GABA AND POTASSIUM EFFECTS ON CORTICOSPINAL AND PRIMARY AFFERENT TRACTS OF NEONATAL RAT SPINAL DORSAL COLUMNS

The neurotransmitter GABA markedly depresses action potential conducti on in neonatal rat spinal dorsal columns. However, GABA sensitivity of the dorsal columns declines with maturation and myelination. At seven to 14 days after birth, the corticospinal tract component of the dors al columns is immature and unmyelinated compared to the cuneate-gracil is fasciculi. GABA and isoguvacine (a GABA(A) receptor agonist) were a pplied to isolated neonatal (seven to 14 days old) dorsal columns duri ng recordings of conducted cuneate-gracilis fasciculi and corticospina l tract action potentials. GABA (10(-4) to 10(-3) M) significantly red uced amplitudes (- 28.9% to - 69.7%) and increased latencies (+ 4.8% t o + 23.9%) of cuneate-gracilis fasciculi responses but had less effect on corticospinal tract response amplitudes (- 1.1% to - 14.7%) and la tencies (+ 0.9% to + 6.2%). Likewise, isoguvacine (10(-5) to 10(-4) M) reduced amplitudes (- 26.7% to - 37.5%) and increased latencies (+ 11 .2% and + 24.0%) of cuneate-gracilis fasciculi responses but had littl e or no effect on corticospinal tract response amplitudes (- 6.2% to - 3.8%) or latencies (- 0.8% to + 1.5%). At 10(-4) and 10(-3) M, GABA r apidly increased extracellular K+([K+]e) from baseline levels of 3.0 m M to 3.7 +/- 0.4 and 6.6 +/- 1.4 mM in cuneate-gracilis fasciculi and increased corticospinal tract [K+]e to 3.9 +/- 0.4 and 4.4 +/- 0.4 mM (mean +/- S.D.). [K+]e declined during drug application and fell below baseline after drug washout. Cuneate-gracilis fasciculi responses, ho wever, did not recover until several minutes after [K+]e returned to b aseline. In separate experiments, increasing bath [K+]e concentrations to 3.7 and 6.6 mM reduced cuneate-gracilis fasciculi response amplitu des by only - 7.6% and - 29.6%. Latencies increased by + 1.3% and + 3. 6% respectively. The results indicate that the cuneate-gracilis fascic uli are more sensitive to GABA than the corticospinal tract and that t he GABA effect is not entirely due to [K+]e changes.