|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our study identified that ErbB4 ablation in parvalbumin interneurons induced GABAergic dysregulation, providing valuable mechanistic insights into the sensorimotor cortico-striatal community structure deficits associated with schizophrenia.
|
31388929 |
2020 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Here, we re-analyzed six published datasets from postmortem studies of schizophrenia to assess molecular markers of glutamate and GABA neurotransmission in the DLPFC at three levels of anatomical resolution: 1) total cortical gray matter, 2) gray matter restricted to layer 3, and 3) a layer 3 local circuit composed of excitatory pyramidal cells and inhibitory, parvalbumin-containing, GABA neurons.
|
31296415 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
<b>Aim:</b> The authors aimed to study cognitive-enhancement- and neuroprotective-effects of Brahmi on novel object recognition memory and GABAergic neuronal density, defined by the presence of calcium binding proteins (CBPs; calbindin (CB), parvalbumin (PV), and calretinin (CR)) in a sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia.
|
31118643 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Given the extant literature exploring the pathological effects of oxidative stress on PV cells in cortical regions linked to schizophrenia, we decided to investigate whether PV neurons in other select brain regions, including sub-cortical structures, may be differentially affected by redox dysregulation induced oxidative stress during neurodevelopment in mice with a genetically compromised glutathione synthesis (Gclm KO mice).
|
30857872 |
2019 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
There is increasing evidence that redox dysregulation, which can lead to oxidative stress and eventually to impairment of oligodendrocytes and parvalbumin interneurons, may underlie brain connectivity alterations in schizophrenia.
|
31283822 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Therefore, progression to disease in schizophrenia-model mice can be prevented by treatments supporting vH-mPFC PV network function during a sensitive time window late in adolescence, suggesting therapeutic strategies to prevent the outbreak of schizophrenia.
|
31474363 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Ventral tegmental area (VTA) DA neuron population activity and vHipp activity was increased 1-2 and 5-6 weeks post-adolescent stress, along with a decrease in the number of PV+, PNN+, PV + /PNN + cells in the vHipp, which are consistent with the MAM model of schizophrenia.
|
31488866 |
2019 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We found that the hippocampus in the methylazoxymethanol acetate (MAM) rodent developmental disruption model of schizophrenia is hyperactive and dysrhythmic, possibly due to loss of parvalbumin interneurons, leading to a hyperresponsive dopamine system.
|
29385549 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Cortical D2 dopamine receptor (Drd2) have mostly been examined in the context of cognitive function regulation and neurotransmission modulation of medial prefrontal cortex by principal neurons and parvalbumin positive, fast-spiking, interneurons in schizophrenia.
|
30295716 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Overall our findings provide tentative support for the hypothesis that the GABAergic system is deficient in schizophrenia and that parvalbumin-containing interneurons offer a potential target for treatment.
|
31529297 |
2019 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These findings suggest that the contribution of each GABA neuron subset to inhibitory regulation of local circuitry normally differs across cortical regions of the visuospatial WM network and that in schizophrenia alterations of PV and SST neurons are a shared feature across these regions, whereas VIP neurons are affected only in V1.
|
30247542 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Region specific knockdown of Parvalbumin or Somatostatin produces neuronal and behavioral deficits consistent with those observed in schizophrenia.
|
31636253 |
2019 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Here, we review findings from both types of studies which converge on the notions that 1) inhibitory GABA signaling in the PFC, especially between parvalbumin positive GABAergic basket cells and excitatory pyramidal cells, is required for gamma oscillatory activity and working memory function; and 2) disturbances in this signaling contribute to altered gamma oscillations and working memory in schizophrenia.
|
29936230 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
For the first time we demonstrate that spindle density is markedly reduced by (i) optogenetic stimulation of a major GABA/PV inhibitory input to TRN arising from basal forebrain parvalbumin neurons (BF-PV) and; (ii) localized pharmacological inhibition of low-threshold calcium channels, implicated as a genetic risk factor for schizophrenia.
|
30837664 |
2019 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In the present study, we investigated the effect of adolescent social isolation (SI) on PV expression in the medial prefrontal cortex in a neurodevelopmental model (MAM-E17) of schizophrenia.
|
30519836 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Downregulation of Npas4 in parvalbumin interneurons and cognitive deficits after neonatal NMDA receptor blockade: relevance for schizophrenia.
|
30792384 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results suggest that PV GABAergic neuron-NMDAR hypofunction in postnatal development confers bidirectional NAc hyper- and mPFC hypo-sensitivity to amphetamine-induced dopamine release, similar to that classically observed in schizophrenia pathophysiology.
|
29394409 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The Role of Parvalbumin-positive Interneurons in Auditory Steady-State Response Deficits in Schizophrenia.
|
31811155 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Because PV protein and PVALB transcript levels were found to be lower in the brain of patients with autism spectrum disorder and schizophrenia, the novel transgenic mouse line might serve as a model to investigate the putative role of PV in these neurodevelopmental disorders.
|
30883994 |
2019 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Maternal immune activation (MIA) in rodents models an environmental risk factor for schizophrenia and recapitulates these PV interneuron changes.
|
31175998 |
2019 |
|
Seizures
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
To study the function of different components of the uPA-uPAR system on behavior and epileptogenesis, and to complement our previous studies on naïve and injured mice deficient in the uPA-encoding gene Plau or the uPAR-encoding gene Plaur, we analyzed the behavioral phenotype, seizure susceptibility, and perineuronal nets surrounding parvalbumin-positive inhibitory interneurons in Plau and Plaur (double knockout dKO) mice.
|
30836238 |
2019 |
|
Seizures
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
Aberrations in glutamatergic neurotransmission has been implicated in some seizure models, and we have recently reported that reduced cortical AMPA receptor (AMPAR) expression (predominantly GluA4- containing AMPARs) in parvalbumin-containing (PV<sup>+</sup>) inhibitory interneurons, could underlie seizure generation in the stargazer mutant mouse.
|
30593850 |
2019 |
|
Seizures
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
To test this, we used a pentylenetetrazole- (PTZ-) kindling model mouse to investigate changes to hippocampal parvalbumin- (PV-) positive neurons, extracellular matrix molecules, and perineuronal nets (PNNs) after the last kindled seizure.
|
31827499 |
2019 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
While decreased PV is considered a hallmark of neuropathology in schizophrenia, previous work elucidating the effects of KET administration on PV are contradictory, with findings suggesting decreased, increased, or no change in PV expression.
|
30296474 |
2018 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Published data suggest that GluN2A is involved in maturation and phenotypic maintenance of parvalbumin interneurons (PVIs), and these interneurons suffer from a deficient glutamatergic neurotransmission via GluN2A-containing NMDARs in schizophrenia.
|
29024713 |
2018 |