We compared the effect of GABA and the serotonin receptor agonist (±)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT) on compound action potential amplitudes, latency, and conduction velocity in the spinal cord isolated from young (eight to 13-day-old) Long-Evans hooded rats. Supramaximally activated conducting action potentials and extracellular K+ activity were recorded with microelectrodes from the cuneatus-gracilis fasciculi and corticospinal tract. In the cuneatus-gracilis fasciculi, 8-OH-DPAT (10-4 M) significantly reduced response amplitudes by 26.1 ± 10.3% (mean ± S.D., P < 0.0001, paired t-test, n = 27) and increased latencies by 20.3 ± 7.9% (P < 0.0001). GABA (10-4 M) reduced amplitudes by 31.7 ± 15.0% (P < 0.0001, n = 28) and increased latencies by 6.1 ± 5.4% (P < 0.0001). However, neither GABA nor 8-OH-DPAT significantly altered conduction velocities, suggesting that the latency shifts are due to changes in activation time and not conduction velocity. In cortical spinal tract, 8-OH-DPAT (10-4 M) depressed response amplitudes by 18.9 ± 9.6% (P < 0.05, n = 5), increased latencies by 23.3 ± 7.2% (P < 0.0001), but reduced conduction velocities by 19.9 ± 10.2%. GABA (10-4 M) reduced amplitudes by 16.4 ± 7.5% (P < 0.01, n = 5), increased latencies by 5.3 ± 2.3% (P < 0.05), and did not change conduction velocities. Bicuculline or picrotoxin blocked the GABA effects but did not affect the 8-OH-DPAT effects on both tracts. The potassium channel blocker tetraethylammonium did not alter the 8-OH-DPAT effects. The Na+/K+-ATPase inhibitor ouabain (10-6 M) markedly enhanced the depressive GABA effects from 27.9 ± 12.0% to 49.4 ± 24.5% (P < 0.01, n = 9), but had no effect on 8-OH-DPAT-mediated effects. These results suggest that GABA and serotonin agonists depress axonal excitability through different and independent mechanisms.
- (±)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT)
- conduction velocities
- extracellular potassium [(K)(e)]
ASJC Scopus subject areas