RGD Reference Report - Neuronal activity and TrkB ligands influence Kv3.1b and Kv3.2 expression in developing cortical interneurons. - Rat Genome Database

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Neuronal activity and TrkB ligands influence Kv3.1b and Kv3.2 expression in developing cortical interneurons.

Authors: Grabert, J  Wahle, P 
Citation: Grabert J and Wahle P, Neuroscience. 2008 Oct 15;156(3):618-29. doi: 10.1016/j.neuroscience.2008.08.008. Epub 2008 Aug 12.
RGD ID: 9685735
Pubmed: PMID:18775767   (View Abstract at PubMed)
DOI: DOI:10.1016/j.neuroscience.2008.08.008   (Journal Full-text)

Among the GABAergic neocortical interneurons, fast-spiking (FS) basket and chandelier cells are essential mediators for feed-forward inhibition, network synchrony and oscillations. The FS properties are in part mediated by the voltage-gated potassium channels Kv3.1b/3.2 which allow the fast repolarization of the membrane necessary for firing non-adapting action potentials at high frequencies. It has been recently reported that the FS phenotype fails to mature in BDNF knockout mice suggesting a role for neurotrophins. We now describe the role of neuronal activity and neurotrophins for Kv3.1b/3.2 expression using organotypic cultures of rat visual cortex as model system. Chronic activity deprivation from 2 days in vitro (DIV) prevented the postnatal developmental increase of Kv3.2, but not Kv3.1b mRNA expression. However, chronic activity deprivation failed to alter Kv3.1b and marginally delayed Kv3.2 protein expression. Activity deprivation by glutamate receptor blockade from 10 to 20 DIV reduced both mRNAs, whereas deprivation with tetrodotoxin (TTX) reduced both mRNAs and the Kv3.2 protein. Thalamic and cortical afferents in cocultures failed to alter the expression. BDNF and NT4 supplemented from 2 DIV onwards increased the expression of Kv3.1b, but not Kv3.2 mRNA in young cultures. Only NT4 increased the expression of both mRNAs later in development. Kv3 protein levels were not changed by exogenous tropomyosin-related kinase B (TrkB) ligands, but the levels decreased upon inhibiting the MAPK signaling suggesting a role for endogenous factors and in particular MEK2 signaling for translation. The results show that Kv3.1b/3.2 expression is differentially controlled by neuronal activity and neurotrophic factors.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to amine  IEP 9685735; 9685735aminophosphonovaleric acidRGD 
response to magnesium ion  IEP 9685735 RGD 
response to nerve growth factor  IEP 9685735brain-derived neurotrophic factor and neurotrophin 4RGD 
response to nerve growth factor  IEP 9685735neurotrophin 4RGD 
response to toxic substance  IEP 9685735; 9685735tetrodotoxinRGD 

Objects Annotated

Genes (Rattus norvegicus)
Kcnc1  (potassium voltage-gated channel subfamily C member 1)
Kcnc2  (potassium voltage-gated channel subfamily C member 2)


Additional Information