Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression changes in the absence of miR-128 in striatal D1-receptor positive neurons

ABSTRACT: MicroRNA regulates protein expression of cells by repressing translation of specific target messenger transcripts. Loss of the neuron specific microRNA miR-128 in Dopamine D1-receptor expressing neurons in the murine striatum (D1-MSNs) lead to increased neuronal excitability, locomotor hyperactivity and fatal epilepsy. To examine expression changes in the absence of miR-128 in D1-MSNs, we used mice expressing EGFP-tagged ribosomes in D1-MSNs with either D1-MSN-specific homozygous deletion of miR-128-2 locus or no deletion. Transcripts co-immunoprecipitated with tagged ribosomes were analyzed by microarray. 9 mutant animals ( D1-MSN-tagged ribosome; D1-MSN specific miR-128-2 homozygous deletion) and 7 age matched littermate control animals (D1-MSN-tagged ribosome only).

ORGANISM(S): Mus musculus

SUBMITTER: Chan Lek Tan

PROVIDER: E-GEOD-48813 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MicroRNA-128 governs neuronal excitability and motor behavior in mice.

Tan Chan Lek CL Plotkin Joshua L JL Venø Morten T MT von Schimmelmann Melanie M Feinberg Philip P Mann Silas S Handler Annie A Kjems Jørgen J Surmeier D James DJ O'Carroll Dónal D Greengard Paul P Schaefer Anne A

Science (New York, N.Y.) 20131201 6163

The control of motor behavior in animals and humans requires constant adaptation of neuronal networks to signals of various types and strengths. We found that microRNA-128 (miR-128), which is expressed in adult neurons, regulates motor behavior by modulating neuronal signaling networks and excitability. miR-128 governs motor activity by suppressing the expression of various ion channels and signaling components of the extracellular signal-regulated kinase ERK2 network that regulate neuronal exci ...[more]

PMID: 24311694

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Project description:The striatum is the main input structure of the basal ganglia, receiving information from the cortex and the thalamus and consisting of D1- and D2- medium spiny neurons (MSNs). D1-MSNs and D2-MSNs are essential for motor control and cognitive behaviors and have implications in Parkinson’s Disease. In the present study, we demonstrated that Sp9 positive progenitors produced both D1-MSNs and D2-MSNs and that Sp9 expression was rapidly downregulated in postmitotic D1-MSNs. Furthermore, we found that sustained Sp9 expression in lateral ganglionic eminence (LGE) progenitor cells and their descendants led to promoting D2-MSNs identity and repressing D1-MSNs identity during striatal development. As a result, sustained Sp9 expression resulted in an imbalance between D1-MSNs and D2-MSNs in the mouse striatum. In addition, the fate-changed D2 like-MSNs survived normally in adulthood. Taken together, our finding supported that Sp9 was sufficient to promote D2-MSNs identity and repress D1-MSNs identity, and Sp9 was a negative regulator of D1-MSNs fate. The striatum is the main input structure of the basal ganglia, receiving information from the cortex and the thalamus and consisting of D1- and D2- medium spiny neurons (MSNs). D1-MSNs and D2-MSNs are essential for motor control and cognitive behaviors and have implications in Parkinson’s Disease. In the present study, we demonstrated that Sp9 positive progenitors produced both D1-MSNs and D2-MSNs and that Sp9 expression was rapidly downregulated in postmitotic D1-MSNs. Furthermore, we found that sustained Sp9 expression in lateral ganglionic eminence (LGE) progenitor cells and their descendants led to promoting D2-MSNs identity and repressing D1-MSNs identity during striatal development. As a result, sustained Sp9 expression resulted in an imbalance between D1-MSNs and D2-MSNs in the mouse striatum. In addition, the fate-changed D2 like-MSNs survived normally in adulthood. Taken together, our finding supported that Sp9 was sufficient to promote D2-MSNs identity and repress D1-MSNs identity, and Sp9 was a negative regulator of D1-MSNs fate.

Dataset Information

Expression changes in the absence of miR-128 in striatal D1-receptor positive neurons

Publications

MicroRNA-128 governs neuronal excitability and motor behavior in mice.

Similar Datasets

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