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Dendritic Elaboration: Morphology and Chemistry

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Neuroscience in the 21st Century

Abstract

Dendrites (from Greek δένδρον déndron, “tree”) are one of the major structural elements of neurons and exhibit enormously diverse forms. They receive, integrate and process thousands of excitatory, and to a lesser extent inhibitory, synaptic inputs terminating either on the dendritic shaft or spine. The morphology and size of dendrites critically determines the mode of connectivity between neurons with dendritic trees ramifying in characteristic spatial domains where they receive specific synaptic inputs. Therefore, dendrites play a critical role in the integration of these inputs and in determining the extent of action potential generation.

Furthermore, the structure and branching of dendrites together with the availability and variation in voltage-gated ion conductances strongly influences how synaptic inputs within a given microcircuit are integrated. This integration is both temporal – involving the summation of signals as well as spatial – entailing the aggregation of excitatory and inhibitory inputs from individual branches. Dendrites were thought to convey electrical signals passively. However, as shown recently dendrites can activly support action potentials and release neurotransmitters, a property that was originally believed to be specific to axons.

Voltage changes at the soma result from activation of distal synapses propagating to the soma without the aid of voltage-gated ion channels. Based on the passive cable theory one can measure how changes in dendritic morphology lead to changes of the membrane voltage, and thus how variation in dendrite architectures affects the overall output characteristics of the neuron. In this context it is also important to know that the membrane of dendrites contain ensembles of various proteins that may contribute to amplify or attenuate synaptic inputs. Sodium, calcium, and potassium channels are all implicated to affect input modulation. Each of these ions has a family of channel types with its own biophysical characteristics relevant to synaptic input modulation thereby controlling the latency of channel opening, the electrical conductance of the ion pore, the activation voltage and duration. This could lead to an amplification of even weak inputs from distal synapses by sodium and calcium currents. One important feature of dendrites, endowed by their active voltage gated conductances, is their ability to propagate action potentials back into the dendritic tree. Known as “backpropagating action potentials,” these signals depolarize the dendritic tree, a mechanism that contributes to synaptic modulation and long- and short-term potentiation and plasticity.

Abnormalities in dendritic structural plasticity are a characteristic feature of many mental, neurological and neurodegenerative brain disorders. Changes in synaptic function or neuronal circuitry associated with disease produce severe structural changes in dendritic length and branching, dramatic loss of spines accompanied also by changes in spine morphology. Thus, pathologies in dendritic structure are followed by remodeling of dendritic and synaptic circuits and changes in learning, memory and mind of the brain.

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Authors and Affiliations

  1. Institute for Neuroscience and Medicine INM-2, Research Centre Jülich, Jülich, 52425, Germany

    Astrid Rollenhagen & Joachim H. R. Lübke

  2. Department of Psychiatry, Psychotherapy and Psychosomatics, RWTH/University Hospital Aachen and JARA Translational Brain Medicine, Aachen, Germany

    Joachim H. R. Lübke

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  1. Astrid Rollenhagen
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  1. Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, New York, USA

    Donald W. Pfaff

  2. National Institute on Drug Abuse (NIDA), National Institutes of Health (NIH), Rockville, Maryland, USA

    Nora D. Volkow

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Rollenhagen, A., Lübke, J.H.R. (2016). Dendritic Elaboration: Morphology and Chemistry. In: Pfaff, D., Volkow, N. (eds) Neuroscience in the 21st Century. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-3474-4_11

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