MMP‑3 deficiency does not influence the length and number of CA1 dendrites of hippocampus of adult mice.

Over the past two decades, metalloproteinases (MMPs), including MMP‑2, MMP‑3, and MMP‑9, have been implicated as important players in mechanisms underlying various forms of neuroplasticity. In particular, MMP‑3 was found to be involved in both cognitive functions and in plasticity phenomena, but the underlying molecular mechanisms remain largely elusive. In general, it is believed that functional plasticity of neurons is associated with morphological alterations. Interestingly, MMP‑9, in addition to playing a key role in synaptic plasticity, was found to affect plasticity‑related spine morphology changes. Whereas the involvement of MMP‑3 in shaping synapse morphology upon induction of synaptic plasticity awaits determination, it has been demostrated that MMP‑3 knockout results in clearly altered apical dendrite morphology in pyramidal neurons in mouse visual cortex. Considering that the involvement of MMP‑3 in synaptic plasticity has been most extensively documented for the CA1 hippocampal region, we decided to investigate whether genetic deletion of MMP‑3 affects neuronal morphology in this area. To this end, we used Golgi staining to compare dendritic morphology of pyramidal neurons in the CA1 region in MMP‑3‑deficient and wild‑type mice. Surprisingly, in contrast to the results obtained in cortex, extensive analysis of dendritic morphology in the CA1 region revealed no significant differences between MMP‑3 knockout and wild‑type groups. These results suggest that the impact of MMP‑3 on neuronal morphology may be region‑specific.