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2017 | 77 | Suppl.1 |

Tytuł artykułu

Gabaergic system in aging. Focus on somatostatin containing interneurons

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Języki publikacji

EN

Abstrakty

EN
INTRODUCTION: Molecular aging, defined as an age‑related transcriptome changes, and biochemical protein-related alterations within synapses weaken the plastic potential of neurons. Previously, we have shown an age-related impairment of learning-related functional plasticity in mouse somatosensory cortex (SI), induced by associative fear learning and visualized with brain mapping using 2-deoxyglucose technique. AIM(S): The aim of the study was to investigate age-related changes in somatostatin-containing GABAergic interneurons, which are involved in learning – related plasticity in mouse SI. METHOD(S): Learning-related plasticity was induced with classical conditioning, where tactile stimulus to large sensory whiskers was coupled to the tail shock. Two groups of mice were used in the experiments: young (3 months old) and aged (1 year old). We have investigated mRNA and protein level of GAD67 (enzyme synthesizing GABA) and SOM (somatostatin) in mouse SI using q-RT-PCR and ELISA, respectively. Using immunofluorescence we compared the number of both types of neurons in SI. RESULTS: Analysis of q-RT-PCR results revealed no change in investigated mRNAs levels between young and aged mice. We also observed an upregulation of GAD67 and GABA levels after training in young but not in aged animals. Immunohistochemistry results showed an increase in the number of GAD67+ cells, however, we did not observe an elevation in the number of SOM+/GAD67+ cells. CONCLUSIONS: Increase in GAD67+ neurons density after sensory training in aged animals without parallel upregulation in GAD67 and GABA levels suggests lower GABA synthesis resulting in reduced effectiveness of aged GABAergic neurons. Lack of increase in SOM+ neurons density after sensory training in aged mice, suggest that upregulation of SOM+ cells is necessary for training induced plasticity. FINANCIAL SUPPORT: Supported by National Science Centre grant 2013/09/B/NZ3/00540.

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77

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Opis fizyczny

p.87

Twórcy

autor
  • Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
  • Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
  • Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

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Bibliografia

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