GABA and potassium effects on corticospinal and primary afferent tracts of neonatal rat spinal dorsal columns.
The neurotransmitter GABA markedly depresses action potential conduction 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 dorsal columns is immature and unmyelinated compared to the cuneate-gracilis fasciculi. GABA and isoguvacine (a GABAA receptor agonist) were applied to isolated neonatal (seven to 14 days old) dorsal columns during recordings of conducted cuneate-gracilis fasciculi and corticospinal tract action potentials. GABA (10(-4) to 10(-3) M) significantly reduced amplitudes (-28.9% to -69.7%) and increased latencies (+4.8% to +23.9%) of cuneate-gracilis fasciculi responses but had less effect on corticospinal tract response amplitudes (-1.1% to -14.7%) and latencies (+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 little 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 rapidly increased extracellular K+([K+]e) from baseline levels of 3.0 mM 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, however, did not recover until several minutes after [K+]e returned to baseline. In separate experiments, increasing bath [K+]e concentrations to 3.7 and 6.6 mM reduced cuneate-gracilis fasciculi response amplitudes by only -7.6% and -29.6%. Latencies increased by +1.3% and +3.6% respectively. The results indicate that the cuneate-gracilis fasciculi are more sensitive to GABA than the corticospinal tract and that the GABA effect is not entirely due to [K+]e changes.
Department of Neurosurgery, New York University Medical Center, NY 10016.
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Honmou
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Sakatani
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Young
D000344:Afferent Pathways / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn; D007539:Isonicotinic Acids / Q000494:pharmacology; D009431:Neural Conduction; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology*; D011712:Pyramidal Tracts / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000187:drug effects* / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D007539:Isonicotinic Acids; D005680:gamma-Aminobutyric Acid; D011188:Potassium; C015300:isoguvacine