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The Relationship of Sodium and Potassium Conductances with Dynamic States of a Mathematical Model of Electrosensory Pyramidal Neurons  [PDF]
Takaaki Shirahata
Applied Mathematics (AM) , 2016, DOI: 10.4236/am.2016.79072
Abstract: Electrosensory pyramidal neurons in weakly electric fish can generate burst firing. Based on the Hodgkin-Huxley scheme, a previous study has developed a mathematical model that reproduces this burst firing. This model is called the ghostbursting model and is described by a system of non-linear ordinary differential equations. Although the dynamic state of this model is a quiescent state during low levels of electrical stimulation, an increase in the level of electrical stimulation transforms the dynamic state first into a repetitive spiking state and finally into a burst firing state. The present study performed computer simulation analysis of the ghostbursting model to evaluate the sensitivity of the three dynamic states of the model (i.e., the quiescent, repetitive spiking, and burst firing states) to variations in sodium and potassium conductance values of the model. The present numerical simulation analysis revealed the sensitivity of the electrical stimulation threshold required for eliciting the burst firing state to variations in the values of four ionic conductances (i.e., somatic sodium, dendritic sodium, somatic potassium, and dendritic potassium conductances) in the ghostbursting model.
Bursts and Isolated Spikes Code for Opposite Movement Directions in Midbrain Electrosensory Neurons  [PDF]
Navid Khosravi-Hashemi, Maurice J. Chacron
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040339
Abstract: Directional selectivity, in which neurons respond strongly to an object moving in a given direction but weakly or not at all to the same object moving in the opposite direction, is a crucial computation that is thought to provide a neural correlate of motion perception. However, directional selectivity has been traditionally quantified by using the full spike train, which does not take into account particular action potential patterns. We investigated how different action potential patterns, namely bursts (i.e. packets of action potentials followed by quiescence) and isolated spikes, contribute to movement direction coding in a mathematical model of midbrain electrosensory neurons. We found that bursts and isolated spikes could be selectively elicited when the same object moved in opposite directions. In particular, it was possible to find parameter values for which our model neuron did not display directional selectivity when the full spike train was considered but displayed strong directional selectivity when bursts or isolated spikes were instead considered. Further analysis of our model revealed that an intrinsic burst mechanism based on subthreshold T-type calcium channels was not required to observe parameter regimes for which bursts and isolated spikes code for opposite movement directions. However, this burst mechanism enhanced the range of parameter values for which such regimes were observed. Experimental recordings from midbrain neurons confirmed our modeling prediction that bursts and isolated spikes can indeed code for opposite movement directions. Finally, we quantified the performance of a plausible neural circuit and found that it could respond more or less selectively to isolated spikes for a wide range of parameter values when compared with an interspike interval threshold. Our results thus show for the first time that different action potential patterns can differentially encode movement and that traditional measures of directional selectivity need to be revised in such cases.
Transcriptional control of dendritic patterning in Drosophila neurons
Michel Tassetto, Fen-Biao Gao
Genome Biology , 2006, DOI: 10.1186/gb-2006-7-7-225
Abstract: Many neurons receive most of their input through thin processes, called dendrites, that form synapses with the axons of other neurons. Dendrites can be highly branched and have complex architecture. The shape and size of the dendrites of a single neuron determine the number and specificity of the axonal contacts it receives. Therefore, the development of the correct pattern of dendritic branching, or arborization, on different neurons is essential for the proper functioning of the nervous system. Neuronal subtypes in mammals and insects can have specific patterns of dendrite branching [1,2], and several unbiased genome-wide 'forward' genetic screens in Drosophila have identified factors that regulate dendritic morphogenesis in both the peripheral and central nervous systems [3-5]. But although these studies uncovered dozens of genes that might have essential roles in dendritic morphogenesis, most of the genes have yet to be cloned and characterized, and the information on genetic pathways has been sparse. Except for a few identified transcription factors that have been implicated in dendritic morphogenesis in flies and mammals [6-14], little is known about the overall transcriptional programs that specify the characteristic patterns of dendritic arborization in different neurons.Over the past few years, however, large-scale 'reverse' genetic approaches such as RNA interference (RNAi) have emerged to help characterize molecular pathways. Screens based on RNAi have been used to analyze cellular processes in cultured insect cells [15,16] and in intact Drosophila embryos [17,18]. In a recent paper in Genes and Development, Parrish et al. [19] report the results of an in vivo RNAi-based screen set up to examine transcription factor networks that control several aspects of dendritic morphogenesis in Drosophila.Parrish and colleagues [19] took advantage of the simple and stereotyped dendrite branching patterns of type I dendritic arborization (DA) neurons in the Drosophila
SIRT1 Regulates Dendritic Development in Hippocampal Neurons  [PDF]
Juan F. Codocedo, Claudio Allard, Juan A. Godoy, Lorena Varela-Nallar, Nibaldo C. Inestrosa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047073
Abstract: Dendritic arborization is required for proper neuronal connectivity. SIRT1, a NAD+ dependent histone deacetylase, has been associated to ageing and longevity, which in neurons is linked to neuronal differentiation and neuroprotection. In the present study, the role of SIRT1 in dendritic development was evaluated in cultured hippocampal neurons which were transfected at 3 days in vitro with a construct coding for SIRT1 or for the dominant negative SIRT1H363Y, which lacks the catalytic activity. Neurons overexpressing SIRT1 showed an increased dendritic arborization, while neurons overexpressing SIRT1H363Y showed a reduction in dendritic arbor complexity. The effect of SIRT1 was mimicked by treatment with resveratrol, a well known activator of SIRT1, which has no effect in neurons overexpressing SIRT1H363Y indicating that the effect of resveratrol was specifically mediated by SIRT1. Moreover, hippocampal neurons overexpressing SIRT1 were resistant to dendritic dystrophy induced by Aβ aggregates, an effect that was dependent on the deacetylase activity of SIRT1. Our findings indicate that SIRT1 plays a role in the development and maintenance of dendritic branching in hippocampal neurons, and suggest that these effects are mediated by the ROCK signaling pathway.
Quantitative analysis of dendritic branching pattern of large neurons in human cerebellum  [PDF]
Milo?evi? Neboj?a T.,Ristanovi? Du?an,Mari? Du?ica L.,Gudovi? Radmila
Vojnosanitetski Pregled , 2010, DOI: 10.2298/vsp1009712m
Abstract: Background/Aim. Dentate nucleus (nucleus dentatus) is the most distant of the cerebellar nuclei and the major system for information transfer in the cerebellum. So far, dendritic branches of four different kinds of large neurons of dentate nucleus, have been considered mainly qualitatively with no quantification of their morphological features. The aim of the study was to test the qualitative hypothesis that the human dentate nucleus is composed of various types of the large neurons by quantitative analysis of their dendritic branching patterns. Methods. Series of horizontal sections of the dentate nuclei were taken from 15 adult human brains, free of diagnosed neurological disorders. The 189 Golgi-impregnated images of large neurons were recorded by a digital camera connected to a light microscope. Dendritic branching patterns of digitized neuronal images were analyzed by modified Sholl and fractal analyses. Results. The number of intersections (Nm), critical radius (rc) and fractal dimension (D) of dendritic branching pattern for four types of the large neurons were calculated, statistically evaluated and analyzed. The results show that there is a significant difference between four neuronal types in one morphometric parameter at least. Conclusion. The present study is the first attempt to analyze quantitatively the dendritic branching pattern of neurons from the dentate nucleus in the human. The hypothesis that the four types of the large neurons exist in this part of human cerebellum is successfully supported.
Computational Modeling Reveals Dendritic Origins of GABAA-Mediated Excitation in CA1 Pyramidal Neurons  [PDF]
Naomi Lewin, Emre Aksay, Colleen E. Clancy
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047250
Abstract: GABA is the key inhibitory neurotransmitter in the adult central nervous system, but in some circumstances can lead to a paradoxical excitation that has been causally implicated in diverse pathologies from endocrine stress responses to diseases of excitability including neuropathic pain and temporal lobe epilepsy. We undertook a computational modeling approach to determine plausible ionic mechanisms of GABAA-dependent excitation in isolated post-synaptic CA1 hippocampal neurons because it may constitute a trigger for pathological synchronous epileptiform discharge. In particular, the interplay intracellular chloride accumulation via the GABAA receptor and extracellular potassium accumulation via the K/Cl co-transporter KCC2 in promoting GABAA-mediated excitation is complex. Experimentally it is difficult to determine the ionic mechanisms of depolarizing current since potassium transients are challenging to isolate pharmacologically and much GABA signaling occurs in small, difficult to measure, dendritic compartments. To address this problem and determine plausible ionic mechanisms of GABAA-mediated excitation, we built a detailed biophysically realistic model of the CA1 pyramidal neuron that includes processes critical for ion homeostasis. Our results suggest that in dendritic compartments, but not in the somatic compartments, chloride buildup is sufficient to cause dramatic depolarization of the GABAA reversal potential and dominating bicarbonate currents that provide a substantial current source to drive whole-cell depolarization. The model simulations predict that extracellular K+ transients can augment GABAA-mediated excitation, but not cause it. Our model also suggests the potential for GABAA-mediated excitation to promote network synchrony depending on interneuron synapse location - excitatory positive-feedback can occur when interneurons synapse onto distal dendritic compartments, while interneurons projecting to the perisomatic region will cause inhibition.
Distinct Mammalian Precursors Are Committed to Generate Neurons with Defined Dendritic Projection Patterns  [PDF]
Wolfgang Kelsch,Colleen P. Mosley,Chia-Wei Lin,Carlos Lois
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0050300
Abstract: The mechanisms that regulate how dendrites target different neurons to establish connections with specific cell types remain largely unknown. In particular, the formation of cell-type–specific connectivity during postnatal neurogenesis could be either determined by the local environment of the mature neuronal circuit or by cell-autonomous properties of the immature neurons, already determined by their precursors. Using retroviral fate mapping, we studied the lamina-specific dendritic targeting of one neuronal type as defined by its morphology and intrinsic somatic electrical properties in neonatal and adult neurogenesis. Fate mapping revealed the existence of two separate populations of neuronal precursors that gave rise to the same neuronal type with two distinct patterns of dendritic targeting—innervating either a deep or superficial lamina, where they connect to different types of principal neurons. Furthermore, heterochronic and heterotopic transplantation demonstrated that these precursors were largely restricted to generate neurons with a predetermined pattern of dendritic targeting that was independent of the host environment. Our results demonstrate that, at least in the neonatal and adult mammalian brain, the pattern of dendritic targeting of a given neuron is a cell-autonomous property of their precursors.
Distinct Mammalian Precursors Are Committed to Generate Neurons with Defined Dendritic Projection Patterns  [PDF]
Wolfgang Kelsch,Colleen P Mosley,Chia-Wei Lin,Carlos Lois
PLOS Biology , 2007, DOI: 10.1371/journal.pbio.0050300
Abstract: The mechanisms that regulate how dendrites target different neurons to establish connections with specific cell types remain largely unknown. In particular, the formation of cell-type–specific connectivity during postnatal neurogenesis could be either determined by the local environment of the mature neuronal circuit or by cell-autonomous properties of the immature neurons, already determined by their precursors. Using retroviral fate mapping, we studied the lamina-specific dendritic targeting of one neuronal type as defined by its morphology and intrinsic somatic electrical properties in neonatal and adult neurogenesis. Fate mapping revealed the existence of two separate populations of neuronal precursors that gave rise to the same neuronal type with two distinct patterns of dendritic targeting—innervating either a deep or superficial lamina, where they connect to different types of principal neurons. Furthermore, heterochronic and heterotopic transplantation demonstrated that these precursors were largely restricted to generate neurons with a predetermined pattern of dendritic targeting that was independent of the host environment. Our results demonstrate that, at least in the neonatal and adult mammalian brain, the pattern of dendritic targeting of a given neuron is a cell-autonomous property of their precursors.
Dendritic spinules in rat nigral neurons revealed by acetylcholinesterase immunocytochemistry and serial sections of the dendritic spine heads.  [cached]
Katsuyoshi Ishii,Tsuyako Hayashida,Tsutomu Hashikawa,Shigeru Tsuji
Folia Histochemica et Cytobiologica , 2004, DOI: 10.5603/4659
Abstract: Dendritic spinules of rat nigral neurons were visualized at electron microscopic level by acetylcholinesterase immunocytochemistry and serial sections of the nigral dendrites. The spinules (at least 150 nm in length and 10-20 nm in width) which protruded from the spine heads are found in extracellular space in the neuropil and particularly between nerve terminals of the presynaptic neurons and fine glial processes. The nigral spinules are, however, not observed as invaginated processes in the nerve terminals. The dendritic spinule may be endowed with synaptic plasticity and metabolic exchange between nerve terminals and glial processes.
The BDNF effects on dendritic spines of mature hippocampal neurons depend on neuronal activity  [PDF]
Yves Kellner,Nina G?decke,Tobias Dierkes,Nils Thieme,Marta Zagrebelsky,Martin Korte
Frontiers in Synaptic Neuroscience , 2014, DOI: 10.3389/fnsyn.2014.00005
Abstract: The fine tuning of neural networks during development and learning relies upon both functional and structural plastic processes. Changes in the number as well as in the size and shape of dendritic spines are associated to long-term activity-dependent synaptic plasticity. However, the molecular mechanisms translating functional into structural changes are still largely unknown. In this context, neurotrophins, like Brain-Derived Neurotrophic Factor (BDNF), are among promising candidates. Specifically BDNF-TrkB receptor signaling is crucial for activity-dependent strengthening of synapses in different brain regions. BDNF application has been shown to positively modulate dendritic and spine architecture in cortical and hippocampal neurons as well as structural plasticity in vitro. However, a global BDNF deprivation throughout the central nervous system (CNS) resulted in very mild structural alterations of dendritic spines, questioning the relevance of the endogenous BDNF signaling in modulating the development and the mature structure of neurons in vivo. Here we show that a loss-of-function approach, blocking BDNF results in a significant reduction in dendritic spine density, associated with an increase in spine length and a decrease in head width. These changes are associated with a decrease in F-actin levels within spine heads. On the other hand, a gain-of-function approach, applying exogenous BDNF, could not reproduce the increase in spine density or the changes in spine morphology previously described. Taken together, we show here that the effects exerted by BDNF on the dendritic architecture of hippocampal neurons are dependent on the neuron's maturation stage. Indeed, in mature hippocampal neurons in vitro as shown in vivo BDNF is specifically required for the activity-dependent maintenance of the mature spine phenotype.
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