Service Electrophysiology
The following data and facts give a rough illustration of the enormous complexity of the human brain: this organ contains about 100 billions of neurons, each of which forms on average 1000 chemical synapses with other neurons. Moreover, the strength of transmission of the electrical nerve cell signals at the resultant approximately 100 trillions of chemical synapses is not fixed. At these synapses, dependent on the type of neuron, different transmission agents (neurotransmitters) are released (e.g. glutamate, GABA, serotonin, and dopamine). The strength of synaptic transmission can short- or long-lastingly become increased or decreased, e.g. by altered concentrations of neurotransmitters, activity-dependent processes (synaptic plasticity), and numerous endogenous and exogenous modulatory substances. In addition to synaptic plasticity, the brain exhibits further forms of plasticity (e.g. structural plasticity) that, inclusive of synaptic plasticity, can be subsumed under the term "neuroplasticity". Due to the structural and physiological features of the brain described above, it is safe to assume that alterations in the “flow” of electrical activity through neuronal networks of the brain play a causal role in the pathogenesis and/or the appearance of symptoms of psychiatric diseases.
The exploration of the pathophysiology of psychiatric diseases does not only represent a big scientific challenge, but is also a prerequisite for hypotheses-guided developments of more effective pharmacological treatments of these diseases. Hence, it appears crucial to uncover changes in neuronal network activity and interneuronal synaptic communication within the brain which significantly participate in, or at least accompany, the genesis and/or the appearance of core symptoms of these diseases. The “Electrophysiology and Neuronal Network Dynamics” Core Unit addresses itself to this task and, in doing so, mainly turns its attention to stress-related psychiatric disorders. The range of methods, applied to different mouse models, involves classical electrophysiological techniques, infrared-guided photostimulation, voltage-sensitive dye imaging, and optogenetic stimulation/inhibition of the electrical activity of local assemblies of neurons. By means of these techniques, we further work on the elucidation of modulatory actions of different endogenous and exogenous substances, among them corticotropin-releasing factor (CRF) and antidepressants.
Methods used:
- Field potential recordings
- Patch-clamp recordings
- Fluorescence microscopy
- Voltage-sensitive dye imaging (VSDI)
- Optogenetic tools
- Infrared-guided photostimulation