![]() J Physiol 399:247–266īarrionuevo G, Brown TH (1983) Associative long-term potentiation in hippocampal slices. CRC Press, Boca RatonĪscher P, Nowak L (1988) The role of divalent cations in the N-methyl- d-aspartate responses of mouse central neurones in culture. Proc Natl Acad Sci USA 98:8071–8076Īltman J, Bayer S (1997) Development of the cerebellar system in relation to its evolution, structure, and functions. Nat Neurosci 3(Suppl):1178–1183Īdams MM, Shah RA, Janssen WG, Morrison JH (2001) Different modes of hippocampal plasticity in response to estrogen in young and aged female rats. This process is experimental and the keywords may be updated as the learning algorithm improves.Ībbott LF, Nelson SB (2000) Synaptic plasticity: taming the beast. These keywords were added by machine and not by the authors. Thus, pathologies in dendritic structure are followed by remodeling of dendritic and synaptic circuits and changes in learning, memory and mind of the brain. 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. 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.Ībnormalities in dendritic structural plasticity are a characteristic feature of many mental, neurological and neurodegenerative brain disorders. One important feature of dendrites, endowed by their active voltage gated conductances, is their ability to propagate action potentials back into the dendritic tree. This could lead to an amplification of even weak inputs from distal synapses by sodium and calcium currents. 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. Sodium, calcium, and potassium channels are all implicated to affect input modulation. 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. 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. ![]() Voltage changes at the soma result from activation of distal synapses propagating to the soma without the aid of voltage-gated ion channels. However, as shown recently dendrites can activly support action potentials and release neurotransmitters, a property that was originally believed to be specific to axons. ![]() Dendrites were thought to convey electrical signals passively. 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. Therefore, dendrites play a critical role in the integration of these inputs and in determining the extent of action potential generation.įurthermore, 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. 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. They receive, integrate and process thousands of excitatory, and to a lesser extent inhibitory, synaptic inputs terminating either on the dendritic shaft or spine. Dendrites (from Greek δένδρον déndron, “tree”) are one of the major structural elements of neurons and exhibit enormously diverse forms.
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