Michael Maibach & Philipp Braaker

Speaker 1

Michael Maibach, PhD student

Investigating Mitochondrial Motility in the Context of Synaptic Plasticity and Development

Abstract

During development, neurons expand their processes and form new connections to establish functional neuronal circuits. However, the establishment of these networks poses a unique logistical challenge for neurons: Synaptic transmission is extremely energy-intensive, and the complex morphology of neurons complicates the distribution of the required energy. It is thus crucial that there are mechanisms in place which ensure energetic demands are met across synapses.

While the specifics of such mechanisms remain uncertain, they are likely to have far reaching consequences for the function of the network as a whole, as the formation, stabilization and elimination of synapses are energy dependent. Mitochondria represent an ideal contender to be at the centre of such a mechanism as they are the main producers of ATP and are able to reposition themselves along neuronal processes. In fact mitochondrial motility is regulated by neuronal activity and disruption of mitochondrial motility during development results in aberrant dendritic growth and network wiring.

In this research project, I am thus investigating the involvement of mitochondria in synaptic plasticity and development. My current approach involves simultaneously recording mitochondrial motility, spontaneous activity and spine plasticity in the dendrites of pyramidal cells within organotypic slice cultures of the primary visual cortex.

I hypothesize that the presence or absence of mitochondria at individual synapses determines their long-term fate, thus influencing the fine scale wiring of the developing brain.

Speaker 2

Philipp Braaker, postdoc

Activity-driven myelin sheath growth is mediated by mGluR5

Abstract

The nervous system employs multiple activity-dependent mechanisms to adapt to challenging tasks. Activity-dependent myelination by oligodendrocytes is such a process, affecting the outcome of learning processes.

I will present recent work establishing an optogenetic platform for zebrafish to drive activity-dependent myelination. Using these optogenetic approaches, I identified metabotropic glutamate receptor 5 signaling to mediate activity-driven myelin sheath elongation.

Together, these findings provide a framework to study how neuronal activity regulates myelination in disease and, in turn, how adaptive myelination influences circuit function and the electrical properties of axons in an intact animal.