INTRODUCTION: Carnosine (beta-alanyl-L-histidine) is predominantly present in skeletal muscle but also in other excitable tissues. It was suggested that muscle carnosine concentration can decrease with ageing. There is growing evidence that supplementation of carnosine can be effective for the treatment of age related disorders as well as neurological disorders e.g. Alzheimer’s disease or Parkinson’s disease. AIM(S): Here we investigate the effects of orally supplemented carnosine in aged rats on motor units (MUs) contractile properties. METHOD(S): 42 male Wistar rats aged 15 months were randomly assigned to three groups: control (CON; n=15), treated with carnosine for 8 months (CAR8M; n=15) or treated with lated and fixed. In one set of experiments the brains were frozen and cut with the use of cryotome. Then, slices were used either for Nissl staining to visualise anatomical structure, or in situ hybridisation for gene expression analysis. In another set of experiments, fixed brains were dissected into two hemispheres, after which a small DiI crystal was inserted into the thalamus. After incubation, the hemispheres were cut with a vibratome and DiI-stained axons were visualised under fluorescent microscope. RESULTS: We show here, that TCF7L2‑deficent mice displayed major changes in the anatomy of the thalamus and habenulae, as well as partial malformations of the striatum. Furthermore, Tcf7l2-/- mice most often completely failed to produce thalamocortical axons; if some were visible, they did not reach their cortical targets. CONCLUSIONS: The study demonstrated a critical involvement of TCF7L2 in thalamic nucleogenesis and establishment of thalamocortical axons. FINANCIAL SUPPORT: Work supported by NCN grants 2011/03/B/NZ3/04480 and 2015/19/B/NZ3/02949.
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