Matrix metalloproteinase-9 (MMP-9) is an extracellularly operating endopeptidase, which cleaves extracellular matrix proteins and plays an important role in synaptic plasticity, learning and memory. It is expressed in neurons in many different brain structures, including the hipocampus, prefrontal cortex and amygdala. MMP-9 is involved in maintenance of long-term potentiation (LTP) in the hipocampus and prefrontal cortex. On the other hand, its role in synaptic plasticity in the amygdala is much less known. It has been shown that the MMP-9 knock-out (MMP-9 KO) mice are impaired in amygdala-dependent appetitively motivated learning. The amygdaloid complex consists of several cytoarchitectonically and functionally distinguishable nuclei. To investigate MMP-9-dependent synaptic plasticity in different amygdalar nuclei, we studied MMP-9 role in LTP evoked in the central (CE), basal (BA) and lateral (LA) nuclei of the amygdala. In our in vitro extracellular recordings we used slices from MMP-9 KO and control mice. LTP in the BACE and LA-BA pathways was induced at the same level in the MMP-9 KO and control slices but it was disrupted several minutes after induction. In contrast, LTP in the external capsule-LA pathway was not disturbed in MMP-9 KO. These data suggests that MMP-9 is involved in stabilization but not in induction of LTP only in particular nuclei of the amygdala.
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