The effect of parvalbumin deficiency on the acoustic startle response and prepulse inhibition in mice

Popelář, Jiří; Rybalko, Natalia; Burianová, Jana; Schwaller, Beat; Syka, Josef

doi:10.1016/j.neulet.2013.08.042

Cited by 12 publications

(9 citation statements)

References 29 publications

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“…A recently published study confirmed alterations of sensorimotor gating (PPI) in both sexes in all 3 mouse mutant lines 12 . In addition, altered numbers of parvalbumin-positive interneurons were observed in the thalamic reticular nucleus (TRN) of these mice, which is consistent with results showing that a deficiency of parvalbumin, a calcium binding protein, is known to affect PPI 13 .…”

Section: Introductionsupporting

confidence: 89%

Polymorphisms in CRYBB2 encoding βB2-crystallin are associated with antisaccade performance and memory function

et al. 2020

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βB2-crystallin (gene symbol: Crybb2/CRYBB2) was first described as a structural protein of the ocular lens before it was detected in various brain regions of the mouse, including the hippocampus and the cerebral cortex. Mutations in the mouse Crybb2 gene lead to alterations of sensorimotor gating measured as prepulse inhibition (PPI) and reduced hippocampal size, combined with an altered number of parvalbumin-positive GABAergic interneurons. Decreased PPI and alterations of parvalbumin-positive interneurons are also endophenotypes that typically occur in schizophrenia. To verify the results found in mice, we genotyped 27 single nucleotide polymorphisms (SNPs) within the CRYBB2 gene and its flanking regions and investigated different schizophrenia typical endophenotypes in a sample of 510 schizophrenia patients and 1322 healthy controls. In the case-control study, no association with schizophrenia was found. However, 3 of the 4 investigated haplotype blocks indicated a decreased CRYBB2 mRNA expression. Two of these blocks were associated with poorer antisaccade task performance and altered working memory-linked functional magnetic resonance imaging signals. For the two haplotypes associated with antisaccade performance, suggestive evidence was found with visual memory and in addition, haplotype block 4 showed a nominally significant association with reduced sensorimotor gating, measured as P50 ratio. These results were not schizophrenia-specific, but could be detected in a combined sample of patients and healthy controls. This is the first study to demonstrate the importance of βB2-crystallin for antisaccade performance and memory function in humans and therefore provides implications for βB2-crystallin function in the human brain.

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Section: Introductionsupporting

confidence: 89%

Polymorphisms in CRYBB2 encoding βB2-crystallin are associated with antisaccade performance and memory function

et al. 2020

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“…Particularly, the differentiation of PV basket cells, a subpopulation of GABAergic neurons that regulate a critical period of plasticity in the cortex which depends on BDNF (for a review, see [54]), may play a role during the alteration of inhibitory strength in BDNF Pax2 -KOs. Likewise, elevated auditory startle amplitude and latencies in PV −/− mice suggested a specific role of PV basket cells for inhibitory circuits in auditory processing [55]. To investigate a role of PV for the observed changes in inhibitory strength in BDNF Pax2 -KO mice, we used antibodies for PV [56, 57] and antibodies for the 67-kDa isoform of GABAergic interneurons.…”

Section: Resultsmentioning

confidence: 99%

BDNF in Lower Brain Parts Modifies Auditory Fiber Activity to Gain Fidelity but Increases the Risk for Generation of Central Noise After Injury

et al. 2015

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For all sensory organs, the establishment of spatial and temporal cortical resolution is assumed to be initiated by the first sensory experience and a BDNF-dependent increase in intracortical inhibition. To address the potential of cortical BDNF for sound processing, we used mice with a conditional deletion of BDNF in which Cre expression was under the control of the Pax2 or TrkC promoter. BDNF deletion profiles between these mice differ in the organ of Corti (BDNFPax2-KO) versus the auditory cortex and hippocampus (BDNFTrkC-KO). We demonstrate that BDNFPax2-KO but not BDNFTrkC-KO mice exhibit reduced sound-evoked suprathreshold ABR waves at the level of the auditory nerve (wave I) and inferior colliculus (IC) (wave IV), indicating that BDNF in lower brain regions but not in the auditory cortex improves sound sensitivity during hearing onset. Extracellular recording of IC neurons of BDNFPax2 mutant mice revealed that the reduced sensitivity of auditory fibers in these mice went hand in hand with elevated thresholds, reduced dynamic range, prolonged latency, and increased inhibitory strength in IC neurons. Reduced parvalbumin-positive contacts were found in the ascending auditory circuit, including the auditory cortex and hippocampus of BDNFPax2-KO, but not of BDNFTrkC-KO mice. Also, BDNFPax2-WT but not BDNFPax2-KO mice did lose basal inhibitory strength in IC neurons after acoustic trauma. These findings suggest that BDNF in the lower parts of the auditory system drives auditory fidelity along the entire ascending pathway up to the cortex by increasing inhibitory strength in behaviorally relevant frequency regions. Fidelity and inhibitory strength can be lost following auditory nerve injury leading to diminished sensory outcome and increased central noise.

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“…Only when KCC3 was targeted in parvalbumin-positive neurons did we detect a locomotor deficit similar to the one observed in the global knockout animals. Parvalbumin is a member of the large family of EF-hand calcium-binding proteins, which comprises more than 200 members in human [22]. It is essential for Ca 2+ homeostasis and the modulation of intracellular Ca 2+ concentration in specific populations of neurons [8].…”

Section: Discussionmentioning

confidence: 99%

Deletion of KCC3 in parvalbumin neurons leads to locomotor deficit in a conditional mouse model of peripheral neuropathy associated with agenesis of the corpus callosum

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2014

Behavioural Brain Research

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Hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum (HMSN/ACC or ACCPN) is an autosomal recessive disease caused by the disruption of the SLC12A6 gene, which encodes the K-Cl cotransporter-3 (KCC3). A ubiquitous deletion of KCC3 in mice leads to severe locomotor deficits similar to ACCPN patients. However, the underlying pathological mechanism leading to the disease remains unclear. Even though a recent study suggests that the neuropathic features of ACCPN are mostly due to neuronal loss of KCC3, the specific cell type responsible for the disease is still unknown. Here we established 4 tissue specific KCC3 knockout mouse lines to explore the cell population origin of ACCPN. Our results showed that the loss of KCC3 in parvalbumin-positive neurons led to significant locomotor deficit, suggesting a crucial role of these neurons in the development of the locomotor deficit. Interestingly, mice in which KCC3 deletion was driven by the neuron-specific enolase (NSE) did not develop any phenotype. Furthermore, we demonstrated that nociceptive neurons targeted with Nav1.8-driven CRE and Schwann cells targeted with a desert hedgehog-driven CRE were not involved in the development of ACCPN. Together, these results establish that the parvalbumin-positive neuronal population is an important player in the pathogenic development of ACCPN.

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The effect of parvalbumin deficiency on the acoustic startle response and prepulse inhibition in mice

Cited by 12 publications

References 29 publications

Polymorphisms in CRYBB2 encoding βB2-crystallin are associated with antisaccade performance and memory function

Polymorphisms in CRYBB2 encoding βB2-crystallin are associated with antisaccade performance and memory function

BDNF in Lower Brain Parts Modifies Auditory Fiber Activity to Gain Fidelity but Increases the Risk for Generation of Central Noise After Injury

Deletion of KCC3 in parvalbumin neurons leads to locomotor deficit in a conditional mouse model of peripheral neuropathy associated with agenesis of the corpus callosum

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