Disease relevance of Pvalb

• Tracing and histological analyses revealed a complete loss of spindles in limb muscles, absence of peripheral and central Ia projections, and lack of cells immunoreactive to parvalbumin in the dorsal root ganglion (DRG) [1].
• The early, severe and selective loss of cortical PV+ neurons in experimental scrapie and CJD suggest selective loss of PV+ GABAergic neurons as important event during disease development, possibly as one basis of excitatory symptoms in TSEs [2].
• In CA1 area and the hilus of the dentate gyrus of the mouse hippocampus, drastic reduction of NeuN, calbindin, calretinin, or parvalbumin immunopositive neurons was shown at 3, 7 and 60 days after pilocarpine-induced status epilepticus [3].
• Parvalbumin deficiency affects network properties resulting in increased susceptibility to epileptic seizures [4].
• Pentylenetetrazole induced generalized tonic-clonic seizures in all genotypes, but the severity of seizures was significantly greater in PV-/- than in PV+/+ animals [4].

Psychiatry related information on Pvalb

• In CJD inoculated mice, loss of PV+ neurons was severe and occurred very early after inoculation [2].
• In view of reports suggesting that somatostatin- and parvalbumin-reactive cortical neurons may be preferentially damaged in Alzheimer's disease, these observations support a hypothesis that the overactivation of non-NMDA receptors could be involved in Alzheimer's disease pathogenesis [5].
• After removal of the vermis a total abolition of tremor, a definite improvement in the balance of affected body parts, an increase in locomotor activity when tested in an open-field matrix, and a strong increase in parvalbumin expression in Weaver mutant deep cerebellar and vestibular nuclei in comparison to wild-types have indeed been found [6].
• Perisomatic inhibition mediated by PV-positive basket cells is pruned by sensory deprivation [7].
• PV also caused prevention against supramaximal electroshock and pentylenetetrazol induced seizures [8].

High impact information on Pvalb

• This correlated with a loss of parvalbumin and carbonic anhydrase-positive neurons in the dorsal root ganglion [9].
• Fluorescently labeled troponin C and parvalbumin did not bind to mitochondria on any other cellular organelle [10].
• This reduction preferentially affects calretinin(+) (bipolar cells) and somatostatin(+) subtypes (for example, bitufted cells), whereas parvalbumin(+) subpopulations (basket cells and chandelier cells) seem to be unaffected [11].
• Here we report that Runx3-deficient (Runx3(-/-)) mice displayed severe motor uncoordination and that few DRG neurons synthesized the proprioceptive neuronal marker parvalbumin [12].
• In Bax(-/-)/NT3(-/-) mice, NT3-dependent neurons survived and expressed the proprioceptive neuronal marker parvalbumin [13].

Chemical compound and disease context of Pvalb

• Expression of the mutant thyroid hormone receptor PV in the pituitary of transgenic mice leads to weight reduction [14].
• Ifenprodil attenuates the loss of parietal cortical parvalbumin immunoreactivity after focal cerebral ischemia in the mouse [15].

Biological context of Pvalb

• However, similar to PV, delayed binding by CB leads to biphasic Ca2+ decay kinetics [16].
• Calbindin, calretinin, or parvalbumin and 5-bromo-2'-deoxyuridine (BrdU) double labeling showed that calcium binding protein immunopositive neurons in gliotic CA1 area at 60 days were surviving instead of newly generated neurons [3].
• Gene locus homology between chromosome 15 of the mouse and chromosome 22 of man (which carries the human PV gene) is discussed [17].
• The restriction fragment patterns of DNA samples from 65 individual offspring of (C57BL/6 x SPE)F1 x C57BL/6 backcrosses were tested with the PV probe and matched, for linkage detection, to pre-existing patterns established with various RFLP probes on the same samples [17].
• A cDNA derived from the 1100 nucleotide parvalbumin transcript was cloned and the sequence for the as yet unknown 3' extended trailer, generated by alternative polyadenylation, was determined [18].

Anatomical context of Pvalb

• Parvalbumin immunostaining in interneurons was well preserved in all groups [19].
• In the cerebella of 8-, 9-, and 12-week-old TM-B05 there was a progressive decrease in PV IR in Purkinje cells compared with nTM and TM-A02 [19].
• In double knock-out mice, the absence of both PV and CB entailed a doubling of spine length, an increase in spine volume and spine surface, a higher spine density along the dendrites, as well as a more clustered spine distribution [20].
• GABAergic neurons containing both PV and nNOS, i.e., PV-immunoreactive (-IR)/nNOS-IR neurons, were rare in Ammon's horn but frequent in the dentate gyrus (DG) [21].
• The density of CB+ cells gradually increased in the pallial amygdala until the first postnatal week and appeared to decrease later, coinciding with the postnatal appearance of parvalbumin cells and raising the possibility of a partial phenotypic shift [22].

Associations of Pvalb with chemical compounds

• Embryonic and postnatal development of GABA, calbindin, calretinin, and parvalbumin in the mouse claustral complex [23].
• Undifferentiated P19-cells were stably transfected with the cDNA for CR, CB or PV, induced to differentiate, and then exposed to NMDA, a glutamate-receptor agonist [24].
• Two of the three PV-transfected clones raised were vulnerable to NMDA-induced excitotoxicity; the third, which expressed the lowest level of PV, was protected to a similar degree as that found for the CR- and CB-transfected clones [24].
• The cultures treated for 24 h with antisense oligos (CaB+PV) showed a significant decrease in [3H]-GABA uptake as compared with the cultures treated with lipofectin alone or with lipofectin + mismatched antisense oligos to CaB and PV mRNA [25].
• The cells at different days in vitro were treated with antisense or mismatched antisense phosphorothioate oligonucleotides for CaB and PV mRNA (complexed with lipofectin) [25].
• NaCl supplementation of Pvalb(-/-) mice increased calciuria at baseline and after furosemide [26].

Regulatory relationships of Pvalb

• Evidence is reviewed that suggests bipolar calretinin expressing interneurons may have distinct origins from those that express parvalbumin or somatostatin [27].
• Group 1 are Renshaw cells and intensely express calbindin and coexpress parvalbumin and calretinin [28].
• Affected subpopulations of interneurons included basket interneurons evident in NCAM-EC transgenic mice intercrossed with a reporter line expressing green fluorescent protein and by parvalbumin staining [29].
• Coexposure to the calcium channel opener BayK, or the group I metabotropic glutamate receptor agonist DHPG [(RS)-3,5-dihydroxyphenylglycine] attenuated the decrease in GAD67 and parvalbumin induced by the NMDA receptor antagonists [30].

Other interactions of Pvalb

• In the present study we determined PV and CaB expression (by immunohistochemical and immunoblot analyses) in Purkinje cells of transgenic mice (TM) expressing the human SCA-1 gene with an expanded (line B05) and normal (line A02) CAG tract, as well as in age-matched nontransgenic mice (nTM) [19].
• This enhanced susceptibility was specific for enkephalin- and tachykinin-positive projection neurons, and also for parvalbumin-positive interneurons [31].
• Thus, the structural gene for PV, designated Pva, maps to chromosome 15 of the mouse whereas the adr mutation shows no linkage with markers on this chromosome [17].
• Cerebellar Purkinje cells of 6-week-old TM-B05, which exhibit no ataxia and even lack demonstrable Purkinje cell loss, also revealed reduction in PV IR [19].
• Of these, mRNAs for parvalbumin and myosin heavy chain IIB were drastically downregulated in myotonic muscle (to < 10% of control) [18].

Analytical, diagnostic and therapeutic context of Pvalb

• This change was matched by a significant decrease in the amount of cerebellar PV in 6-week-old TM-B05 as determined by Western blot analysis [19].
• The result of Southern blot hybridization is consistent with a single copy gene for parvalbumin [17].
• Peripheral innervation patterns of proprioceptive afferents from dorsal root ganglia and the mesencephalic trigeminal nucleus were assessed in trkC-deficient mice using immunohistochemistry for protein gene product 9.5 and parvalbumin [32].
• Electron microscopy revealed enriched GluR3 immunoreactivity in parvalbumin-containing perikarya at cytoplasmic and postsynaptic sites [33].
• Parvalbumin mRNA was assayed by Northern blot analysis in muscles from normal and dystropic (mdx) mice [34].

References