DECREASED DURATION OF CA2-MEDIATED PLATEAU POTENTIALS IN STRIATAL NEURONS FROM AGED RATS()

1. The influence of age on striatal neuron Ca2+ physiology was studied through an analysis of intracellularly recorded Ca2+-mediated plateau potentials. In vitro brain slices from young and aged rats were treat ed with the K+ channel blocker tetraethylammonium (30 mM) to facilitat e the expression of plateau potentials. A sample of neurons was also f illed with biocytin and post hoc correlations were performed between m orphology and physiology. 2. Testing of sampling parameters in neurons from young rats revealed that tetrodotoxin did not affect the amplitu de or duration of plateau potentials. The membrane potential induced d uring plateau testing and the rate of plateau potential generation, ho wever, had to be held constant because these variables affected platea u potential duration. 3. A significant age-related decrease was found in the duration of Ca2+-mediated plateau potentials that could not be explained by alterations in the activation or inactivation properties of the plateau potential. Investigation into relationships between cel l morphology and plateau potential duration revealed a number of corre lations. Soma size and dendritic length were correlated with plateau p otential duration, independent of age (hierarchical regression), and a n age-related decrease in dendritic length but not in soma size was fo und. Spine density and plateau potential duration were also correlated , but the significance depended on the variance associated with age. T hese data indicate that the extent of somadendritic membrane (includin g spines) affects plateau potential duration in striatal neurons and t hat dendrite and spine loss in aged animals may contribute to age-rela ted decreases in plateau potential duration. 4. The response to replac ement of Ca2+ with Ba2+ was age dependent, with Ba2+ causing a greater increase in the duration of plateau potentials in young neurons. Thes e data rule out an increase in Ca2+-mediated inactivation of Ca2+ chan nels as a primary cause for the shortening of plateau potentials in ag ed neurons. Our morphological findings suggest that dendritic regressi on in aged neurons may have reduced the number of Ca2+ channels partic ipating in plateau potential generation, but other mechanisms related to changes in the type of Ca2+ channel expressed and possible differen ces in their inactivation kinetics may also contribute to the age rela ted change in plateau potential duration.