprotein particles (RNPs). Furthermore, these neurons have a significantly reduced dendritic tree and develop fewer synapses. Homozygous stau1 tm1Apa mutant mice are viable and show no obvious deficits in development, fertility, health, overall brain morphology, and a variety of behavioral assays, e.g., hippocampus-dependent learning. However, we did detect deficits in locomotor activity. Our data suggest that Stau1 is crucial for synapse development in vitro but not critical for normal behavioral function.

The literature on the neuroanatomical changes that occur during normal, non-demented aging is reviewed here with an emphasis on the improved accuracy of studies that use stereological techniques. Loss of neural tissue involved in cognition occurs during aging of humans as well as the other mammals that have been examined. There is considerable regional specificity within the cerebral cortex and the hippocampus in both the degree and cellular basis for loss. The anatomy of the prefrontal cortex is especially vulnerable to the effects of aging while the major subfields of the hippocampus are not. A loss of neurons, dendrites and synapses has been documented, as well as changes in neurotransmitter systems, in some regions of the cortex and hippocampus but not others. Species differences are also apparent in the cortical white matter and the corpus callosum where there are indications of loss of myelin in humans, but most evidence favors preservation in rats. The examination of whether ...

Rubin, Daniel B. and Thomas A. Cleland. Dynamical mechanisms of odor processing in olfactory bulb mitral cells. . In the olfactory system, the contribution of dynamical properties such as neuronal oscillations and spike synchronization to the representation of odor stimuli is a matter of substantial debate. While relatively simple computational models have sufficed to guide current research in large-scale network dynamics, less attention has been paid to modeling the membrane dynamics in bulbar neurons that may be equally essential to sensory processing. We here present a reduced, conductance-based compartmental model of olfactory bulb mitral cells that exhibits the complex dynamical properties observed in these neurons. Specifically, model neurons exhibit intrinsic subthreshold oscillations with voltage-dependent frequencies that shape the timing of stimulus-evoked action potentials. These oscillations rely on a persistent sodium conductance, an inactivating potassium conductance, and a calcium-dependent potassium conductance and are reset via inhibitory input such as that delivered by periglomerular cell shunt inhibition. Mitral cells fire bursts, or clusters, of spikes when continuously stimulated. Burst properties depend critically on multiple currents, but a progressive deinactivation of I A over the course of a burst is an important regulator of burst termination. Each of these complex properties exhibits appropriate dynamics and pharmacology as determined by electrophysiological studies. Additionally, we propose that a second, inconsistently observed form of infrathreshold bistability in mitral cells may derive from the activation of ATP-activated potassium currents responding to hypoxic conditions. We discuss the integration of these cellular properties in the larger context of olfactory bulb network operations.

Minicolumns are thought to be the smallest cortical modules within the hierarchical organization of the isocortex. Several reports suggest alterations in minicolumnar morphometry may be involved in psychiatric disorders such as autism, dyslexia, and schizophrenia. Thus far anatomical studies of minicolumns have primarily relied on measurements of pyramidal cell arrays. This study expands on a recursive trace line segmentation method used to define morphometric measures for myelinated axon bundles. The results were compared against those of pyramidal cell arrays derived from immediately adjacent serial sections. Width estimates based on cell somas and myelinated axon bundles were highly correlated (r = 0.9888). Histograms of signal intensity using the recursive trace line method produced expected features of myeloarchitectonics; that is, bundles of Meynert and intervening interradiary plexus. The close correspondence of derived values for myelinated axon bundles and pyramidal cell arrays suggests their participation and interaction within the same modular arrangement of the isocortex.

Low current cortex stimulation produces a sparse and distributed set of activated cells often with distances of several hundred micrometers between cell bodies and the microelectrode. A modeling study based on recently measured densities of high threshold sodium channels Nav1.2 in dendrites and soma and low threshold sodium channels Nav1.6 in the axon shall identify spike initiation sites including a discussion on dendritic spikes. Varying excitability along the neural axis has been observed while studying different electrode positions and configurations. Although the axon initial segment (AIS) and nodes of Ranvier are most excitable, many thin axons and dendrites which are likely to be close to the electrode in the densely packed cortical regions are also proper candidates for spike initiation sites. Cathodic threshold ratio for thin axons and dendrites is about 1:3, whereas 0.2 μm diameter axons passing the electrode tip in 10 μm distance can be activated by 100 μs pulses with 2.6 μA. Direct cathodic excitation of dendrites requires a minimum electrode-fiber distance, which increases with dendrite diameter. Therefore thin dendrites can profit from the stronger electrical field close to the electrode but low current stimulation cannot activate large diameter dendrites, contrary to the inverse recruitment order known from peripheral nerve stimulation. When local depolarization fails to generate a dendritic spike, stimulation is possible via intracellular current flow that initiates an action potential, for example 200 μm distant in the low threshold AIS or in certain cases at the distal dendrite ending. Beside these exceptions, spike initiation site for cathodic low current stimulation appears rather close to the electrode.

Dendrite morphology, a neuron's anatomical fingerprint, is a neuroscientist's asset in unveiling organizational principles in the brain. However, the genetic program encoding the morphological identity of a single dendrite remains a mystery. In order to obtain a formal understanding of dendritic branching, we studied distributions of morphological parameters in a group of four individually identifiable neurons of the fly visual system. We found that parameters relating to the branching topology were similar throughout all cells. Only parameters relating to the area covered by the dendrite were cell type specific. With these areas, artificial dendrites were grown based on optimization principles minimizing the amount of wiring and maximizing synaptic democracy. Although the same branching rule was used for all cells, this yielded dendritic structures virtually indistinguishable from their real counterparts. From these principles we derived a fully-automated model-based neuron reconstruction procedure validating the artificial branching rule. In conclusion, we suggest that the genetic program implementing neuronal branching could be constant in all cells whereas the one responsible for the dendrite spanning field should be cell specific.

Unraveling the molecular mechanisms governing long-term synaptic plasticity is a key to understanding how the brain stores information in neural circuits and adapts to a changing environment. Brain-derived neurotrophic factor (BDNF) has emerged as a regulator of stable, late phase long-term potentiation (L-LTP) at excitatory glutamatergic synapses in the adult brain. However, the mechanisms by which BDNF triggers L-LTP are controversial. Here, we distill and discuss the latest advances along three main lines: 1) TrkB receptor-coupled translational control underlying dendritic protein synthesis and L-LTP, 2) Mechanisms for BDNF-induced rescue of L-LTP when protein synthesis is blocked, and 3) BDNF-TrkB regulation of actin cytoskeletal dynamics in dendritic spines. Finally, we explore the inter-relationships between BDNF-regulated mechanisms, how these mechanisms contribute to different forms of L-LTP in the hippocampus and dentate gyrus, and outline outstanding issues for future research.

Solidification patterns in crystalline systems are one the most aesthetically pleasing examples of pattern formation in nature. During solidification when a planar solid/liquid interface becomes unstable, it reorganizes itself into cellular and dendritic micro arrangements. These interfacial patterns appear as fractal features and their level of complexity is characterized by their fractal dimension or by their primary and secondary arms spacing. In metallic systems, because solidification microstructure is a defining link between production techniques and the mechanical properties, it is technologically crucial and economically favored to achieve desired properties of the final product through a controlled solidification process.
One of the major obstacles for the solidification studies in metallic systems is its occurrence at high temperatures and the lack of experimental techniques to observe this phenomenon in real-time. Hence all the previous in-situ research was carried out on substitute transparent materials, which mimic the forms of solidification in metallic systems. The real-time technologies and adequate techniques to observe patterning in metallic-systems-themselves were only introduced in the recent years eventually proving the possibility to answer the fundamental question: to what extend the substitute transparent materials can mimic the forms of solidification in metallic systems?
Our proposed study uses a high-temperature Laser-Scanning Confocal Microscopy (LSCM) combined with in-house technological advancements to make real-time observations of phase transformations at high temperatures and such system was used to observe pattern formations during steel solidification. Using the Concentric Solidification technique, pattern formations during solidification of steel were observed in real-time and subsequently the effect of cooling rate and alloy composition on the cellular spacing were discussed morphologically and analytically.