Aging differentially affects LTCC function in hippocampal CA1 and piriform cortex pyramidal neurons

Author:

Maziar Aida1,Critch Tristian N R H Y1,Ghosh Sourav1,Rajani Vishaal1,Flynn Cassandra M1,Qin Tian1,Reinhardt Camila1,Man Kwun Nok Mimi2,Lee Amy3,Hell Johannes W2,Yuan Qi1ORCID

Affiliation:

1. Division of Biomedical Sciences , Faculty of Medicine, Memorial University, St. John's, NL A1B 3V6, Canada

2. Department of Pharmacology , School of Medicine, University of California-Davis, Sacramento, CA 95817, United States

3. Department of Neuroscience , University of Texas-Austin, Austin, TX 78712, United States

Abstract

Abstract Aging is associated with cognitive decline and memory loss in humans. In rats, aging-associated neuronal excitability changes and impairments in learning have been extensively studied in the hippocampus. Here, we investigated the roles of L-type calcium channels (LTCCs) in the rat piriform cortex (PC), in comparison with those of the hippocampus. We employed spatial and olfactory tasks that involve the hippocampus and PC. LTCC blocker nimodipine administration impaired spontaneous location recognition in adult rats (6–9 months). However, the same blocker rescued the spatial learning deficiency in aged rats (19–23 months). In an odor-associative learning task, infusions of nimodipine into either the PC or dorsal CA1 impaired the ability of adult rats to learn a positive odor association. Again, in contrast, nimodipine rescued odor associative learning in aged rats. Aged CA1 neurons had higher somatic expression of LTCC Cav1.2 subunits, exhibited larger afterhyperpolarization (AHP) and lower excitability compared with adult neurons. In contrast, PC neurons from aged rats showed higher excitability and no difference in AHP. Cav1.2 expression was similar in adult and aged PC somata, but relatively higher in PSD95− puncta in aged dendrites. Our data suggest unique features of aging-associated changes in LTCCs in the PC and hippocampus.

Funder

National Institutes of Health

Publisher

Oxford University Press (OUP)

Subject

Cellular and Molecular Neuroscience,Cognitive Neuroscience

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