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Abstract Neurons are highly polarized, specialized cells that must overcome immense challenges to ensure the health and survival of the organism in which they reside. They can spread over meters and persist for decades yet communicate at sub-millisecond and millimeter scales. Thus, neurons require extreme levels of spatial-temporal control. Neurons employ molecular motors to transport coding and noncoding RNAs to distal synapses. Intracellular trafficking of RNAs enables neurons to locally regulate protein synthesis and synaptic activity. The way in which RNAs get loaded onto molecular motors and transported to their target locations, particularly following synaptic plasticity, is explored below. 

Abstract The molecular mechanisms underlying age‐related declines in learning and long‐term memory are still not fully understood. To address this gap, our study focused on investigating the transcriptional landscape of a singularly identified motor neuron L7 in Aplysia, which is pivotal in a specific type of nonassociative learning known as sensitization of the siphon‐withdraw reflex. Employing total RNAseq analysis on a single isolated L7 motor neuron after short‐term or long‐term sensitization (LTS) training of Aplysia at 8, 10, and 12 months (representing mature, late mature, and senescent stages), we uncovered aberrant changes in transcriptional plasticity during the aging process. Our findings specifically highlight changes in the expression of messenger RNAs (mRNAs) that encode transcription factors, translation regulators, RNA methylation participants, and contributors to cytoskeletal rearrangements during learning and long noncoding RNAs (lncRNAs). Furthermore, our comparative gene expression analysis identified distinct transcriptional alterations in two other neurons, namely the motor neuron L11 and the giant cholinergic neuron R2, whose roles in LTS are not yet fully elucidated. Taken together, our analyses underscore cell type‐specific impairments in the expression of key components related to learning and memory within the transcriptome as organisms age, shedding light on the complex molecular mechanisms driving cognitive decline during aging.