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.
Highlights
Matrix metalloproteinase-9 (MMP-9) is a member of a matrix metalloproteinase family of zinc-dependent extracellular and membrane bound endopeptidases that cleave components of the extracellular matrix
To address the question about molecular heterogeneity of the amygdalar nuclei at the level of synaptic plasticity we investigated the role of matrix metalloproteinase 9 (MMP-9) in LTP measured at three different amygdalar pathways: from the external capsule (EC) to the lateral amygdala (LA), from the LA to the basal amygdala (BA) and from the BA to the medial section of the central amygdala (CeAm)
Thereafter LTP in MMP-9 KO declined to the baseline level, whereas it remained stable in MMP-9 WT mice (repeated measures ANOVA: F(1,12) = 5.95, p = 0.04 for comparison between two groups for the last 50 min of recording, Figure 1B)
Summary
Matrix metalloproteinase-9 (MMP-9) is a member of a matrix metalloproteinase family of zinc-dependent extracellular and membrane bound endopeptidases that cleave components of the extracellular matrix. It has been observed that MMP-9 knockout mice display a deficit in late phase of long term potentiation (L-LTP), but not in its early phase (E-LTP) in the hippocampal CA3 to CA1 pathway (Nagy et al, 2006). Chemical inhibition of MMP-9 causes destabilization of LTP in the mossy fibers-CA3 pathway (Wojtowicz and Mozrzymas, 2010). Deficits in spatial learning and contextual fear conditioning were observed in MMP-9 knock-out mice (Nagy et al, 2006). It has been demonstrated that overexpression of TIMP-1 in vivo, as well as specific chemical inhibition of MMP-9 in acute slice preparation block late phase of LTP in the subiculum to medial prefrontal cortex pathway (Okulski et al, 2007). Very little is known about the role of MMP-9 in neuronal plasticity in other brain structures, including the amygdala
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