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PubMed1992

Wisteria floribunda agglutinin-labelled nets surround parvalbumin-containing neurons.

Net-like structures surrounding several types of neurones contain glycoconjugates which are detectable by lectins specific for N-acetylgalactosamine. Wisteria floribunda agglutinin (WFA) was introduced as a further marker for the visualization of such perineuronal nets, which were also revealed in regions of the rat brain where these structures could not be clearly demonstrated using other lectins. The WFA-labelled perineuronal nets resembled in detail those which could be visualized using Vicia villosa agglutinin, colloidal iron or hyaluronectin as markers. Furthermore, WFA-stained perineuronal net components appeared to be similar to proteoglycan-immunoreactive structures. Dual-peroxidase experiments and fluorescence double labelling demonstrated that WFA-binding structures frequently ensheath GABAergic neurons containing the calcium-binding protein parvalbumin in the areas investigated.

Animals↗
PubMed1994

Compartmental distribution of parvalbumin and calbindin D-28k in rat globus pallidus.

The cellular localization of parvalbumin (PV) and calbindin D-28k (CB) in the globus pallidus (GP) of rats was studied with double-immunohistochemical methods applied to single sections. The two calcium-binding proteins were found to be differentially distributed in GP. PV-positive cells were largely concentrated in the lateral part of GP where CB immunostaining was minimal. Their number and location varied along the rostrocaudal axis of GP. Pallidal PV cells were either large and multipolar or small and fusiform. In contrast, the medial part of GP was markedly enriched with CB neuropil but largely devoid of PV-positive cells. This spatial segregation indicates the existence of at least two different functional domains in the rat GP.

Animals↗
PubMed1999

Variation in the spatial relationship between parvalbumin immunoreactive interneurones and pyramidal neurones in rat somatosensory cortex.

The morphology of pyramidal neurones was revealed by intracellular injection of Lucifer Yellow (LY) in fixed tangential cortical slices taken from rat primary somatosensory cortex. Slices were processed with a combination of antibodies to allow visualization of both the LY-injected neurones and parvalbumin immunoreactive (PV-ir) cell bodies, by confocal microscopy. Basal dendritic fields of pyramidal neurones in layer V were larger and more complex than those of layer III. Furthermore, the number of PV-ir cell bodies contained within the basal dendritic territories of pyramidal neurones in layer V was significantly greater than in layer III (mean +/- s.e.m., 36.3 +/- 3.0 and 20.9 +/- 1.6, respectively). These findings have functional implications both in terms of physiological characteristics, and inhibitory modulation of receptive field properties, of cortical neurones.

Animals↗
PubMed2000

Recurrent mossy fibers preferentially innervate parvalbumin-immunoreactive interneurons in the granule cell layer of the rat dentate gyrus.

Detection of vesicular zinc and immunohistochemistry against markers for different interneuron subsets were combined to study the postsynaptic target selection of zinc-containing recurrent mossy fiber collaterals in the dentate gyrus. Mossy fiber collaterals in the granule cell layer selectively innervated parvalbumin-containing cells, with numerous contacts per cell, whereas the granule cells were avoided. Under the electron microscope, those boutons made asymmetrical contacts on dendrites and somata. These findings suggest that, in addition to the hilar perforant path-associated (HIPP) interneurons, the basket and chandelier cells also receive a powerful feed-back drive from the granule cells, and thereby are able to control population synchrony in the dentate gyrus. On the other hand, the amount of monosynaptic excitatory feed-back among granule cells is shown to be negligible.

Animals↗
PubMed2002

Parvalbumin positive dendrites co-localize with apical dendritic bundles in rat retrosplenial cortex.

The granular retrosplenial cortex in rats, involved in learning and memory, has a highly modular organization in layer 1. Apical dendrites of layer 2 pyramidal neurons form bundles, which correspond to patchy thalamic input. Here, we demonstrate that dendrites of parvalbumin-immunoreactive (PV-ir) GABAergic neurons in layers 2/3 also form bundles, and that these co-localize in layer 1 with the apical dendritic bundles, as verified by double immunofluorescence for PV and microtuble-associated protein. Deeper, at the border of layers 1/2, the PV-ir bundles merge into a honeycomb-like structure, with walls consisting of PV-ir neuropil. Compartmentalization in layers 1/2 is characteristic of other periallocortical structures. Further work is necessary to determine whether these specializations may be specifically related to learning and memory.

Acetylcholinesterase↗
PubMed2004

Calbindin-D28K, parvalbumin and calretinin in primate lower motor neurons.

It has been suggested that lower motor neurons containing calcium-binding proteins (CBP) may be resistant to degeneration in motor neuron disease. The testing of this hypothesis is hampered by lack of comprehensive information regarding the presence of CBPs in motor neurons. To address this shortcoming, we investigated the distribution of the CBPs calbindin-D28K (CB), parvalbumin (PV) and calretinin (CRT) in lower motor neurons in the normal human and two non-human primates (rhesus monkey and common marmoset) using immunohistochemistry. A variable proportion of motor neurons in cranial nerve motor nuclei contained immunoreactivity for one or more CBPs. A subpopulation of spinal cord alpha-motor neurons was also CBP-positive. Comparison of staining for choline acetyltransferase (ChAT) and CBPs in the human spinal cord demonstrated that approximately 63% of ventral horn motor neurons contained PV, 53% contained CRT and 56% contained CB. CBP immunoreactivity within motor neurons was of variable staining intensity. It remains to be established whether the presence of these CBPs confers protection against the pathogenic mechanisms of motor neuron disease.

Aged↗
PubMed1997

Disproportionate loss of CA4 parvalbumin-immunoreactive interneurons in patients with Ammon's horn sclerosis.

We studied differences in the number and morphology of parvalbumin-immunoreactive (PV-IR) interneurons in 43 hippocampal specimens from patients with classical Ammon's horn sclerosis (AHS) who underwent anterior temporal lobectomy, as compared with 14 autopsy and non-AHS surgical control specimens. PV-IR neuronal loss in the AHS specimens varied significantly from that expected based on overall AHS-associated pyramidal and granule neuron loss. Most striking was the loss of PV-IR interneurons in CA4 of the AHS specimens, which was 12 times greater than AHS-associated pyramidal neuron loss, and significantly exceeded the PV-IR interneuron loss observed in the other sectors of the hippocampus. In addition, the PV-IR interneurons in the AHS specimens had markedly smaller and less defined cell bodies and shortened and simplified dendritic arbors compared with the PV-IR interneurons in the control specimens. Other differences noted in the AHS specimens included prominent dendritic varicosities; the loss or interruption of a band formed by PV-IR terminals in the dentate gyrus; and the virtual absence of a small, intensely staining PV-IR interneuron with a short, exuberant dendritic arbor that was readily identified in the autopsy specimens. We discuss these findings in relationship to the development of classical AHS and complex partial seizures (CPS).

Adolescent↗
PubMed1997

Distribution of parvalbumin-immunoreactive neurons in brain correlates with hippocampal and temporal cortical pathology in Creutzfeldt-Jakob disease.

There is a distinctive pattern of hippocampal involvement in Creutzfeldt-Jakob disease (CJD) and evidence for selective vulnerability of GABAergic neurons in experimental and human prion disease. We studied hippocampus and temporal cortex from human CJD and control autopsy brains and surgical cryptogenic temporal lobe epilepsy specimens for distribution and density of parvalbumin (PV) and calbindin-D28K (Cal) -positive neurons that are subpopulations of GABAergic neurons. Pathology was evaluated semiquantitatively in 8 regions in 23 CJD brains for severity of spongiform change, astrogliosis and pathological prion protein deposition. In CJD, pathology was severe in pre-parasubiculum and temporal cortex, and little or absent in CA1-4; PV+ neurons were severely reduced or absent in all cases, whereas Cal+ neurons were largely preserved. In controls, the density of PV+ neurons was highest in pre-parasubiculum and temporal cortex, and lowest in CA1-4. In cTLE, loss of PV+ neurons was seen only in CA1-4. The diffuse and severe loss of PV+ neurons in CJD, and the topographical correlation of tissue lesioning in CJD with density of PV+ neurons in controls suggest selective vulnerability and early loss of this subset of inhibitory neurons in CJD. This might relate to characteristic CJD symptoms such as myoclonus and the distinctive EEG pattern.

Adult↗
PubMed2005

Role of parvalbumin in estrogen protection from ethanol withdrawal syndrome.

BACKGROUND: Parvalbumin (PA) is a calcium-binding protein that has been implicated in protecting neurons from hyperexcitability by sequestering intracellular calcium. This study examined whether ethanol exposure and/or ethanol withdrawal (EW) alter the levels of PA in a manner that is protected by 17beta-estradiol (E2). METHODS: Ovariectomized rats implanted with E2 (EW/E2) or oil pellets (EW/Oil) received chronic ethanol (7.5% w/v, 5 weeks) or control dextrin (Dex/Oil and Dex/E2) diets. At 0 hr, 24 hr, and 2 weeks of EW, three brain areas (the cerebellum, hippocampus, and cortex) were prepared for immunoblotting and immunohistological assessment of PA. RESULTS: At 24 hr of EW, the EW/Oil group showed reduced levels of PA protein and PA-positive neurons in the cerebellum and hippocampus compared with the dextrin control and the EW/E2 groups. At 2 weeks of EW, the reduced levels of PA persisted in the cerebellum but recovered toward the control levels in the hippocampus. The cortex showed no change in PA levels in any of the treatment groups. When tested at 24 hr of EW, the magnitude of EW signs inversely correlated with the levels of PA in the cerebellum and hippocampus. Ethanol exposure itself did not affect PA levels. CONCLUSION: These data suggest that EW, rather than ethanol exposure, reduces PA levels in a manner that is brain region specific and that is protected by estrogen. Disturbed PA homeostasis is hypothesized to play a role in the hyperexcitability of EW signs.

Animals↗
PubMed2004

The expression of PARP, NF-kappa B and parvalbumin is increased in Parkinson disease.

Immunohistochemical techniques revealed a significant increase of poly(ADP-ribose) polymerase (PARP)-containing nuclei in the dopaminergic neurons of the substantia nigra (SN) in Parkinson disease and in diffuse Lewy body disease as compared with a group of patients with other neurodegenerative diseases and normal controls. The nuclear translocation of nuclear factor kappa B (NF-kappa B) was also noted in the same cells. The over-activation of PARP and the transcriptional activation of NF-kappa B can contribute to the pathomechanism of the disease specific lesion of the neurons in the SN. However, in another subgroup of dopaminergic cells of the SN an increased parvalbumin content was detected reflecting a natural protective mechanism against the putative increase of intracellular calcium caused by excitotoxic injury and oxidative stress.

Humans↗
PubMed1986

Skin calcium-binding protein is a parvalbumin of the panniculus carnosus.

Skin calcium-binding protein (SCaBP) is a calcium binding protein purified from whole rat skin. It has a molecular weight of approximately 12,000 daltons but migrates at Mr 13,000 on sodium dodecyl sulfate (SDS)-polyacrylamide gels. On nitrocellulose blots of SDS-polyacrylamide gels, 6 different antisera to SCaBP reacted equally well with SCaBP and parvalbumin (PV), an 11,500-dalton calcium-binding protein purified from rat skeletal muscle, which also migrates at Mr 13,000 on SDS-polyacrylamide gels. Rabbit antiserum to muscle PV also recognized both PV and SCaBP, and either protein absorbed specific antibodies against either antigen from both types of antisera. Soluble protein extracts from whole adult rat and mouse skin contained a Mr 13,000 protein which was recognized on nitrocellulose blots of SDS gels by both antisera. Blots of extracts from epidermis, dermis, whole skin, and skin scraped on the dermal side to remove hypodermal tissue revealed that the Mr 13,000 PV/SCaBP cross-reacting antigen was restricted to the hypodermal tissue removed by scraping. Immunofluorescent staining of Bouin-fixed skin sections with these antisera confirmed the localization of PV/SCaBP to the panniculus carnosus, a hypodermal muscle layer. Newborn mouse skin does not contain this antigen. Additional polypeptides of Mr 10,500 and 12,000 on SDS gels of extracts from the epidermis of newborn and adult rats and mice were found to be immunoreactive with anti-SCaBP serum. These polypeptides were not recognized by the PV antiserum, and the reactivity of anti-SCaBP for these antigens was not absorbed by purified PV or SCaBP. Our results indicate that SCaBP is antigenically indistinguishable from PV and is localized in the adult rodent panniculus carnosus, and that antisera to SCaBP are polyspecific, recognizing epidermal proteins in addition to SCaBP/PV.

Animals↗
PubMed1996

Chimeras of parvalbumin and oncomodulin involving exchange of the complete CD site show that the Ca2+/Mg2+ specificity is an intrinsic property of the site.

Rat parvalbumin (PV) and oncomodulin (OM) differ in the affinity and selectivity of metal binding to their CD site, which is a high-affinity Ca2+/Mg(2+)-mixed site in PV and a low-affinity Ca(2+)-specific site in OM. To assess to what degree the Ca2+/Mg2+ specificity and affinity of an EF-hand motif in a protein is intrinsically determined by its sequence, the complete CD sites were exchanged, yielding two chimeras, [S41-Q71]PV and [D41-S71]OM. The optical characteristics of a Trp102, inserted in the hydrophobic core of PV, OM and the two chimeras, are very similar in all four proteins, which suggests that the hydrophobic core is qualitatively similar in the chimeras as in the parent proteins. Direct Ca2+ and Mg2+ binding monitored by flow dialysis and gel filtration revealed that [S41-Q71]PV binds only one Mg2+ with an intrinsic affinity K'Mg2+ of 3.0 x 10(4) M-1 and two Ca2+ with an identical K'Ca2+ of 4.4 x 10(6) M-1, whereas [D41-S71]OM binds two Mg2+ with a mean K'Mg2+ of 2 x 10(4) M-1 and two Ca2+ with a K'Ca2+ of 1.3 x 10(7) M-1. K'Ca2+ of the CD site of [S41-Q71]PV was 2.5-fold higher than of the CD site in [W102]OM, but 5-6-fold lower than that of the CD site in [W102]PV. In [D41-S71]OM, K'Ca2+ of the CD site was twofold lower than in [W102]PV, but eightfold higher than in [W102]OM. These results indicate that the sequence of the CD site determines its Ca2+/Mg(2+)-specificity, whereas its affinity for Ca2+ influenced by the protein into which the CD site is inserted. The inserted CD site in turn influences the affinity of the EF site to which it is paired in the host protein and the paired sites display an equalized affinity for Ca2+. Mg2+ decreases the affinity of the chimeras for Ca2+, but not according to a simple competition model. The Mg2+ antagonism is much more pronounced in [D41-S71]OM than in [S41-Q71]PV, but in each chimera the CD and EF site are quantitatively affected in the same manner. Thus, [S41-Q71]PV which can only bind a single Mg2+ ion, displays a Ca2+/Mg(2+)-antagonism for both sites with a KMg.compet of 2.3 x 10(2) M-1. These results confirm the 'equalizer' principle in the cation-binding parameters of [S41-Q71]PV: both sites display the same Ca2+ affinity and Mg2+ antagonism. In [D41-S71]OM with its two Ca2+/Mg2+ sites the antagonism shows qualitatively the same complexity as in wild-type PV, although it is somewhat weaker in amplitude.

Animals↗
PubMed1996

Pre-exposure to subtoxic levels prevents kainic acid lesions in organotypic hippocampal slice cultures: effects of kainic acid on parvalbumin-immunoreactive neurons and expression of heat shock protein 72 following the induction of tolerance.

The effects of kainic acid on the survival of principal neurons and parvalbumin-immunoreactive (PARV-IR) neurons, and on the expression of heat shock protein 72 immunoreactivity (HSP72-IR) were investigated in organotypic hippocampal slice cultures. Untreated cultures displayed an organotypic organization and the development and morphology of PARV-IR neurons in the hippocampus paralleled that reported to occur in vivo, with the exception of the hilar region of the dentate gyrus which exhibited a marked lack of PARV-IR neurons. No constitutive expression of HSP72 was found in untreated cultures. The lesion of CA3 neurons and the reduction in numbers of PARV-IR neurons in both CA3 and CA1 after chronic exposure to 5 microM kainic acid were similar to those reported to occur in vivo. Exposure to 1 microM doses of kainic acid resulted in a widespread appearance of HSP72-IR and the induction of tolerance to a previously toxic dose of kainic acid. These results suggest the presence of endogenous neuroprotective mechanisms, activated by a stress response which induces HSP72, and is reminiscent of the induced tolerance reported to occur after a mild ischaemic insult.

Animals↗
PubMed1996

Thalamic and basal forebrain afferents modulate the development of parvalbumin and calbindin D28k immunoreactivity in the barrel cortex of the rat.

In the adult barrel cortex of the rat the calcium-binding proteins calbindin D28k (CALB) and parvalbumin (PARV) are found in separate populations of GABAergic nonpyramidal neurons. 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. The aim of this study was to investigate the influence of subcortical afferents on the neurochemical differentiation of cortical PARV- and CALB-immunoreactive nonpyramidal neurons during development of the barrel cortex. We produced unilateral excitotoxic lesions with a single injection of ibotenic acid (0.5 microl, 0.05 M) in different subcortical nuclei in 7- to 8-day-old rats. Lesions involving the ventroposterior thalamic nuclei resulted in delayed development of PARV and CALB immunoreactivity in the barrel cortex. One week after ibotenic acid injections a transient decrease in the number of PARV-immunoreactive neurons in layer IV was observed, together with increased numbers of CALB-immunoreactive neurons in all cortical layers. The number of nonpyramidal neurons displaying coexistence of PARV and CALB in the lesioned hemisphere also increased compared with the numbers in the control hemisphere or control littermates. In contrast, lesions affecting the globus pallidus, zona incerta and reticular thalamic nucleus transiently increased the number of PARV-immunoreactive neurons in layers II and III, but had no effect on the number of CALB-positive cells. From 3 weeks onwards no differences were found between control and lesioned hemispheres after injections into either the ventroposterior thalamic nuclei or the magnocellular basal forebrain. These results suggest that CALB and PARV expression in nonpyramidal cortical neurons can be reversibly modulated in opposite directions by different cortical afferents during postnatal development.

Analysis of Variance↗
PubMed2000

Kinetics of Ca2+ binding to parvalbumin in bovine chromaffin cells: implications for [Ca2+] transients of neuronal dendrites.

kappaS1. The effect of parvalbumin (PV) on [Ca2+] transients was investigated by perfusing adrenal chromaffin cells with fura-2 and fluorescein isothiocyanate (FITC)-labelled PV. As PV diffused into cells, the decay of [Ca2+] transients was transformed from monophasic into biphasic. The proportion of the initial fast decay phase increased in parallel with the fluorescence intensity of FITC, indicating that PV is responsible for the initial fast decay phase. The relationship between the fast decay phase and the [Ca2+] level was investigated using depolarizing trains of stimuli. Within a train the relative amplitude of the fast decay phase was inversely dependent on the [Ca2+] level preceding a given stimulus. Based on these observations, we estimated the Ca2+ binding ratio of PV (kappaP), the apparent dissociation constant of PV for Ca2+ (Kdc, app), and the unbinding rate constant of Ca2+ from PV (kc-) in the cytosol of chromaffin cells. Assuming free [Mg2+] to be 0.14 mM, we obtained values of 51.4 +/- 2.0 nM (n = 3) and 0.95 +/- 0.026 s-1 (n = 3), for Kdc,app and kc-, respectively. With the parameters obtained in the perfusion study, we simulated [Ca2+] transients, using two different Ca2+ extrusion rates (gamma) - 20 and 300 s-1 - which represent typical values for chromaffin cells and neuronal dendrites, respectively. The simulation indicated that Ca2+ is pumped out before it is equilibrated with PV, when gamma is comparable to the equilibration rates between PV and Ca2+, resulting in the fast decay phase of a biexponential [Ca2+] transient. From these results we conclude that Ca2+ buffers with slow kinetics, such as PV, may cause biexponential decays in [Ca2+] transients, thereby complicating the analysis of endogenous Ca2+ binding ratios (kappaS) based on time constants. Nevertheless, estimates of kappaS based on Ca2+ increments provide reasonable estimates for Ca2+ binding ratios before equilibration with PV.

Animals↗
PubMed2006

Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy.

PURPOSE: We analyzed 26 surgically treated patients operated on for intractable epilepsy associated with type IA (architectural) cortical dysplasia, to investigate neuropathologic and immunocytochemical features, particularly of the gamma-aminobutyric acid (GABA)ergic system, and to compare the findings with those observed in normal cortex. METHODS: Routinely stained slides and serial sections immunostained for neurofilaments (SMI 311), microtubule-associated protein-2 (MAP-2), neuron-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), parvalbumin (PV), calbindin (CB), and calretinin (CR) were processed. Some sections were processed by using single-immunoperoxidase procedures; others were processed for double immunofluorescence labelling and observed by confocal microscopy. The density of inhibitory PV-immunoreactive interneurons was quantitatively assessed in all patients and control cases by using a two-dimensional cell-counting technique on PV immunostained sections. RESULTS: The density of PV-immunoreactive interneurons was significantly reduced in this group of patients, whereas CB- and CR- positivity appeared similar to those in normal cortex. In five cases, architectural abnormalities, in addition to those that defined type 1A dysplasia, were present and characterized by abnormal clusters of neurons and laminar cellular loss in superficial cortical laminate. CONCLUSIONS: The reduction of PV expression in type IA cortical dysplasia suggests an impairment of the GABAergic system as a possible mechanism for the epileptogenicity; in addition, PV immunoreactivity can be helpful in the neuropathologic characterization of this form of cortical dysplasia.

Adolescent↗
PubMed2006

Parvalbumin deficiency in fast-twitch muscles leads to increased 'slow-twitch type' mitochondria, but does not affect the expression of fiber specific proteins.

Parvalbumin (PV), a small cytosolic protein belonging to the family of EF-hand calcium-binding proteins, is highly expressed in mammalian fast-twitch muscle fibers. By acting as a 'slow-onset' Ca2+ buffer, PV does not affect the rapid contraction phase, but significantly contributes to increase the rate of relaxation, as demonstrated in PV-/- mice. Unexpectedly, PV-/- fast-twitch muscles were considerably more resistant to fatigue than the wild-type fast-twitch muscles. This effect was attributed mainly to the increased fractional volume of mitochondria in PV-/- fast-twitch muscle, extensor digitorum longus, similar to levels observed in the slow-twitch muscle, soleus. Quantitative analysis of selected mitochondrial proteins, mitochondrial DNA-encoded cytochrome oxidase c subunit I and nuclear DNA-encoded cytochrome oxidase c subunit Vb and F1-ATPase subunit beta revealed the PV-/- tibialis anterior mitochondria composition to be almost identical to that in wild-type soleus, but not in wild-type fast-twitch muscles. Northern and western blot analyses of the same proteins in different muscle types and in liver are indicative of a complex regulation, probably also at the post-transcriptional level. Besides the function in energy metabolism, mitochondria in both fast- and slow-twitch muscles act as temporary Ca2+ stores and are thus involved in the shaping of Ca2+ transients in these cells. Previously observed altered spatio-temporal aspects of Ca2+ transients in PV-/- muscles are sufficient to up-regulate mitochondria biogenesis through the probable involvement of both calcineurin- and Ca2+/calmodulin-dependent kinase II-dependent pathways. We propose that 'slow-twitch type' mitochondria in PV-/- fast muscles are aimed to functionally replace the slow-onset buffer PV based on similar kinetic properties of Ca2+ removal.

Adenosine Triphosphate↗
PubMed2006

Soybean isoflavones alter parvalbumin in hippocampus of mid-aged normal female, ovariectomized female, and normal male rats.

AIM: To investigate the long-term effect of soybean isoflavones on changes in parvalbumin (PV) immunoreactivity in the hippocampus in normal female, ovariectomized (OVX) female and normal male rats. METHODS: Ten-month-old rats were assigned to one of 9 groups (n = 7 in each group) based on body weight using a randomized complete-block design. The groups were: control diet-treated females, OVX females, and males; 0.3 g/kg isoflavone-treated females, OVX females, and males; and 1.2 g/kg isoflavone-treated females, OVX females, and males. The PV immunostaining was conducted by using the standard avidin-biotin complex method. RESULTS: PV immunoreactivity and the number of PV-immunoreactive neurons in all the groups after isoflavone treatment were significantly changed in the hippocampal CA1 region and in the dentate gyrus, but not in the hippocampal CA2/3 region. PV immunoreactivity and the number of PV-immunoreactive neurons in the control diet OVX females were similar to those in the control diet, and were greater than those in the control diet normal females. PV immunoreactivity and the number of PV-immunoreactive neurons in all the isoflavone-treated groups decreased dose-dependently after isoflavone treatment. CONCLUSION: Long-term administration of isoflavones may induce a reduction of PV in interneurons in the hippocampal CA1 region and in the dentate gyrus. The reduction of PV in these regions suggests that the long-term administration of isoflavones may cause a change in calcium homeostasis in the hippocampal CA1 region and in the dentate gyrus.

Animals↗