Interval timing deficits and their neurobiological correlates in aging mice

Gur E., Duyan Y. A., Arkan S., KARSON A., Balci F.

NEUROBIOLOGY OF AGING, cilt.90, ss.33-42, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 90
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1016/j.neurobiolaging.2020.02.021
  • Dergi Adı: NEUROBIOLOGY OF AGING
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Abstracts in Social Gerontology, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Psycinfo, Veterinary Science Database
  • Sayfa Sayıları: ss.33-42
  • Kocaeli Üniversitesi Adresli: Evet

Özet

Age-related neurobiological and cognitive alterations suggest that interval timing (as a related function) is also altered in aging, which can, in turn, disrupt timing-dependent functions. We investigated alterations in interval timing with aging and accompanying neurobiological changes. We tested 4-6, 10-12, and 18-20 month-old mice on the dual peak interval procedure. Results revealed a specific deficit in the termination of timed responses (stop-times). The decision processes contributed more to timing variability (vs. clock/memory process) in the aged mice. We observed age-dependent reductions in the number of dopaminergic neurons in the VTA and SNc, cholinergic neurons in the medial septum/diagonal band (MS/DB) complex, and density of dopaminergic axon terminals in the DLS/DMS. Negative correlations were found between the number of dopaminergic neurons in the VTA and stop times, and the number of cholinergic neurons in MS/DB complex and the acquisition of stop times. Our results point at age-dependent changes in the decisional components of interval timing and the role of dopaminergic and cholinergic functions in these behavioral alterations. (C) 2020 Elsevier Inc. All rights reserved.