Abstract
We characterized spontaneous electrical activity in the aging guinea pig prostate. Membrane potential recordings were made using conventional single microelectrode recording techniques. Three types of spontaneous waveforms were recorded, including spikes, slow waves and spontaneous transient depolarizations. Spikes were classified as hyperactive or active. Active cells showed a mean +/- SEM frequency of 5.06 +/- 0.63 minutes(-1), significantly different from that in hyperactive cells (362.05 +/- 151.82 minutes(-1), p <0.05). After hyperpolarization amplitude was also significantly different in the active and hyperactive groups (17.80 +/- 1.98 vs 9.96 +/- 1.05 mV). Spike activity was abolished by 1 microM nifedipine in 7 preparations (p <0.05). Slow wave activity occurred at a frequency of 5.2 +/- 0.5 minutes(-1). The spike component of slow wave activity was abolished by 1 microM nifedipine, although the depolarizing transient remained unaltered from control values (8.1 +/- 3.1 mV, paired Student's t test p >0.05). Spontaneous transient depolarizations were recorded in the presence of slow waves in 10 preparations and of spikes in 13, and in quiescent cells in 9. Spontaneous transient depolarization frequency was highest in otherwise quiescent cells (24.55 +/- 6.48 minutes(-1)) compared to that in the presence of slow waves or spikes. Adding 1 microM nifedipine in 5 preparations did not significantly affect any measured parameters (p >0.05). Pacemaker potentials were not recorded in the aging prostate. With increased age there is an increase in spike activity, which could conceivably explain the increased prostatic tone that accompanies aging. Spike activity and the spike component of the slow wave were abolished by nifedipine, suggesting a role for L-type channels. Finally, spontaneous transient depolarizations were unaffected by nifedipine, suggesting that mechanisms other than Ca(2+) entry via L-type channels are responsible for their generation and maintenance.
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