The response of main subclasses of GABAergic interneurons to plasticity induction and aging: changes in mRNA levels

• Autorzy: Rozycka A. , Zakrzewska R. , Liguz-Lecznar M.
• Języki publikacji: EN

Abstrakty

EN

INTRODUCTION: Inhibitory interneurons undergo age-related alterations that may have tremendous consequences on cellular and network computations and account for cognitive and behavioral deficits. Accordingly, we have shown that mechanisms governing fear learning‑induced plasticity were weakened in aged (1 y.o.) mice somatosensory cortex, hampering manifestation of plastic changes, while in old (2 y.o.) mice the plasticity was absent. AIM(S): To investigate age-related mRNA changes of distinct markers that are characteristic of GABAergic interneurons, define their main subtypes, and correlate potential changes with age‑related plasticity impairments. METHOD(S): Plasticity was induced with a classical conditioning paradigm, in which tactile stimulus to one row of whiskers was paired with a tail electric shock. Three groups of mice were used: young (3 months old), aged (1 y.o.) and old (2 y.o.). Using qRT‑PCR, we investigated mRNA levels of GAD67, GAD65, parvalbumin (PV), somatostatin (SST), calretinin (CR), calbindin (CB), vasoactive intestinal polypeptide (VIP), and Neuropeptide Y (NPY). RESULTS: qRT‑PCR analysis showed changes in mRNA levels, resulting from both aging itself and from plasticity induction. mRNA level of CB decreased in aged and old animals, whereas PV increased in the old group. After plasticity induction, we observed a reduction of NPY in the young group, while aged animals presented a decline of VIP mRNA levels. We observed decrease in CB along with an increase in PV mRNA levels, which may result in calcium homeostasis disruption in neurons and may consequently be involved in the plasticity impairments observed in aged and old animals. CONCLUSIONS: Being a part of the VIP-SST disinhibitory circuit that exist in many cortical areas, VIP mRNA changes may contribute to dysregulation of this important mechanism controlling plasticity. FINANCIAL SUPPORT: National Science Centre grant 2013/09/B/NZ3/00540.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2019
• Tom: 79
• Numer: Suppl.1
• Opis fizyczny: p.LXIV-LXV

Twórcy

autor

Rozycka A.

• Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland

autor

Zakrzewska R.

• Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland

autor

Liguz-Lecznar M.

• Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland