Abstract
Crosstalk between excitatory principal cells and interneurons
controls any kind of network activity. 10–15% of the neuronal
population of the basolateral amygdala (BLA) is composed of a
diverse group of GABAergic interneurons, which innervate
distinct subcellular domains of projection neurons and are
thought to shape fear memory. However, the involvement of
local circuits formed by GABAergic inhibitory interneurons
projecting in different sub compartments of principal neurons
within the amygdala and their detailed function in shaping fear
memory and cognitive flexibility are not well studied.
With our unique lentiviral tool we are capable of modifying
GABAergic synapses from the different sub compartment (axon
initial segment, somata, dendrite) of principal neurons. We could
manipulate GABAergic synapses from the AIS via neurofascin
knockdown while soma and proximal dendritic GABAergic
synapses are modified via EphA7 knockdown. Interestingly, this
differential GABAergic synapse manipulation affects behavior in
different manner. Neurofascin knockdown affects the fear
extinction severely [1] while anxiety is unaffected whereas
EphA7 knockdown leads to severe anxiety deficit but fear
extinction behavior is completely normal. Moreover, neurofascin
knockdown also impairs behavioral flexibility in reversal learning.
With our in vivo electrophysiological recordings we confirmed
that modification in the BLA inhibitory synapses causes
metaplastic changes towards medial prefrontal cortex
controls any kind of network activity. 10–15% of the neuronal
population of the basolateral amygdala (BLA) is composed of a
diverse group of GABAergic interneurons, which innervate
distinct subcellular domains of projection neurons and are
thought to shape fear memory. However, the involvement of
local circuits formed by GABAergic inhibitory interneurons
projecting in different sub compartments of principal neurons
within the amygdala and their detailed function in shaping fear
memory and cognitive flexibility are not well studied.
With our unique lentiviral tool we are capable of modifying
GABAergic synapses from the different sub compartment (axon
initial segment, somata, dendrite) of principal neurons. We could
manipulate GABAergic synapses from the AIS via neurofascin
knockdown while soma and proximal dendritic GABAergic
synapses are modified via EphA7 knockdown. Interestingly, this
differential GABAergic synapse manipulation affects behavior in
different manner. Neurofascin knockdown affects the fear
extinction severely [1] while anxiety is unaffected whereas
EphA7 knockdown leads to severe anxiety deficit but fear
extinction behavior is completely normal. Moreover, neurofascin
knockdown also impairs behavioral flexibility in reversal learning.
With our in vivo electrophysiological recordings we confirmed
that modification in the BLA inhibitory synapses causes
metaplastic changes towards medial prefrontal cortex
| Original language | English |
|---|---|
| Pages (from-to) | S539 |
| Number of pages | 1 |
| Journal | European Neuropsychopharmacology |
| Volume | 27 |
| Issue number | 4 |
| DOIs | |
| State | Published - Oct 2017 |