Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model

Table 1

Summary of PA-induced changes from our laboratory.

Reference	Time after PA	Brain area	Main findings	Concluding remarks
Capani et al. 2009 [24]	6 months	Striatum	Thickening in PSDs and high ubiquitination levels related to injury duration and severity.; Hypothermia prevented changes.	Long-term protein misfolding/aggregation in PSDs may drive synaptic dysfunction/neuronal damage.
Grimaldi et al. 2012 [25]	1 month	Striatum	Thickening in PSDs and high ubiquitination levels related to injury duration and severity.	Early misfolding/aggregation of synaptic proteins could induce long-term changes and neurodegeneration.
Saraceno et al. 2012 [26]	1 month	Striatum	Accumulation of cytoskeletal F-actin in dendritic spines.; Increased number of mushroom-shaped spines.; Reduced number of neurons.	Early synaptic alteration/neuronal damage might be linked to cytoskeletal F-actin accumulation.
Muñiz et al. 2014 [27]	2 months	Striatum	Increased number of mushroom-shaped F-actin dendritic spines.; Hypothermia prevented changes.	Sustained synaptic and cytoskeletal changes were found.
Saraceno et al. 2012 [28]	4 months	Hippocampus	Thickening in PSDs and high ubiquitination levels.; Reduced number of F-actin stained spines.	Long-term actin cytoskeleton might play a role in PA-induced PSD alterations.
Saraceno et al. 2016 [29]	1 month	Hippocampus	Thickening in PSDs and increased number of F-actin stained spines.; Enhanced filopodium formation and synaptogenesis.; Habituation memory changes.	Likely dysfunctional synapses might result in late readaptive decrease in F-actin levels.; Overplasticity might affect the adequate establishment of neural circuits.

PSDs: postsynaptic densities. See text for more details.