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How to Detect Amygdala Activity with Magnetoencephalography using Source Imaging
Published on: June 3, 2013
Priming of LTP in amygdala and hippocampus by prior paired pulse facilitation paradigm in mice lacking brain
Christine Gebhardt1, Valentina Mosienko2, Natalia Alenina2,3
1Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Abstract:
This study focuses on analyzing long-term potentiation (LTP) changes in the lateral nucleus of the amygdala (LA) and in the CA1 region of the hippocampus in slices derived from mice deficient in tryptophan hydroxylase 2 (TPH2-/- ), the rate-limiting enzyme for 5-HT synthesis in the brain. We found a reduced LTP in both brain structures in TPH2-/- mice. However, we found no changes in the magnitude of LTP in TPH2-/- mice compared to wildtype mice when it was preceded by a paired pulse protocol. Whereas the magnitude of long-term depression (LTD) did not differ between wildtype and TPH2-/- mice, priming synapses by LTD-induction facilitated subsequent CA1-LTP in wildtype mice to a greater extent than in TPH2-/- mice. In the LA we found no differences between the genotypes in this protocol of metaplasticity. These data show that, unlike exogenous 5-HT application, lack of 5-HT in the brain impairs cellular mechanisms responsible for induction of LTP. It is supposed that suppression of LTP observed in TPH2-/- mice might be compensated by mechanisms of metaplasticity induced by paired pulse stimulation or low frequency stimulation before the induction of LTP.
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