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Front Cell Neurosci. 2015 Mar 11;9:73. doi: 10.3389/fncel.2015.00073. eCollection 2015.

Matrix metalloproteinase 9 (MMP-9) is indispensable for long term potentiation in the central and basal but not in the lateral nucleus of the amygdala.

Frontiers in cellular neuroscience

Tomasz Gorkiewicz, Marcin Balcerzyk, Leszek Kaczmarek, Ewelina Knapska

Affiliations

  1. Department of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences Warszawa, Poland ; Department of Biophysics, Warsaw University of Life Sciences Warszawa, Poland.
  2. Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences Warszawa, Poland ; Unidad Ciclotron, Centro Nacional de Aceleradores (Universidad de Sevilla - CSIC - Junta de Andalucia) Sevilla, Spain.
  3. Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences Warszawa, Poland.
  4. Department of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences Warszawa, Poland.

PMID: 25814930 PMCID: PMC4356064 DOI: 10.3389/fncel.2015.00073

Abstract

It has been shown that matrix metalloproteinase 9 (MMP-9) is required for synaptic plasticity, learning and memory. In particular, MMP-9 involvement in long-term potentiation (LTP, the model of synaptic plasticity) in the hippocampus and prefrontal cortex has previously been demonstrated. Recent data suggest the role of MMP-9 in amygdala-dependent learning and memory. Nothing is known, however, about its physiological correlates in the specific pathways in the amygdala. In the present study we show that LTP in the basal and central but not lateral amygdala (LA) is affected by MMP-9 knock-out. The MMP-9 dependency of LTP was confirmed in brain slices treated with a specific MMP-9 inhibitor. The results suggest that MMP-9 plays different roles in synaptic plasticity in different nuclei of the amygdala.

Keywords: LTP; MMP-9; amygdala; learning; synaptic plasticity

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