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Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation.

Bencsik N, Szíber Z, Liliom H, Tárnok K, Borbély S, Gulyás M, Rátkai A, Szűcs A, Hazai-Novák D, Ellwanger K, Rácz B, Pfizenmaier K, Hausser A, Schlett K - J. Cell Biol. (2015)

Bottom Line: In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways.Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation.We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.

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PKD activity regulates spine morphology in cultured neurons. (A) Representative inverted fluorescent images of tertiary dendritic branches of EGFP-transfected neurons treated with 20 mM KCl and/or 3 µM kbNB 142-70 or transfected with kdPKD-EGFP. Bars, 2 µm. (B and C) Morphological characteristics of dendritic spines in EGFP-transfected neurons, plotted along their head/neck width ratio (HN index) and length (B) and mean proportion of filamentous, mushroom, or stubby spines upon 16 h of 20 mM KCl and/or 3 µM kbNB 142-70 treatments (C). (D) Mean protrusion density on the tertiary branches of EGFP or kdPKD-EGFP–expressing neurons. (E) Mean proportion of filamentous, mushroom, or stubby spines in neurons transfected with EGFP or kdPKD-EGFP. (F and G) Morphological characteristics of dendritic spines in EGFP (F)- or kdPKD-EGFP (G)–transfected neurons, plotted along their head/neck width ratio (HN index) and length. Data were obtained from three to four independent cultures; the number of spines is indicated in the legends. All data are displayed as mean ± SEM. Asterisks represent significance compared with control values (white columns), and the $ symbol indicates significant differences between data pairs. *, P < 0.05; ** or $$, P < 0.01; *** or $$$, P < 0.001.
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fig3: PKD activity regulates spine morphology in cultured neurons. (A) Representative inverted fluorescent images of tertiary dendritic branches of EGFP-transfected neurons treated with 20 mM KCl and/or 3 µM kbNB 142-70 or transfected with kdPKD-EGFP. Bars, 2 µm. (B and C) Morphological characteristics of dendritic spines in EGFP-transfected neurons, plotted along their head/neck width ratio (HN index) and length (B) and mean proportion of filamentous, mushroom, or stubby spines upon 16 h of 20 mM KCl and/or 3 µM kbNB 142-70 treatments (C). (D) Mean protrusion density on the tertiary branches of EGFP or kdPKD-EGFP–expressing neurons. (E) Mean proportion of filamentous, mushroom, or stubby spines in neurons transfected with EGFP or kdPKD-EGFP. (F and G) Morphological characteristics of dendritic spines in EGFP (F)- or kdPKD-EGFP (G)–transfected neurons, plotted along their head/neck width ratio (HN index) and length. Data were obtained from three to four independent cultures; the number of spines is indicated in the legends. All data are displayed as mean ± SEM. Asterisks represent significance compared with control values (white columns), and the $ symbol indicates significant differences between data pairs. *, P < 0.05; ** or $$, P < 0.01; *** or $$$, P < 0.001.

Mentions: 16 h of KCl-induced depolarization significantly increased the ratio of mushroom spines (Fig. 3, A and C) without affecting spine density (not depicted). KCl-induced changes in spine morphology were also evident when individual spines were plotted according to their length and HN index (head/neck width ratio; Fig. 3 B). As this happened at the expense of thin, filamentous spines, we assume that long-term depolarization leads to F-actin stabilization and, consequently, the expansion of dendritic spine heads. Collectively, our data indicate decreased actin dynamics when enlarged dendritic spine heads are already stabilized.


Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation.

Bencsik N, Szíber Z, Liliom H, Tárnok K, Borbély S, Gulyás M, Rátkai A, Szűcs A, Hazai-Novák D, Ellwanger K, Rácz B, Pfizenmaier K, Hausser A, Schlett K - J. Cell Biol. (2015)

PKD activity regulates spine morphology in cultured neurons. (A) Representative inverted fluorescent images of tertiary dendritic branches of EGFP-transfected neurons treated with 20 mM KCl and/or 3 µM kbNB 142-70 or transfected with kdPKD-EGFP. Bars, 2 µm. (B and C) Morphological characteristics of dendritic spines in EGFP-transfected neurons, plotted along their head/neck width ratio (HN index) and length (B) and mean proportion of filamentous, mushroom, or stubby spines upon 16 h of 20 mM KCl and/or 3 µM kbNB 142-70 treatments (C). (D) Mean protrusion density on the tertiary branches of EGFP or kdPKD-EGFP–expressing neurons. (E) Mean proportion of filamentous, mushroom, or stubby spines in neurons transfected with EGFP or kdPKD-EGFP. (F and G) Morphological characteristics of dendritic spines in EGFP (F)- or kdPKD-EGFP (G)–transfected neurons, plotted along their head/neck width ratio (HN index) and length. Data were obtained from three to four independent cultures; the number of spines is indicated in the legends. All data are displayed as mean ± SEM. Asterisks represent significance compared with control values (white columns), and the $ symbol indicates significant differences between data pairs. *, P < 0.05; ** or $$, P < 0.01; *** or $$$, P < 0.001.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4555815&req=5

fig3: PKD activity regulates spine morphology in cultured neurons. (A) Representative inverted fluorescent images of tertiary dendritic branches of EGFP-transfected neurons treated with 20 mM KCl and/or 3 µM kbNB 142-70 or transfected with kdPKD-EGFP. Bars, 2 µm. (B and C) Morphological characteristics of dendritic spines in EGFP-transfected neurons, plotted along their head/neck width ratio (HN index) and length (B) and mean proportion of filamentous, mushroom, or stubby spines upon 16 h of 20 mM KCl and/or 3 µM kbNB 142-70 treatments (C). (D) Mean protrusion density on the tertiary branches of EGFP or kdPKD-EGFP–expressing neurons. (E) Mean proportion of filamentous, mushroom, or stubby spines in neurons transfected with EGFP or kdPKD-EGFP. (F and G) Morphological characteristics of dendritic spines in EGFP (F)- or kdPKD-EGFP (G)–transfected neurons, plotted along their head/neck width ratio (HN index) and length. Data were obtained from three to four independent cultures; the number of spines is indicated in the legends. All data are displayed as mean ± SEM. Asterisks represent significance compared with control values (white columns), and the $ symbol indicates significant differences between data pairs. *, P < 0.05; ** or $$, P < 0.01; *** or $$$, P < 0.001.
Mentions: 16 h of KCl-induced depolarization significantly increased the ratio of mushroom spines (Fig. 3, A and C) without affecting spine density (not depicted). KCl-induced changes in spine morphology were also evident when individual spines were plotted according to their length and HN index (head/neck width ratio; Fig. 3 B). As this happened at the expense of thin, filamentous spines, we assume that long-term depolarization leads to F-actin stabilization and, consequently, the expansion of dendritic spine heads. Collectively, our data indicate decreased actin dynamics when enlarged dendritic spine heads are already stabilized.

Bottom Line: In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways.Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation.We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.

Show MeSH
Related in: MedlinePlus