Article Figures & Data
Figures
- Figure 1.
A subset of aged rats exhibits impaired performance in the Morris water maze. A, Learning curves in the Morris water maze illustrating the performance of young and the AU and AI subgroups of aged rats as a function of path length to reach the hidden platform (Y, n = 9; AU, n = 8; AI, n = 10). Esc., Escape. B, Probe scores for each group were assessed on the fifth day of training. #p < 0.05 compared with the AU group.
- Figure 2.
The sAHP is enlarged in CA1 neurons of AI rats. A, Representative waveforms (average, n = 5 sweeps) taken from a young (Y), an AU, and an AI rat. In each case, the sAHP was evoked with a 50 ms current pulse sufficient to trigger four action potentials. The Vm was held at -50 mV by tonic current injection. B, Summary of sAHP amplitudes from all cells recorded from either resting or depolarized potentials using a constant or pulsed current injection protocol to elicit action potentials. #p < 0.001 compared with the AU or young groups (Y, n = 32; AU, n = 40; AI, n = 30). C, Distribution of sAHP amplitudes from all cells examined recorded from 50 mV using a 50 ms square wave current pulse to elicit action potentials.
- Figure 3.
sAHP amplitude covaries with water maze performance among aged rats. Linear regression analysis of sAHP amplitude reached statistical significance for both the mean escape (Esc.) path length (days 3-5) during training (A) as well as two probe measures (B, C) that were used as an index of the subjects' reliance on a spatial strategy in the maze. Each data point reflects the mean sAHP amplitude of all cells (n = 3-9) examined from that animal. The data point in each panel depicting the mean performance for young rats was not included in the regression analysis.
- Figure 4.
CA1 neurons from AI rats exhibit depressed excitability. A, Representative recordings from young (Y) and AI CA1 neurons during tonic current injection (-100, +450 pA; 800 ms). The dashed line represents 0 mV. Calibration: 20 mV, 0.2 s. B, Summary of all cells illustrated in A (Y, n = 18; AU, n = 14; AI, n = 17). C, Instantaneous firing frequency of the first four interspike intervals from the same group of cells. *p < 0.05; #p < 0.01 compared with AU group; two-factor repeated-measures ANOVA followed by Tukey-Kramer post hoc test. I-pulse, Current pulse.
- Figure 5.
Suppression of the sAHP reveals no age-related difference in the mAHP. A, Intracellular dialysis of CA1 neurons with 50 μm 8-CPT-cAMP virtually abolished the sAHP while preserving the mAHP. Representative waveforms (n = 5 sweeps) were acquired with or without cAMP from two cells in the same slice of an AI rat (Vm = -50 mV). Calibration: 2 mV, 1 s. B, mAHP amplitude, measured either at resting (RMP) or at Vh = -50 mV, is not affected by aging: Y, n = 18 neurons, 3 rats; AU, n = 18 neurons, 4 rats; AI, n = 14 neurons, 3 rats. C, After dialysis with 8-CPT-cAMP, a residual sAHP can be detected at depolarized potentials. D, Prolonged (800 ms) current injection (-100, +450 pA) in the same two cells shown in A illustrates the dramatic effect of the cAMP analog on accommodation. E, Summary of cell firing from experiments as shown in D, in which all cells were dialyzed with 8-CPT-cAMP. F, Instantaneous firing frequency (Freq.) of the first four interspike intervals from the same set of neurons as in E. I-pulse, Current pulse.
- Figure 6.
The calcium spike in CA1 neurons is driven essentially by L-typechannels. A, Representative calcium spike (young rat) illustrating where measurements were taken. B, Bath application of (-)BayK8644 (BayK; 1 μm) increases peak width and tail of the spike (young rat) without dramatically altering its peak amplitude. Inset, Early part of the tail on the expanded time scale. C, Summary of experiments depicted in B (n = 4 neurons). D, Bath application of (-)BayK8644 (1 μm) amplifies the sAHP. Example sAHP waveforms evoked by four spikes before and after exposure to 1 μm BayK86444 are shown. Calibration: 2.5 mV, 1 s.
- Figure 7.
The calcium spike is enhanced in CA1 neurons of AI rats. A, Calcium spike width, but not its peak or plateau amplitude, is larger in AI rats. *p < 0.05 compared with AU rats. B, Calcium spike tail amplitude is ∼40% larger compared with young or AU rats. #p < 0.001 compared with AU rats. C, Integrated tail potentials of the calcium spike from AI rats exhibit a right-shifted distribution (compare with Fig. 2C); the AI group mean is statistically different from the AU (p < 0.05) and Y (p < 0.01) groups. The sample sizes are as follows: Y, n = 31 neurons, 9 rats; AU, n = 49 neurons, 11 rats; AI, n = 40 neurons, 8 rats.
- Figure 8.
The calcium spike correlates with water maze acquisition but not probe performance. A, Linear regression and Spearman's rank plots of the relationship between calcium spike tail amplitude (p < 0.01) and days 3-5 mean escape path length or latency in the water maze. B, Linear regression plots of calcium spike tail amplitude and two probe measures: dwell time in the target zone and mean distance to platform location, both of which failed to reach significance (p > 0.05). The solid line depicts regression for aged rats only; the dashed line reflects analysis of both young and aged subjects. Each data point reflects the mean tail amplitude of all cells examined from that animal (n = 3-7).
Tables
Spike properties Group Vm(mV) Rin(MΩ) Threshold (MV) Half-width (mV) Amplitude (mV) Young (n = 32) −61.6 ± 0.4 88 ± 3 −40.2 ± 0.5 1.02 ± 0.02 78 ± 1 AU (n = 48) −61.4 ± 0.3 99 ± 4 −40.0 ± 0.4 1.02 ± 0.02 76 ± 1 AI (n = 30) −61.1 ± 0.4 109 ± 4* −41.2 ± 0.4 1.02 ± 0.01 77 ± 1 -
The number of neurons examined (in parentheses) was derived from nine rats for each group. *p<0.001 compared with young rats (ANOVA with Tukey-Kramer post hoc test).
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