Fig. 2.

Postinjury MMP response in hippocampus and olfactory bulb following deafferentation. a Rodent MMP expression after entorhinal cortical lesion (ECL) deafferentation. X-axis shows degeneration/regeneration time course. MMP-3 transcript and protein increase acutely, in tandem with membrane-type MT5-MMP and ADAM10 protein (left panel). MMP-3 remains elevated throughout synapse regeneration, while the membrane-type enzymes return to baseline with synapse maturation at 15 d. Inducible activity of pro-enzyme is similarly elevated 1–2 d postlesion, with MMP-9 rapidly reduced by 7 d (right panel). By contrast, ADAMTS activity is below baseline at 1–2 d, but peaks at 7-d onset of terminal sprouting. The hippocampus shows time-dependent MMP response during reactive synaptogenesis. MMPs are prominent during acute degeneration and during the onset of synapse regeneration ¹[1]; ²[10]; ³[26]; ⁴[13]; ⁵[12]. b Rodent MMP expression after olfactory bulb deafferentation (nerve transection [TX] or sensory neuron nasal chemical lesion [CL]). X-axis shows degeneration/regeneration time course. Rapid acute MMP-9 upregulation, peaks in degenerative phase, with a delayed MMP-2 induction at onset of synaptic repair. Nerve transection vs. sensory neuron lesion exhibits different response. MMP-9 rise is delayed after chemical lesion and peaks much higher. MMP-2 shows the opposite temporal pattern, where chemical lesion produces a modest 5-d peak relative vs. > 5X rise at 10-d rise with nerve transection. Olfactory bulb shows a time-dependent MMP response with deafferentation-induced synaptic plasticity and illustrates how injury modality alters cued MMP response ¹[15]; ²[14]; ³[17]