Neuroscience

Memory
Ingrid Ehrlich, University of Tuebingen

The ability to adapt behavior through learning and memory formation is thought to depend on activity driven and selective changes in the efficacy of synaptic connections in the brain. The study of cellular models for plasticity such as long-term potentiation (strengthening) and long-term depression (weakening) of excitatory synapses, have revealed a plethora of mechanisms for induction and expression of synaptic changes. These include functional changes in pre- and postsynaptic properties that lead to alteration of synaptic strength. At the postsynapse, the regulated trafficking (i.e. insertion or removal) of glutamate receptors has emerged as a key mechanism regulating synaptic strength, and more recently has been demonstrated to participate in experience- and learning-driven plasticity in various brain regions. However, it has remained a challenge to directly relate plasticity at a specific set of synaptic connections and neurons to distinct behavioural changes. Some of the strongest links come from studying Pavlovian fear conditioning and its neural substrates in the amygdala, an important structure for fear memory storage. Here, long-term potentiation of inputs carrying sensory information about stimuli to amygdala principal cells appears to be a key mechanism for conditioning and has attracted most attention. However, little is known about other cells types and changes in amygdala networks. Using an ex-vivo approach, we started to address this issue focusing on a group of interneurons that critically control amygdala output and fear responses. We characterize their different inputs, and determine if these inputs and their properties and efficacy can be modified by activity-dependent plasticity as well as by fear and extinction learning.

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Neuroscience

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