OOD SOC

Research

Background:

 We and most animals obtain information about our environment by analyzing the sound patterns that arrive at our ears. A large proportion of neurons in the brainstem and midbrain, organized in multiple nuclei, are devoted for the analysis these sound patterns. They are extensively interconnected and analyze sound signals by integrating the excitatory and inhibitory inputs with high temporal precision. We are interested how these neural circuits emerge and refine during postnatal development and how genetic and environmental factors can disturb this development. Ultimately, we want to find out to what extend genetic and environment mechanisms interact and, moreover, elucidate measures how this altered brain connectivity can be prevented. We study these questions with a combination of in vivo and in vitro electrophysiological and anatomical techniques including whole-cell patch clamp recordings of synaptic transmission and integration in acute brain slices. We use genetically modified mouse models that help us to target specific neuronal populations and circuits or as models for human diseases. 

Current Projects:

1. Development and function of a large synapse in the auditory brainstem

A population of neurons in the ventral nucleus of the lateral lemniscus receives extremely large excitatory synapses that originate from the “fastest” neurons in the brain, the octopus cells in the cochlear nucleus. We are interested in the molecular mechanisms that underlie the development of this large synapse, and whether activity dependent mechanisms play a role. Ultimately, we want to know to what extent the correct function of this synapse influences the processing of complex sound pattern, such as for example speech, in the auditory midbrain.

2. Auditory brainstem processing in Fragile X mice

The Fragile X Syndrome is the most common inherited cause of mental retardation. People with Fragile X Syndrome suffer a range of symptoms including autism, sensory processing deficits and auditory hypersensitivity. The Fragile X Syndrome is caused by a mutation in the X-linked FMR1-gene that causes a knockdown of the FMR1 protein, a transcription factor with a multitude of targets. We use a mouse model with the general knockdown of the FMR1 protein to study alterations in synaptic transmission, neural connectivity in the auditory brainstem and relate them to deficits in sound processing.

 3. Inhibitory neurons in the auditory midbrain

Neurons in the auditory midbrain (inferior colliculus=IC) integrate ascending and descending projections to analyze sound patterns. Local projections of excitatory and inhibitory neurons within the auditory midbrain contribute to this analysis. We use a transgenic mouse line that labels inhibitory neurons under the promoter of VGAT to investigate the development and function of these inhibitory neurons within the IC. 

4. Hearing in naked mole rats

Naked mole rats live in large colonies in extensive but narrow burrows, an environment with specific acoustic features. Low frequency signals, such as the  large repertoire of vocalization signals, propagate exceptionally well in these narrow tunnels, whereas sound localization cues are largely absent. We are interested how the ascending auditory system of these exceptional (ugly J) animals is adapted to this specialized environment.


Member of:

·        SFB 870 “Development and function of neural circuits in sensory processing

·        Priority Program 1608: “Ultrafast and temporally precise information
         processing: Normal and dysfunctional hearing”