Effects of anoxia on rat midbrain dopamine neurons

N. B. Mercuri, A. Bonci, S. W. Johnson, F. Stratta, P. Calabresi, G. Bernardi

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Abstract

1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100- 1,000 pA) associated with an increase in the apparent input conductance. 2. The mean reversal potential of the anoxia-induced response at 2.5 and 12.5 mM [K+] was -86 and -66 mV, respectively. 3. The effect of anoxia was not blocked by tetrodotoxin (TTX), saclofen, (-)sulpiride, or strychnine. Superfusate containing low calcium (0.5 mM CaCl2 and 10 mM MgCl2 or 0.5-1 mM CaCl2 and 1 mM CoCl2) or low sodium (25-40% of control) reduced the anoxia-induced outward current. 4. Extracellular barium (0.1-1 mM) blocked the anoxia-induced hyperpolarization/outward current. Other K+ channel blockers (tetraethylammonium, apamin, quinine, and glibenclamide) failed to reduce anoxia-induced current. 5. When the dopamine-containing neurons were loaded with cesium (1-2 mM), anoxia caused a reversible membrane depolarization and a block of the firing activity. This depolarization was voltage dependent; it was decreased or blocked by the hyperpolarization of the membrane. 6. Perfusion of the cells with 0.5-1 μM TTX did not affect the membrane depolarization/inward current caused by anoxia. These were also present when the cells were treated with the excitatory amino acid receptor antagonists D,L-2-amino-5-phosphonovalerate (APV) (30 μM) and 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX) (10 μM). 7. The exposure of the neurons with low-sodium, low-calcium solutions reversibly reduced the depolarizing/inward effects of anoxia. 8. It is concluded that under control condition anoxia hyperpolarizes dopamine-containing neurons. However, when the potassium current is blocked by intracellular cesium, it depolarizes these cells.

Original languageEnglish
Pages (from-to)1165-1173
Number of pages9
JournalJournal of Neurophysiology
Volume71
Issue number3
Publication statusPublished - 1994

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Dopaminergic Neurons
Mesencephalon
Cesium
Membranes
Tetrodotoxin
Hypoxia
Sodium
6-Cyano-7-nitroquinoxaline-2,3-dione
Calcium
2-Amino-5-phosphonovalerate
Apamin
Strychnine
Excitatory Amino Acid Antagonists
Sulpiride
Magnesium Chloride
Tetraethylammonium
Quinine
Glyburide
Glutamate Receptors
Barium

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Mercuri, N. B., Bonci, A., Johnson, S. W., Stratta, F., Calabresi, P., & Bernardi, G. (1994). Effects of anoxia on rat midbrain dopamine neurons. Journal of Neurophysiology, 71(3), 1165-1173.

Effects of anoxia on rat midbrain dopamine neurons. / Mercuri, N. B.; Bonci, A.; Johnson, S. W.; Stratta, F.; Calabresi, P.; Bernardi, G.

In: Journal of Neurophysiology, Vol. 71, No. 3, 1994, p. 1165-1173.

Research output: Contribution to journalArticle

Mercuri, NB, Bonci, A, Johnson, SW, Stratta, F, Calabresi, P & Bernardi, G 1994, 'Effects of anoxia on rat midbrain dopamine neurons', Journal of Neurophysiology, vol. 71, no. 3, pp. 1165-1173.
Mercuri NB, Bonci A, Johnson SW, Stratta F, Calabresi P, Bernardi G. Effects of anoxia on rat midbrain dopamine neurons. Journal of Neurophysiology. 1994;71(3):1165-1173.
Mercuri, N. B. ; Bonci, A. ; Johnson, S. W. ; Stratta, F. ; Calabresi, P. ; Bernardi, G. / Effects of anoxia on rat midbrain dopamine neurons. In: Journal of Neurophysiology. 1994 ; Vol. 71, No. 3. pp. 1165-1173.
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abstract = "1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100- 1,000 pA) associated with an increase in the apparent input conductance. 2. The mean reversal potential of the anoxia-induced response at 2.5 and 12.5 mM [K+] was -86 and -66 mV, respectively. 3. The effect of anoxia was not blocked by tetrodotoxin (TTX), saclofen, (-)sulpiride, or strychnine. Superfusate containing low calcium (0.5 mM CaCl2 and 10 mM MgCl2 or 0.5-1 mM CaCl2 and 1 mM CoCl2) or low sodium (25-40{\%} of control) reduced the anoxia-induced outward current. 4. Extracellular barium (0.1-1 mM) blocked the anoxia-induced hyperpolarization/outward current. Other K+ channel blockers (tetraethylammonium, apamin, quinine, and glibenclamide) failed to reduce anoxia-induced current. 5. When the dopamine-containing neurons were loaded with cesium (1-2 mM), anoxia caused a reversible membrane depolarization and a block of the firing activity. This depolarization was voltage dependent; it was decreased or blocked by the hyperpolarization of the membrane. 6. Perfusion of the cells with 0.5-1 μM TTX did not affect the membrane depolarization/inward current caused by anoxia. These were also present when the cells were treated with the excitatory amino acid receptor antagonists D,L-2-amino-5-phosphonovalerate (APV) (30 μM) and 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX) (10 μM). 7. The exposure of the neurons with low-sodium, low-calcium solutions reversibly reduced the depolarizing/inward effects of anoxia. 8. It is concluded that under control condition anoxia hyperpolarizes dopamine-containing neurons. However, when the potassium current is blocked by intracellular cesium, it depolarizes these cells.",
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N2 - 1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100- 1,000 pA) associated with an increase in the apparent input conductance. 2. The mean reversal potential of the anoxia-induced response at 2.5 and 12.5 mM [K+] was -86 and -66 mV, respectively. 3. The effect of anoxia was not blocked by tetrodotoxin (TTX), saclofen, (-)sulpiride, or strychnine. Superfusate containing low calcium (0.5 mM CaCl2 and 10 mM MgCl2 or 0.5-1 mM CaCl2 and 1 mM CoCl2) or low sodium (25-40% of control) reduced the anoxia-induced outward current. 4. Extracellular barium (0.1-1 mM) blocked the anoxia-induced hyperpolarization/outward current. Other K+ channel blockers (tetraethylammonium, apamin, quinine, and glibenclamide) failed to reduce anoxia-induced current. 5. When the dopamine-containing neurons were loaded with cesium (1-2 mM), anoxia caused a reversible membrane depolarization and a block of the firing activity. This depolarization was voltage dependent; it was decreased or blocked by the hyperpolarization of the membrane. 6. Perfusion of the cells with 0.5-1 μM TTX did not affect the membrane depolarization/inward current caused by anoxia. These were also present when the cells were treated with the excitatory amino acid receptor antagonists D,L-2-amino-5-phosphonovalerate (APV) (30 μM) and 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX) (10 μM). 7. The exposure of the neurons with low-sodium, low-calcium solutions reversibly reduced the depolarizing/inward effects of anoxia. 8. It is concluded that under control condition anoxia hyperpolarizes dopamine-containing neurons. However, when the potassium current is blocked by intracellular cesium, it depolarizes these cells.

AB - 1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100- 1,000 pA) associated with an increase in the apparent input conductance. 2. The mean reversal potential of the anoxia-induced response at 2.5 and 12.5 mM [K+] was -86 and -66 mV, respectively. 3. The effect of anoxia was not blocked by tetrodotoxin (TTX), saclofen, (-)sulpiride, or strychnine. Superfusate containing low calcium (0.5 mM CaCl2 and 10 mM MgCl2 or 0.5-1 mM CaCl2 and 1 mM CoCl2) or low sodium (25-40% of control) reduced the anoxia-induced outward current. 4. Extracellular barium (0.1-1 mM) blocked the anoxia-induced hyperpolarization/outward current. Other K+ channel blockers (tetraethylammonium, apamin, quinine, and glibenclamide) failed to reduce anoxia-induced current. 5. When the dopamine-containing neurons were loaded with cesium (1-2 mM), anoxia caused a reversible membrane depolarization and a block of the firing activity. This depolarization was voltage dependent; it was decreased or blocked by the hyperpolarization of the membrane. 6. Perfusion of the cells with 0.5-1 μM TTX did not affect the membrane depolarization/inward current caused by anoxia. These were also present when the cells were treated with the excitatory amino acid receptor antagonists D,L-2-amino-5-phosphonovalerate (APV) (30 μM) and 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX) (10 μM). 7. The exposure of the neurons with low-sodium, low-calcium solutions reversibly reduced the depolarizing/inward effects of anoxia. 8. It is concluded that under control condition anoxia hyperpolarizes dopamine-containing neurons. However, when the potassium current is blocked by intracellular cesium, it depolarizes these cells.

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