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Christian Lohmann

Publications and source records attributed to Christian Lohmann.

5 recordsLinked to original sources

Local calcium transients regulate the spontaneous motility of dendritic filopodia.

During development, dendrites, and in particular dendritic filopodia, undergo extensive structural remodeling, presumably to help establish synaptic contacts. Here, we investigated the role of calcium signaling in dendritic plasticity by simultaneously recording calcium dynamics and filopodial growth in rat hippocampal slice cultures. Local calcium transients occurred in dendritic filopodia and shafts, often at putative synaptic sites. These events were highly correlated with filopodial motility: comparatively rare when individual filopodia emerged from the dendrite, they became more frequent after filopodia started growing, finally causing them to halt. Accordingly, an experimental reduction of the frequency of local calcium transients elicited filopodial growth and, conversely, calcium uncaging reduced filopodial motility. Our observations suggest that low levels of local calcium transients facilitate filopodial outgrowth, whereas high levels inhibit the formation of filopodia and stabilize newly formed ones. This process may facilitate synapse formation and may serve as a homeostatic mechanism distributing synapses evenly along developing dendrites.

2-Amino-5-phosphonovalerate↗

Regulation of dendritic growth and plasticity by local and global calcium dynamics.

The dendritic arbors of neurons are organized into unique spatial patterns that are well suited for their specific functions. Although the intracellular signaling pathways that determine dendritic arbor size and branching patterns during development are not completely understood, it is evident that neurotransmission-mediated elevation in intracellular calcium levels ([Ca2+]i) plays a major role. Recent advances in calcium imaging and genetic approaches have provided new insight into how calcium acts to regulate dendritic growth and remodeling. Global increases in [Ca2+]i that occur upon neuronal depolarization control dendritic arbor growth by regulating transcription. However, the detailed branching patterns of dendritic arbors are regulated by local calcium signaling. Calcium-induced calcium release (CICR) from intracellular stores acts to locally stabilize dendritic branches, presumably triggered by neurotransmission upon contact with newly established inputs. The effects of global and local increases in [Ca2+]i on dendritic structure are cell type- and age-dependent. Unraveling the signaling pathways evoked by local and global rises in [Ca2+]i that shape the developing dendritic arbor at each developmental stage remains challenging but highly important.

Calcium↗

Heat stress-dependent DNA binding of Arabidopsis heat shock transcription factor HSF1 to heat shock gene promoters in Arabidopsis suspension culture cells in vivo.

Using UV laser cross-linking and immunoprecipitation we measured the in vivo binding of Arabidopsis heat shock transcription factor HSF1 to the promoters of target genes, Hsp18.2 and Hsp70. The amplification of promoter sequences, co-precipitated with HSF1-specific antibodies, indicated that HSF1 is not bound in the absence of heat stress. Binding to promoter sequences of target genes is rapidly induced by heat stress, continues throughout the heat treatment, and declines during subsequent recovery at room temperature. The molecular mechanisms underlying the differences between Hsp18.2 and Hsp70 in the kinetics of HSF1/promoter binding and corresponding mRNA expression profiles are discussed.

Arabidopsis↗

Imaging calcium dynamics in the nervous system by means of ballistic delivery of indicators.

The use of fluorescence-based calcium indicators has, over the years, unraveled important calcium-dependent mechanisms underlying neuronal function and development. However, difficulties associated with the loading of calcium indicators have limited their widespread use, particularly for the study of neuronal processing in the adult nervous system. Here, we show that in the central and peripheral nervous systems, populations of neurons and their processes, including dendritic spines and filopodia, can be labeled rapidly and efficiently by delivering calcium indicator-coated particles using a 'gene gun'. Importantly, neuronal labeling occurred both in vitro and in vivo, and across a wide range of ages and preparations. The labeled cells demonstrate spontaneous and evoked calcium transients, indicating that particle-mediated delivery is not deleterious to neuronal function. Furthermore, unlike loading with patch pipettes, cytoplasmic content is preserved following ballistic loading. This enables the study of calcium-dependent second messenger pathways without loss of signaling components. The ballistic delivery of calcium indicators thus opens up many new avenues for further exploration of the structure and function of the nervous system from single spines to neuronal networks.

Animals↗

Transmitter-evoked local calcium release stabilizes developing dendrites.

In the central nervous system, dendritic arborizations of neurons undergo dynamic structural remodelling during development. Processes are elaborated, maintained or eliminated to attain the adult pattern of synaptic connections. Although neuronal activity influences this remodelling, it is not known how activity exerts its effects. Here we show that neurotransmission-evoked calcium (Ca(2+)) release from intracellular stores stabilizes dendrites during the period of synapse formation. Using a ballistic labelling method to load cells with Ca(2+) indicator dyes, we simultaneously monitored dendritic activity and structure in the intact retina. Two distinct patterns of spontaneous Ca(2+) increases occurred in developing retinal ganglion cells--global increases throughout the arborization, and local 'flashes' of activity restricted to small dendritic segments. Blockade of local, but not global, activity caused rapid retraction of dendrites. This retraction was prevented locally by focal uncaging of caged Ca(2+) that triggered Ca(2+) release from internal stores. Thus, local Ca(2+) release is a mechanism by which afferent activity can selectively and differentially regulate dendritic structure across the developing arborization.

Acetylcholine↗