Related Experiment Video
Updated: Aug 8, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
Electrochemical aging responses in pisum: cellular adaptations or recovery from injury?
1Department of Biological Sciences, California State College, Stanislaus, Turlock, California 95380.
Abstract:
Following excision, etiolated epicotyl segments of Pisum sativum L. cv. Alaska exhibit a marked hyperpolarization of membrane potential which is followed by a linear accumulation of K(+) when segments are incubated in Higinbotham nutrient solution. Segments aged for several hours and then reexcised display only a slight depolarization of membrane potential and no delay in ion accumulation; thus, recovery from injury appears an unlikely explanation for these responses. Substances originating in either the plumule or the cotyledons do not seem to be directly involved in these "aging" responses. However, locally produced substances, such as ethylene, or substances originating in the roots have not been eliminated as causative factors. Cold temperatures and cycloheximide prolong the lag in K(+) accumulation indicating a metabolic explanation for the induced K(+) accumulation. However, similar specific activities of plasma membrane-bound ATPase were found in isolates from fresh and aged epicotyl segments. Reactivation of an ion transport mechanism, perhaps responsible for the osmotic control of growth in immature cells, is suggested as a possible explanation for the pattern of ion accumulation characteristic of excised pea epicotyl tissue.
Related Concept Videos
Aging
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Cellular Adaptation I: Introduction and Atrophy
Cellular Injury I: Introduction
Responses to Heat and Cold Stress
Neurogenesis and Regeneration of Nervous Tissue
Cellular Injury V: Apoptosis and Autophagy
