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The diffusional properties of dendrites depend on the density of dendritic spines
Santamaria, Fidel,Wils, Stefan,De Schutter, Erik,Augustine, George J. Blackwell Publishing Ltd 2011 The European journal of neuroscience Vol.34 No.4
<P><B>Abstract</B></P><P>We combined computational modeling and experimental measurements to determine the influence of dendritic structure on the diffusion of intracellular chemical signals in mouse cerebellar Purkinje cells and hippocamal CA1 pyramidal cells. Modeling predicts that molecular trapping by dendritic spines causes diffusion along spiny dendrites to be anomalous and that the value of the anomalous exponent (<I>d</I><SUB><I>w</I></SUB>) is proportional to spine density in both cell types. To test these predictions we combined the local photorelease of an inert dye, rhodamine dextran, with two‐photon fluorescence imaging to track diffusion along dendrites. Our results show that anomalous diffusion is present in spiny dendrites of both cell types. Further, the anomalous exponent is linearly related to the density of spines in pyramidal cells and <I>d</I><SUB><I>w</I></SUB> in Purkinje cells is consistent with such a relationship. We conclude that anomalous diffusion occurs in the dendrites of multiple types of neurons. Because spine density is dynamic and depends on neuronal activity, the degree of anomalous diffusion induced by spines can dynamically regulate the movement of molecules along dendrites.</P>
A Model of Induction of Cerebellar Long-Term Depression Including RKIP Inactivation of Raf and MEK
Hepburn, Iain,Jain, Anant,Gangal, Himanshu,Yamamoto, Yukio,Tanaka-Yamamoto, Keiko,De Schutter, Erik Frontiers Media S.A. 2017 Frontiers in molecular neuroscience Vol.10 No.-
<P>We report an updated stochastic model of cerebellar Long Term Depression (LTD) with improved realism. Firstly, we verify experimentally that dissociation of Raf kinase inhibitor protein (RKIP) from Mitogen-activated protein kinase kinase (MEK) is required for cerebellar LTD and add this interaction to an earlier published model, along with the known requirement of dissociation of RKIP from Raf kinase. We update Ca<SUP>2+</SUP> dynamics as a constant-rate influx, which captures experimental input profiles accurately. We improve α-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid (AMPA) receptor interactions by adding phosphorylation and dephosphorylation of AMPA receptors when bound to glutamate receptor interacting protein (GRIP). The updated model is tuned to reproduce experimental Ca<SUP>2+</SUP> peak vs. LTD amplitude curves at four different Ca<SUP>2+</SUP> pulse durations as closely as possible. We find that the updated model is generally more robust with these changes, yet we still observe some sensitivity of LTD induction to copy number of the key signaling molecule Protein kinase C (PKC). We predict natural variability in this number by stochastic diffusion may influence the probabilistic LTD response to Ca<SUP>2+</SUP> input in Purkinje cell spines and propose this as an extra source of stochasticity that may be important also in other signaling systems.</P>