Hypoxic changes in rat locus coeruleus neurons in vitro.

Nieber, K; Ševčı́k, Jan; Illéš, Peter

doi:10.1113/jphysiol.1995.sp020788

Cited by 63 publications

(32 citation statements)

References 45 publications

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“…However, transmembrane fluxes of acidbase equivalents through ion channels or activation of glial Na+-HCO3-cotransport might also be involved (Chesler, 1990 (Trapp & Ballanyi, 1995). The observations that the Erev of the glucose-dependent hyperpolarizations was also close to the estimated equilibrium potential for K+ (Trapp & Ballanyi, 1995; see also Spuler, Endres & Grafe, 1988;Murphy & Greenfield, 1992;Nieber et al 1995) and that sulphonylureas blocked these hyperpolarizations indicate that KATP channels also mediate this response. As discussed in detail elsewhere, a complex set of cellular constituents seems to determine the activity state of these metabolism-related K+ channels (Trapp & Ballanyi, 1995; see also Terzic, Kung & Kurachi, 1994).…”

Section: Effects Of Energy Depletionmentioning

confidence: 93%

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Ballanyi

Doutheil

Brockhaus

1996

The Journal of Physiology

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1. Brainstem slices were taken from mature rats. In the dorsal vagal nucleus (DVNX), membrane potentials (Em) of neurons (DVNs) and glia, as well as extracellular oxygen, K+ and pH (Po2, aKO, pHO), were analysed during metabolic disturbances.2. Postsynaptic potentials of DVNs, elicited by repetitive electrical stimulation of the solitary tract (TS), led to a secondary glial depolarization of up to 25 mV, a fall in Po. of up to 150 mmHg, a rise in extracellular aKo of up to 9 mm, and a fall in pHo of about 0-2 pH units.3. Hypoxic superfusates produced tissue anoxia, leading to an aK. increase of less than 2 mM and a pHo fall of 024 + 0 04 pH units (mean + S.D.). Glucose-free solution evoked, after a delay of more than 8 min, a slow rise in aKo of 1-9 + 0-8 mm, accompanied by a mean increase in pHo of 0-24 + 0-13 pH units. After pre-incubation in glucose-free solution, anoxia elevated aKo by up to 15 mm, whereas the anoxia-induced pHo decrease was completely blocked. 4. In 45 of 118 DVNs, anoxia elicited a persistent hyperpolarization of 15'6 + 5 0 mV. In the remaining DVNs, anoxic exposure either did not produce a change in Em (37 %) or led to a depolarization of less than 10 mV (25 %). A stable depolarization of 9 + 3 8 mV was detected in glial cells during anoxia. Similar responses were revealed in oxygenated glucose-free solution after a delay of 12-60 min.5. The metabolism-related hyperpolarizations were blocked by 100-500 /uM tolbutamide or 20-100 AM glibenclamide, leading to recovery of spontaneous (0-5-6 Hz) spike discharge. In these cells, 400-500 uM diazoxide evoked hyperpolarizations and blockade of spontaneous activity. 6. In DVNs and glial cells, a progressive depolarization of up to 40 mV in amplitude developed during anoxic exposure after pre-incubation in glucose-free solution. 7. The results show that oxygen or glucose depletion does not impair the viability of DVNX cells. The contribution of neuronal ATP-sensitive K+ (KATP) channels to this tolerance is discussed.

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Section: Effects Of Energy Depletionmentioning

confidence: 93%

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Ballanyi

Doutheil

Brockhaus

1996

The Journal of Physiology

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“…Similarly, in hippocampal CA3 pyramidal cells, glibenclamide did not block anoxic hyperpolarization (Ben-Ari, 1990) or the increase in conductance seen after hypoglycaemia (Knbpfel, Spuler, Grafe & Gahwiler, 1990). Tolbutamide, but not glibenclamide, inhibited the hyperpolarization induced by hypoglycaemia or hypoxia in neurones of the hypothalamus and locus coeruleus (Ashford, Boden & Treherne, 1990;Nieber, Sevcik & Illes, 1995). However, in cultured hippocampal neurones, glibenclamide blocked a K+ channel by metabolic inhibition with oligomycin (Politi & Rogawski, 1991).…”

Section: Discussionmentioning

confidence: 99%

Effect of metabolic inhibition on K+ channels in pyramidal cells of the hippocampal CA1 region in rat brain slices.

Hyllienmark¹,

Brismar²

1996

The Journal of Physiology

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1. The effect of metabolic inhibition on membrane potential and ionic conductances of K+ channels was studied with the patch-clamp technique in pyramidal cells in the CAl region of the hippocampus. Individual cells were visualized in brain slices from rats aged between 9 and 19 days using infrared video microscopy. Excitability was inhibited by tetrodotoxin. 2. Dinitrophenol (DNP), carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) and cyanide hyperpolarized the majority of the cells. The resting potential (V) was -55-3 + 0-23 mV (n = 147). In response to DNP the change in V was -3-9 + 0-76 mV (n = 59), with a normal distribution ranging between +9 0 and -16 mV.3. Metabolic inhibition increased the resting conductance (grest) and the conductance related to the delayed outward current measured at V = -20 mV (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), and decreased the conductance of the early outward A-current (gA).

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“…Conversely, the inward current of type A neurons corresponds to the well-described phenomenon of hypoxic membrane depolarisation [16,17,27,28] and presumably indicates a collapse in ionic homeostasis, causing acute neuronal injury [29,30] . Our results confirm the observation that a delay or attenuation of this hypoxic depolarisation could provide a protective effect [31] .…”

Section: Discussionmentioning

confidence: 99%

The Delta-Opioid Receptor Agonist D-Ala2-D-Leu2-Enkephalin Enhances Hypoxic Depression of Excitatory Synaptic Transmission and Improves Recovery of Rat Cortical Neurons from Hypoxia in vitro

Merkenschlager

Bloßfeld²,

Nieber³

2016

Pharmacology

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We investigated the influence of the delta-opioid receptor-preferring agonist D-Ala2-D-Leu2-enkephalin (DADLE) in vitro during long- and short-term hypoxia on the single cortical neuron membrane currents, the postsynaptic currents (PSCs), and the postsynaptic potentials (PSPs) in rats. Rat cortical pyramidal neurons showed 2 distinct and prognostically relevant responses to hypoxia. Type A neurons that responded to hypoxia by an inward current, followed by a steady outward current, were shown to recover during subsequent reoxygenation. In contrast, type B neurons that responded by a steady inward current, indicative of gradual anoxic depolarisation, suffered irreversible membrane dysfunction and did not recover completely during reoxygenation. Pre-treatment with 1 µmol/l DADLE attenuated the hypoxic inward current and favored complete recovery of holding current and input resistance during reoxygenation, even when neurons were challenged by a second exposure to hypoxia. DADLE enhanced the inhibitory effect of hypoxia on PSPs and PSCs. We assume that this neuroprotective effect is transmitted by the additive effects of DADLE on the hypoxic PSP/PSC suppression, thereby inhibiting presynaptic glutamate release.

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Hypoxic changes in rat locus coeruleus neurons in vitro.

Cited by 63 publications

References 45 publications

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

Effect of metabolic inhibition on K+ channels in pyramidal cells of the hippocampal CA1 region in rat brain slices.

The Delta-Opioid Receptor Agonist D-Ala2-D-Leu2-Enkephalin Enhances Hypoxic Depression of Excitatory Synaptic Transmission and Improves Recovery of Rat Cortical Neurons from Hypoxia in vitro

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