Low-Voltage Activated Calcium Currents Increase in Basal Forebrain Neurons
from Aged Rats.
Murchison, David, and William H. Griffith.
Department of Medical Pharmacology and Toxicology, College of Medicine,
Texas A&M University, College Station, TX 77843.
APStracts 2:0132N, 1995.
SUMMARY AND CONCLUSIONS
1. Whole-cell patch clamp recordings were made of low-voltage activated (LVA)
calcium (Ca 2+ ) currents using 2 mM barium (Ba 2+ ) as charge carrier.
Acutely dissociated neurons from medial septum (MS) and the nucleus of the
diagonal band (nDB) were examined in young adult (1-3 months) and aged (24-26
months) Fischer 344 rats. 2. Most neurons in both age groups displayed LVA
currents: 84% of young cells (110/131) and 87% in aged cells (62/71). Using
cell capacitance as an indication of cell size, aged cells were significantly
(p<0.05) smaller (mean 15.4 + 0.6 pF) than young cells (18.0 ¯+ 0.5 pF),
although a single distribution of cell sizes was present in both populations.
3. The LVA currents were enhanced in cells from aged animals. When LVA
currents were studied without activation of high voltage activated (HVA)
currents, the current density (pA/pF) was significantly (p<0.05)
increased at negative potentials in aged neurons (young: 4.92 +/- 0.35 pA/pF;
Aged: 5.92 +/- 0.45 pA/pF, at a pre-pulse potential of -110 mV). No change in
voltage-dependent activation or inactivation was seen. The time course of
recovery from inactivation was also unchanged. 4. Kinetic parameters of LVA
currents were compared in both age groups. No age-related difference in time-
dependent activation or inactivation was observed. A single distribution of
decay time constants of LVA currents was present in both age groups. 5. These
results show that MS/nDB cells maintain robust LVA currents and have increased
current densities in very old rats. An increased LVA current in the aged
neurons suggests that their ability to fire rhythmically or in bursts is
retained or enhanced and that the resulting increase in intracellular Ca 2+
may contribute to an altered Ca 2+ homeostasis.
Received 6 March 1994; accepted in final form 18 April 1995.
APS Manuscript Number J144-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.