Disease relevance of Pvalb

• The apparent decrease in the number of PV and CR immunoreactive hilar neurons was correlated with the duration of the SE and was most extensive in rats with a progressive form of epilepsy [1].
• These studies provide the first detailed characterization of the distribution of vulnerable neurons within the NRT after experimental ischemia and suggest that immunocytochemistry of PV is a useful tool for quantitative analysis of the lesion for use in further experiments to elucidate the mechanisms of selective vulnerability of the NRT [2].
• Loss of parvalbumin immunoreactivity defines selectively vulnerable thalamic reticular nucleus neurons following cardiac arrest in the rat [2].
• PV appeared in the outer nuclear layer at birth (P0) and, by P7, was observed in the ganglion cell layer, amacrine cells, and horizontal cells [3].
• Immunoreactive staining for the calcium-binding proteins calbindin and parvalbumin in lower brainstem auditory nuclei shows abnormalities in areas susceptible to the effects of hyperbilirubinemia and provides a sensitive new way to assess bilirubin toxicity in the auditory system [4].

Psychiatry related information on Pvalb

• Decrease in parvalbumin-expressing neurons in the hippocampus and increased phencyclidine-induced locomotor activity in the rat methylazoxymethanol (MAM) model of schizophrenia [5].
• In rats stimulated by novel environmental cues during the period of wakefulness preceding perfusion, Fos-positive neurons increased markedly relative to unstimulated animals, and involved the majority of the calbindin- or parvalbumin-labeled cell populations (60-75% and over 95%, respectively) [6].
• When compared with the controls, however, concentrations of parvalbumin in parahippocampal gyrus of patients with Alzheimer's disease (4.0 +/- 0.9 ng/mg protein) were significantly low (P less than 0.01), showing less than a half of the control values [7].

High impact information on Pvalb

• Prolonged afferent stimulation of the rat dentate gyrus in vivo leads to degeneration only of those cells that lack immunoreactivity for the calcium binding proteins parvalbumin and calbindin [8].
• The specific role of parvalbumin in GABA-containing cortical cells may be related to controlling the effectiveness of their inhibitory action [9].
• Parvalbumin in most gamma-aminobutyric acid-containing neurons of the rat cerebral cortex [9].
• With semithin frozen sections, it is possible to demonstrate that most GABA neurons in the rat somatosensory cortex contain the calcium-binding protein parvalbumin and that parvalbumin is found virtually only in GABA neurons [9].
• The diffusion of Ca(2+) was severely retarded due to interactions with parvalbumin and a general restriction of small molecule mobility [10].

Chemical compound and disease context of Pvalb

• Thus, selective vulnerability of GABA-containing neurons and relative resistance of neurons in which PV or CB immunoreactivity is present or is expressed later, occur in the hippocampus after neonatal anoxia [11].
• The influence of kainic acid, which induces status epilepticus, on the expressions of calbindin D28k, parvalbumin and calretinin was examined in the rat striatum by immunohistochemistry and microdensitometry [12].
• To investigate the role of PA for the genesis of diabetic neuropathy, the levels of PA in the sciatic nerve of normal and streptozotocin-induced diabetic rats were measured by radioimmunoassay (RIA) for PA [13].
• To assess whether these effects are SERCA2a specific, we overexpressed a skeletal-muscle protein, PV, to examine whether Ca(2+) buffering alone can mitigate ventricular arrhythmias [14].
• CONCLUSION: Elevated levels of TGF-beta1 derived from glomerular or extraglomerular sources are capable of increasing glomerular Palb via superoxide and hydroxyl radicals and may lead to proteinuria in vivo [15].

Biological context of Pvalb

• Virtually every PARV-positive neuron innervated by GABAergic septohippocampal baskets expressed NGF mRNA (86%), whereas 39-59% of CALR- and CALB-positive interneurons that were contacted by GABAergic septohippocampal axons showed NGF gene expression [16].
• However, DA receptor activation did not appear to account for the PV up-regulation in AMPH-treated rats at 7 day withdrawal [17].
• Using in situ hybridization on adult rat tissue, we demonstrated that ALS-resistant motor pools robustly express mRNA for the calcium binding protein parvalbumin, while no measurable parvalbumin expression is found in ALS-sensitive motor neuron populations [18].
• Remodeling of the AB site of rat parvalbumin and oncomodulin into a canonical EF-hand [19].
• Their position with respect to the parvalbumin amino acid sequence corresponded to the intron locations found in genes of several other Ca2+-binding proteins [20].

Anatomical context of Pvalb

• Mixed-effects statistical models, adapted specifically for these analyses, indicated that perturbations of amygdalar inputs to the hippocampus significantly alter the drive that hippocampal PVB-, CR-, and CB-IR neurons within the dentate gyrus/CA4 region exercise on CCK-IR terminals within the same region as well as in CA3-1 [21].
• The numerical density (Nd) of somata showing immunoreactivity (IR) for parvalbumin (PVB) was decreased in dentate gyrus (DG) and the CA4-2 region, while that of calretinin (CR)-IR was decreased in DG and CA2 [21].
• PV-labelled neurones had round somata (diameters between 6 and 10 microm) and were bi-tufted, with beaded dendrites [22].
• Parvalbumin-positive neurons constituted 19-43% of GABA-immunoreactive neurons in the basolateral amygdala, depending on the nucleus [23].
• Parvalbumin, calbindin, or calretinin in cortically projecting and GABAergic, cholinergic, or glutamatergic basal forebrain neurons of the rat [24].

Associations of Pvalb with chemical compounds

• The results show that the majority of PV (100%), SOM (89.8%) and CR (93.9%) staining neurons are GABA positive [25].
• Parvalbumin interneurons showed significant reductions in the strata oriens and pyramidale of CA1, the stratum pyramidale of CA3, and the dentate hilus [26].
• Combined dual-immunofluorescence and confocal microscopy revealed that somatodendritic alpha4 nicotinic acetylcholine receptors colocalized with cortical neurons stained positively for CR, PV or CB [27].
• We tested in an animal model if redox imbalance (GSH deficit and excess extracellular dopamine) during postnatal development would affect PV-expressing neurons [28].
• QA produced degeneration of numerous medium-sized neurons, but not those enriched in Bcl-2-i. Many Bcl-2-i-enriched interneurons including those with CAT+ and PARV+ survived QA injection, while medium-sized neurons labeled for calbindin D-28K (CAL D-28+) did not [29].

Physical interactions of Pvalb

• These data indicate that PA and CA antisera identify two cell populations in whisker-related regions of the V brainstem complex and that PA cells are somatotopically patterned in PrV, SpI, and SpC [30].
• 5-HT1A receptor-immunoreactive GABAergic cells in the MSDB were also demonstrated to contain the calcium-binding protein parvalbumin, a marker for septohippocampal projecting GABAergic neurons [31].

Co-localisations of Pvalb

• From the second week, in addition to labeling vestibular afferents in their specific target areas, parvalbumin was also found colocalized with calbindin in mature Purkinje cell afferents [32].
• Estrogen receptor-beta colocalizes extensively with parvalbumin-labeled inhibitory neurons in the cortex, amygdala, basal forebrain, and hippocampal formation of intact and ovariectomized adult rats [33].
• Double-label immunofluorescence showed that, in the outer part of the IPL, 75% of the alpha 1-immunoreactive puncta were colocalized with recoverin-positive bipolar cell axons and 71% of the alpha 1-immunoreactive puncta were colocalized with parvalbumin-positive All-amacrine processes [34].
• Parvalbumin-positive dendrites did not display any increase in co-localizing gephyrin-positive structures [35].

Regulatory relationships of Pvalb

• In layers II to IV of the barrel cortex most PARV-immunoreactive neurons are likely to derive from a subpopulation of CALB-immunoreactive neurons whose CALB immunoreactivity ceases when they begin to express PARV between the second and third postnatal weeks [36].
• Calretinin-containing neurons which co-express parvalbumin and calbindin D-28k in the rat spinal and cranial sensory ganglia; triple immunofluorescence study [37].
• Our results show that NT-3 promotes the survival of a DRG subpopulation of which over 75% expresses parvalbumin (PV) [38].
• More than 90% of the parvalbumin-positive neurons in the hippocampal formation strongly expressed the DOR gene [39].
• Within the infralimbic, agranular insular, primary motor, parietal association, perirhinal, and lateral entorhinal cortices, an average of 95.6% +/- 0.8% (intact) and 94.5% +/- 1.4% (ovx) of all ER-beta-immunoreactive cells coexpress parvalbumin, and this proportion is strikingly similar across these diverse cortical regions [33].

Other interactions of Pvalb

• All of these are PV, CB, SOM and NOS negative [25].
• No coexistence of NC with PV, SOM or NPY was found in any hippocampal region [40].
• From dual immunostaining for the CBPs and glutamic acid decarboxylase (GAD), it appeared that the vast majority (>90%) of the Parv(+) group was GAD(+), whereas only a small minority (<10%) of the Calb(+) or Calret(+) group was GAD(+) [24].
• Despite the common feature of low GluR-B subunit expression, PV- and CR-containing interneurons differ with respect to the density and combination of their expressed AMPAR subunits [41].
• The majority of these PV-positive NT-3-dependent DRG neurons were large 'type A' neurons [38].

Analytical, diagnostic and therapeutic context of Pvalb

• Parvalbumin and calbindin immunocytochemistry reveal functionally distinct cell groups and vibrissa-related patterns in the trigeminal brainstem complex of the adult rat [30].
• In fact, double in situ hybridization analysis confirmed that most NT-3+ neurons also expressed NGF mRNA, indicating coexpression of both neurotrophins in subpopulations of PARV+ and CALR+ neurons [42].
• In the present study, immunofluorescence histochemical double staining for PKCgamma and CB, CR or PV was performed in the rat medullary dorsal horn [43].
• Electron microscopy showed that the immunoreactive products of calbindin or parvalbumin were mostly in the dendrites or cell bodies [44].
• RNA amplification following single cell dissection of immunohistochemically labeled cells from layers II to VI revealed that PV cells, in contrast to CR cells, express the m2 muscarinic receptor (M2AchR) protein [45].

References