Max Planck Institute for Dynamics and Self-Organization -- Department for Nonlinear Dynamics and Network Dynamics Group
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BCCN/BFNT AG-Seminar

Tuesday, 01.04.2014 17 c.t.

Stress, GABA, Calcium Stores and Hippocampal Plasticity

by Prof. Dr. Menahem Segal
from Weizmann Institute of Sience, Dept. Neurobiology, Rehovot, Israel

Contact person: Ahmed El Hady

Location

MPI für experimentelle Medizin

Abstract

Recent functional studies suggest that cognitive processes are localized primarily within the dorsal/septal sector (dorsal hippocampus, DH) while the ventral/temporal hippocampus (VH) is associated with emotional memories. We attempt to outline the cellular basis for the distinction between ability to express plasticity in the DH and VH. We confirmed earlier observations that CA1 region of VH slices expresses much smaller long term potentiation (LTP) of reactivity to afferent stimulation, than that produced by the DH. Strikingly, this reduced ability to express LTP could be easily reversed by priming stimulation, by activation of metabotropic glutamate receptors, voltage gated calcium channels and by release of calcium from stores. Stress has been shown to modulate synaptic plasticity, in different directions and magnitudes. We found that following acute stress, LTP was impaired in DH slices. Strikingly, LTP was enhanced in VH following stress. Low exogenous corticosterone mimicked this differential effect of stress in both sectors of the hippocampus. There was a striking difference between the two hippocampal regions in the effects of calcium released from stores on the ability to generate LTP: low concentration of ryanodine (0.2µM) was able to convert short-term potentiation (STP) into LTP only in VH. The effects of ryanodine was reversed in stressed animals. These effects are postsynaptic and reflect a higher concentration of ryanodine receptors (RyRs) in the VH compared to the DH. RyRs are co-localized with synaptopodin, a protein associated with the spine apparatus, assumed to link calcium stores with the dendritic spine. Indeed, synaptopodin is correlated with the ability of the spine to handle calcium load, and thus, synaptopodin is assumed to underlie the role of the stores in synaptic plasticity.

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