Abstract
How aging affects the communication between neurons is poorly understood. To address this question, we have studied the electrophysiological properties of identified neuron R15 of the marine mollusk Aplysia californica. R15 is a bursting neuron in the abdominal ganglia of the central nervous system and is implicated in reproduction, water balance, and heart function. Exposure to acetylcholine (ACh) causes an increase in R15 burst firing. Whole-cell recordings of R15 in the intact ganglia dissected from mature and old Aplysia showed specific changes in burst firing and properties of action potentials induced by ACh. We found that while there were no significant changes in resting membrane potential and latency in response to ACh, the burst number and burst duration is altered during aging. The action potential waveform analysis showed that unlike mature neurons, the duration of depolarization and the repolarization amplitude and duration did not change in old neurons in response to ACh. Furthermore, single neuron quantitative analysis of acetylcholine receptors (AChRs) suggested alteration of expression of specific AChRs in R15 neurons during aging. These results suggest a defect in cholinergic transmission during aging of the R15 neuron.
Highlights
Normal aging is characterized by progressive deterioration of several functions [1,2,3]
To study how aging affects the electrophysiological properties of neurons, we have raised a cohort of 34 animals at the National Facility for Aplysia at the University of Miami Rosenstiel School of Medicine and carried out intracellular recordings of the R15 neuron from Aplysia at two different growth stages (6-7 months and 11-12 months old)
We explored the advantages of Aplysia and examined age dependent changes in basal electrophysiological properties, response to acetylcholine and quantified mRNA expression levels of multiple acetylcholine receptors in single neurons
Summary
Normal aging is characterized by progressive deterioration of several functions [1,2,3]. What is the neurophysiological basis for the decline in brain function during normal aging? This results in weaker synapses, which form less efficient circuits [4]. Brain aging is characterized by the loss of synapses. Electrophysiological and anatomical studies of the CA1 and dentate gyrus of hippocampus in older rats have shown significant loss of synapses, deficits in induction and maintenance of long-term potentiation (LTP), lower thresholds for long-term depression (LTD) and depotentiation [3,5,6,7]. Almaguer et al showed that aging impairs communication between the amygdala and hippocampus in older rats [8]
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