Parvalbumin deficiency affects network properties resulting in increased susceptibility to epileptic seizures

PV KO mice are more likely to experience status epilepticus compared to controls following increased doses of pentylenetetrazol (PTZ), a GABAA receptor blocker.

“For example, PV KO mice are more likely to experience status epilepticus compared to controls following increased doses of pentylenetetrazol (PTZ), a GABAA receptor blocker (Schwaller et al., 2004).”

The positive correlation between parvalbumin and perineuronal net labeling in the current study is unlikely to be due to lower parvalbumin expression causing lower perineuronal net labeling, because mice lacking parvalbumin have normal Wisteria floribunda agglutinin labeling.

“In contrast, our findings of a positive correlation between PV and PNN labeling is unlikely to be due to lower PV expression causing lower PNN labeling because mice lacking PV have normal WFA labeling (Schwaller et al, 2004).”

VVA staining was used as a reliable marker for visualizing Pvalb neurons, irrespective of reduced or absent PV expression.

“Since neither the morphology nor the distribution of PNNs were shown to be altered in PV+/- and PV-/- mice in comparison to PV+/+ mice [57, 69], VVA staining was used as reliable marker for visualizing the specific neuronal subpopulation of “PV-FSI” cells, defined as Pvalb neurons, irrespective of reduced or absent PV expression in PV+/- and PV-/- mice, respectively.”

Calbindin D-28k (CB) levels were unaltered in PV-/- mice and in Shank1-/- and Shank3B-/- brains, supporting their use as loading controls.

“The levels of PV signals were normalized to calbindin D-28k (CB) signals, a protein previously shown to be unaltered in PV-/- mice [57, 66] to control for differences in loading. CB levels were found to be unaltered in Shank1-/- and Shank3B-/- brains (data not shown).”

A quantitative and systematic analysis of Pvalb neurons by unbiased stereology in mPFC, SSC and striatum was still missing.

“a quantitative and systematic analysis of Pvalb neurons by unbiased stereology in different brain regions including ASD-implicated regions such as the medial prefrontal cortex (mPFC), somatosensory cortex (SSC) and striatum was still missing.”

In agreement with previous results in cortex and hippocampus of adult PV-/- mice, there was no indication of a cell decrease/loss of Pvalb neurons.

“In agreement with previous results obtained in the cortex and hippocampus of adult PV-/- mice [55, 57], there was no indication of a cell decrease/loss of Pvalb neurons.”