Parvalbumin - Positive Neurons in the Neocortex: A Review.

The calcium binding protein parvalbumin (PV) in the mammalian neocortex is expressed in a subpopulation of cortical GABAergic inhibitory interneurons. PV - producing interneurons represent the largest subpopulation of neocortical inhibitory cells, exhibit mutual chemical and electrical synaptic contacts and are well known to generate gamma oscillation. This review summarizes basic data of the distribution, afferent and efferent connections and physiological properties of parvalbumin expressing neurons in the neocortex. Basic data about participation of PV-positive neurons in cortical microcircuits are presented. Autaptic connections, metabolism and perineuronal nets (PNN) of PV positive neurons are also discussed.

Differences in expression of calcium binding proteins in the perirhinal and retrosplenial cortex of the rat.

The main aim was to describe interneuronal population expressing calcium binding proteins calretinin (CR) and parvalbumin (PV) in the perirhinal (PRC) and retrosplenial (RSC) cortex of the rat. These two cortical areas differ strikingly in their connectivity and function, which could be caused also by different structure of the interneuronal populations. Having a precise knowledge of the cellular composition of any cerebral area forms one of the basic input parameters and tenets for computational modelling of neuronal networks and for understanding some pathological conditions, like generating and spreading of epileptic activity. PRC possesses higher absolute and relative densities of CR+ and PV+ neurons than RSC, but the CR : PV ratio is higher in the RSC, which is similar to the neocortex. The bipolar/bitufted neurons are most common type of CR+ population, while the majority of PV+ neurons show multipolar morphology. Current results indicate that main difference between analysed areas is in density of CR+ neurons, which was significantly higher in the PRC. Our results coupled with works of other authors show that there are significant differences in the interneuronal composition and distribution of heretofore seemingly similar transitional cortical areas. These results may contribute to the better understanding of the mechanism of function of this cortical region in normal and diseased states.

Influence of early life status epilepticus on the developmental expression profile of the GluA2 subunit of AMPA receptors.

AMPA receptors (AMPARs) are responsible for fast excitatory neurotransmission, and their prolonged activation can result in the generation and spread of epileptic seizures. At early stages of postnatal development, the majority of AMPARs are permeable to both Na(+) and Ca(2+) ions. This permeability, which increases neuronal excitability, is due to the lack of the GluA2 subunit, encoded by the GRIA2A gene, and/or the presence of an unedited GluA2 subunit Q/R site (glutamine instead of arginine). Lithium chloride- and pilocarpine-induced status epilepticus (LiCl/Pilo-SE) in rodents represents a model of severe seizures that result in development of temporal lobe epilepsy (TLE). The aim of this study was to determine how LiCl/Pilo-SE induced early in life (at postnatal day 12; P12) alters normal expression of the GRIA2A gene and GluA2 protein. SE was interrupted by an injection of paraldehyde (Para). Control groups were 1) naïve animals, and 2) siblings of SE rats receiving only LiCl and paraldehyde (LiCl/Para). The expression profile of GRIA2A mRNA was determined via qPCR, and GluA2 protein levels were measured by western blotting. The analysis was performed at 3h (protein levels), and then 3-, 6-, 13-, and 60days, following LiCl/Pilo-SE or LiCl/Para injection (i.e. at P12, P15, P18, P25, P72 respectively). Six different brain regions were analyzed: frontal (CXFR), parietal (CXPAR), and occipital (CXOC) cortex, dorsal (HD) and ventral (HV) hippocampus, and thalamus (TH). There was a significant increase in GRIA2A mRNA expression in the CXFR, CXPAR, and CXOC of P18 SE animals. In CXFR and HD, increased expression of GluA2 AMPAR subunit protein was detected, as well as a surge in GRIA2A mRNA and GluA2 protein expression especially at P18. In HD the surge was detected not only during development (P18), but also later in life (P72). Since high levels of GluA2 can be neuroprotective (by decreasing Ca(2+) permeability), our data suggest that the neocortex and dorsal hippocampus are able to activate endogenous antiepileptic mechanisms. A marked decrease in the overall expression of GluA2 protein in the HV in the LiCl/Pilo-SE and LiCl/Para rats, suggests that the HV is predisposed to excitotoxicity, not only during development, but even in adulthood. Interestingly, LiCl in combination with paraldehyde can also strongly alter the normal ontogeny of GRIA2A mRNA as well as GluA2 subunit protein expression.