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.

This study investigated the striatopallidal complex’s involvement in status epilepticus (SE) caused by morphological neurodegenerative changes in a post-natal immature developing brain in a lithium−pilocarpine male Wistar albino rat model of mesial temporal lobe epilepsy. One hundred experimental pups were grouped by age as follows: 12, 15, 18, 21, and 25 days. SE was induced by lithium−pilocarpine. Brain sections were microscopically examined by Fluoro-Jade B fluorescence stain at intervals of 4, 12, 24, and 48 h and 1 week after SE. Each interval was composed of four induced SE pups and a control. Fluoro-Jade B positive neurons in the dorsal striatum (DS) were screened and plotted on stereotaxic rat brain maps. The DS showed consistent neuronal damage in pups aged 18, 21, and 25 days. The peak of the detected damage was observed in pups aged 18 days, and the start of the morphological sequela was observed 12 h post SE. The neuronal damage in the DS was distributed around its periphery, extending medially. The damaged neurons showed intense Fluoro-Jade B staining at the intervals of 12 and 24 h post SE. SE neuronal damage was evidenced in the post-natal developing brain selectively in the DS and was age-dependent with differing morphological sequela.

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.

The aim of the present study was to analyze the location of degenerating neurons in the dorsal (insular) claustrum (DCL, VCL) and the dorsal, intermediate and ventral endopiriform nucleus (DEn, IEn, VEn) in rat pups following lithium–pilocarpine status epilepticus (SE) induced at postnatal days [P]12, 15, 18, 21 and 25. The presence of Fluoro-Jade B-positive neurons was evaluated at 4, 12, 24, 48 h and 1 week later. A small number of degenerated neurons was observed in the CL, as well as in the DEn at P12 and P15. The number of degenerated neurons was increased in the CL as well as in the DEn at P18 and above and was highest at longer survival intervals. The CL at P15 and 18 contained a small or moderate number of degenerated neurons mainly close to the medial and dorsal margins also designated as DCl (“shell”) while isolated degenerated neurons were distributed in the VCl (“core”). In P21 and 25, a larger number of degenerated neurons occurred in both subdivisions of the dorsal claustrum. The majority of degenerated neurons in the endopiriform nucleus were found in the intermediate and caudal third of the DEn. A small number of degenerated neurons was dispersed in the whole extent of the DEn with prevalence to its medial margin. Our results indicate that degenerated neurons in the claustrum CL and endopiriform nucleus are distributed mainly in subdivisions originating from the ventral pallium; their distribution correlates with chemoarchitectonics of both nuclei and with their intrinsic and extrinsic connections.