Upregulated expression of oncomodulin, the beta isoform of parvalbumin, in perikarya and axons in the diencephalon of parvalbumin knockout mice

B. Csillik, B. Schwaller, A. Mihály, T. Henzi, E. Losonczi, E. Knyihár-Csillik

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The calcium-binding proteins parvalbumin, calbindin D-28k, calretinin and calcineurin are present in subsets of GABAergic gigantic calyciform presynaptic terminals of the reticular thalamic nucleus (RTN). Previously it was hypothesized that GABA and calcium-binding proteins including parvalbumin are not only colocalized in the same neuron subpopulation, but that GABA synthesis and parvalbumin expression could be also genetically regulated by a common mechanism. Moreover, parvalbumin expression levels could influence GABA synthesis. For this, we analyzed GABA immunoreactivity in RTN gigantic calyciform presynaptic terminals of parvalbumin-deficient (PV-/-) mice. With respect to GABA immunoreactivity we found no differences compared to wild-type animals. However, using a polyclonal parvalbumin antibody raised against full-length rat muscle parvalbumin on brain sections of PV-/- mice, we observed paradoxical parvalbumin immunoreactivity in partly varicose axons in the diencephalon, mainly in the lamina medullaris externa surrounding the thalamus. A detailed immunohistochemical, biochemical and molecular biological analysis revealed this immunoreactivity to be the result of an upregulation of oncomodulin (OM), the mammalian beta isoform of parvalbumin in PV-/- mice. In addition, OM was present in a sparse subpopulation of neurons in the thalamus and in the dentate gyrus. OM expression has not been observed before in neurons of the mammalian brain; its expression was restricted to outer hair cells in the organ of Corti. Our results indicate that the absence of parvalbumin has no major effect on the GABA-synthesizing system in RTN presynaptic terminals excluding a direct effect of parvalbumin on this regulation. However, a likely homeostatic mechanism is induced resulting in the upregulation of OM in selected axons and neuronal perikarya. Our results warrant further detailed investigations on the putative role of OM in the brain.

Original languageEnglish
Pages (from-to)749-757
Number of pages9
JournalNeuroscience
Volume165
Issue number3
DOIs
Publication statusPublished - Feb 3 2010

Fingerprint

Parvalbumins
Diencephalon
Knockout Mice
Axons
Protein Isoforms
gamma-Aminobutyric Acid
Thalamic Nuclei
Presynaptic Terminals
Calcium-Binding Proteins
Thalamus
Outer Auditory Hair Cells
oncomodulin
Brain
Up-Regulation
Calbindin 2
Neurons
Calbindins
Organ of Corti
GABAergic Neurons
Wild Animals

Keywords

  • GABA
  • oncomodulin
  • parvalbumin
  • regeneration
  • reticular thalamic nucleus
  • thalamus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Upregulated expression of oncomodulin, the beta isoform of parvalbumin, in perikarya and axons in the diencephalon of parvalbumin knockout mice. / Csillik, B.; Schwaller, B.; Mihály, A.; Henzi, T.; Losonczi, E.; Knyihár-Csillik, E.

In: Neuroscience, Vol. 165, No. 3, 03.02.2010, p. 749-757.

Research output: Contribution to journalArticle

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AU - Mihály, A.

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AU - Losonczi, E.

AU - Knyihár-Csillik, E.

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