prikaz prve stranice dokumenta Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration
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Scientific paper - Original scientific paper
Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration
Scientific Reports, 7 (2017), 1; 7273. https://doi.org/10.1038/s41598-017-07839-9
Herrera-Molina, Rodrigo; Mlinac-Jerković, Kristina; Ilić, Katarina; Stöber, Franziska; Vemula, Sampath Kumar; Sandoval, Mauricio; Jovanov Milošević, Nataša; Šimić, Goran; Smalla, Karl-Heinz; Goldschmidt, Jürgen; Kalanj Bognar, Svjetlana; Montag, Dirk

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Herrera Molina, R., Mlinac Jerković, K., Ilić, K., Stöber, F., Vemula, S. K., Sandoval, M. ... Montag, D. (2017). Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration. Scientific Reports, 7. (1), 7273. doi: 10.1038/s41598-017-07839-9

Herrera Molina, Rodrigo, et al. "Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration." Scientific Reports, vol. 7, no. 1, 2017, p. 7273. https://doi.org/10.1038/s41598-017-07839-9

Herrera Molina, Rodrigo, Kristina Mlinac Jerković, Katarina Ilić, Franziska Stöber, Sampath Kumar Vemula, Mauricio Sandoval, Nataša Jovanov Milošević, et al. "Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration." Scientific Reports 7, no. 1 (2017): 7273. https://doi.org/10.1038/s41598-017-07839-9

Herrera Molina, R., et al. (2017) 'Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration', Scientific Reports, 7(1), p. 7273. doi: 10.1038/s41598-017-07839-9

Herrera Molina R, Mlinac Jerković K, Ilić K, Stöber F, Vemula SK, Sandoval M, and sur.. Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration. Scientific Reports [Internet]. 2017 August 04 [cited 2024 May 05];7(1):7273. doi: 10.1038/s41598-017-07839-9

R. Herrera Molina, et al., "Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration", Scientific Reports, vol. 7, no. 1, p. 7273, August 2017. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:105:063386. [Accessed: 05 May 2024]

Metadata
Title (english)Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration
AuthorRodrigo Herrera-Molina
AuthorKristina Mlinac-Jerković
AuthorKatarina Ilić
AuthorFranziska Stöber
AuthorSampath Kumar Vemula
AuthorMauricio Sandoval
AuthorNataša Jovanov Milošević
AuthorGoran Šimić
AuthorKarl-Heinz Smalla
AuthorJürgen Goldschmidt
AuthorSvjetlana Kalanj Bognar
AuthorDirk Montag
Author's institutionUniversity of Zagreb
School of Medicine
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
The cell adhesion molecule neuroplastin (Np) is a novel candidate to influence human intelligence. Np-deficient mice display complex cognitive deficits and reduced levels of Plasma Membrane Ca2+ ATPases (PMCAs), an essential regulator of the intracellular Ca2+ concentration ([iCa2+]) and neuronal activity. We show abundant expression and conserved cellular and molecular features of Np in glutamatergic neurons in human hippocampal-cortical pathways as characterized for the rodent brain. In Nptn lox/loxEmx1Cre mice, glutamatergic neuron-selective Np ablation resulted in behavioral deficits indicating hippocampal, striatal, and sensorimotor dysfunction paralleled by highly altered activities in hippocampal CA1 area, sensorimotor cortex layers I-III/IV, and the striatal sensorimotor domain detected by single-photon emission computed tomography. Altered hippocampal and cortical activities correlated with reduction of distinct PMCA paralogs in Nptn lox/loxEmx1Cre mice and increased [iCa2+] in cultured mutant neurons. Human and rodent Np enhanced the post-transcriptional expression of and co-localized with PMCA paralogs in the plasma membrane of transfected cells. Our results indicate Np as essential for PMCA expression in glutamatergic neurons allowing proper [iCa2+] regulation and normal circuit activity. Neuron-type-specific Np ablation empowers the investigation of circuit-coded learning and memory and identification of causal mechanisms leading to cognitive deterioration.
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review
Publication versionPublished version
Journal titleScientific Reports
Numberingvol. 7, no. 1, p. 7273
p-ISSN2045-2322
DOIhttps://doi.org/10.1038/s41598-017-07839-9
URN:NBNurn:nbn:hr:105:063386
Publication2017-08-04
Document URLhttps://doi.org/10.1038/s41598-017-07839-9
Type of resourceText
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2024-04-09 05:48:57