Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.
1. The effects of anoxia on membrane properties of 119 dorsal vagal motoneurones (DVMs) were investigated in an in vitro slice preparation of the rat medulla. 2. Membrane potential was unaffected by anoxia in 11% of DVMs. An hyperpolarization accompanied by a decrease in input resistance occurred in 44% of DVMs; the remaining 45% depolarized with either an increase (60%) or decrease in input resistance (40%). TTX at a concentration of 0.3-1 microM did not significantly affect these responses. 3. Anoxic artificial cerebrospinal fluid (ACSF) containing 20 mM-TEA reversed the response of DVMs that hyperpolarized in standard ACSF to reveal a depolarization of 7.4 +/- 2.1 mV, and increased the anoxic depolarization from 5.0 +/- 0.7 to 8.7 +/- 1.4 mV. 4. Anoxic depolarization was converted to an hyperpolarization of 7.3 +/- 2.1 mV in ACSF containing 5 mM-4-aminopyridine (4-AP) and 1 microM-TTX. A residual depolarization of 4.5 +/- 3.5 mV was then observed in ACSF containing 5 mM-4-AP, 1 microM-TTX and 20 mM-TEA. Anoxic hyperpolarization was increased from 7.8 +/- 1.8 to 10.0 +/- 3.9 mV in 5 mM-4-AP and 1 microM-TTX and converted to a depolarization of 5.3 +/- 4.5 mV in 5 mM-4-AP, 1 microM-TTX and 20 mM-TEA. 5. In anoxic ACSF containing TEA, the action potential width was increased from 0.92 +/- 0.04 to 8.1 +/- 1.1 ms in hyperpolarizing DVMs, and from 0.85 +/- 0.01 to 2.4 +/- 1.0 ms in depolarizing DVMs. The increase in width was prevented by 2-3 mM-Mn2+. 6. The long after-hyperpolarization (AHP) of DVMs, which is contributed to by both an apamin-sensitive IK(Ca) and an apamin, charybdotoxin and TEA insensitive IK(Ca) was decreased in duration from 2.59 +/- 0.14 to 1.94 +/- 0.12 s during anoxia. 7. It is concluded that anoxia enhances the delayed rectifier current (IK(DR)) and an inward current, probably ICa, but suppresses the A currents (IA). In DVMs that hyperpolarize during anoxia, the increase in IK(DR) outweighs the increase in ICa and the decrease in IA. In depolarizing DVMs the decrease in IA and increase in ICa outweight the increase in IK(DR). The change in input resistance is determined by the relative sizes of current enhancement or suppression.
Cowan
A I
AI
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT.
Martin
R L
RL
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D000860:Hypoxia; D007477:Ions; D008297:Male; D008345:Manganese / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology*; D010100:Oxygen / Q000097:blood*; D051381:Rats; D017208:Rats, Wistar; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D014630:Vagus Nerve / Q000502:physiology*
D007477:Ions; D013757:Tetraethylammonium Compounds; D001030:Apamin; D008345:Manganese; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D010100:Oxygen