O2 deprivation in the central nervous system: On mechanisms of neuronal response, differential sensitivity and injury

Haddad, Gabriel G.; Jiang, Chun

doi:10.1016/0301-0082(93)90014-j

Cited by 297 publications

(177 citation statements)

References 194 publications

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“…The precise chain of events as it relates to the particular insult is still unclear. In addition, the observation that neuronal subtypes differ in their degree of vulnerability to acute insults complicates this area of study even further (Haddad & Jiang, 1993). However, neuronal subtypes that are more vulnerable are more likely to be affected by milder insults.…”

Section: Cellular Theoriesmentioning

confidence: 99%

Impaired cognitive function and mental performance in mild dehydration

2003

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Dehydration is a reliable predictor of impaired cognitive status. Objective data, using tests of cortical function, support the deterioration of mental performance in mildly dehydrated younger adults. Dehydration frequently results in delirium as a manifestation of cognitive dysfunction. Although, the occurrence of delirium suggests transient acute global cerebral dysfunction, cognitive impairment may not be completely reversible. Animal studies have identified neuronal mitochondrial damage and glutamate hypertransmission in dehydrated rats. Additional studies have identified an increase in cerebral nicotinamide adenine dinucleotide phosphate-diaphorase activity (nitric oxide synthase, NOS) with dehydration. Available evidence also implicates NOS as a neurotransmitter in long-term potentiation, rendering this a critical enzyme in facilitating learning and memory. With ageing, a reduction of NOS activity has been identified in the cortex and striatum of rats. The reduction of NOs synthase activity that occurs with ageing may blunt the rise that occurs with dehydration, and possibly interfere with memory processing and cognitive function. Dehydration has been shown to be a reliable predictor of increasing frailty, deteriorating mental performance and poor quality of life. Intervention models directed toward improving outcomes in dehydration must incorporate strategies to enhance prompt recognition of cognitive dysfunction.

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Section: Cellular Theoriesmentioning

confidence: 99%

Impaired cognitive function and mental performance in mild dehydration

2003

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“…Moderate hypoxia or a brief period of hypoxia/ischemia may induce adaptive responses in some tissues prolonging cellular survival (Hochachka et al, 1996;Semenza, 2001). Adaptation may include down-regulation of energy demand (Duffy et al, 1975;Vannucci and Duffy, 1976), reduced protein synthesis (Haddad and Jiang, 1993;Gu and Haddad, 2001;Munns et al, 2003), and changes in the expression of genes and enzymes necessary for survival (Semenza 2001). The distinction between hypoxia-tolerance in cells possessing adaptive mechanisms and hypoxia-sensitivity in cells with few survival mechanisms has been discussed by Hochachka et al (1996).…”

Section: Introductionmentioning

confidence: 99%

Effects of continuous hypoxia on energy metabolism in cultured cerebro-cortical neurons

et al. 2008

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Mechanisms underlying hypoxia-induced neuronal adaptation have not been fully elucidated. In the present study we investigated glucose metabolism and the activities of glycolytic and TCA cycle enzymes in cerebro-cortical neurons exposed to hypoxia (3 days in 1% of O 2 ) or normoxia (room air). Hypoxia led to increased activities of LDH (251%), PK (90%), and HK (24%) and decreased activities of CS (15%) and GDH (34%). Neurons were incubated with [1-13 C]glucose for 45 and 120 min under normoxic or hypoxic (120 min only) conditions and 13 C enrichment determined in the medium and cell extract using 1 H-{ 13 C}-NMR. In hypoxia-treated neurons [3-13 C]lactate release into the medium was 428% greater than in normoxia-treated controls (45-min normoxic incubation) and total flux through lactate was increased by 425%. In contrast glucose oxidation was reduced significantly in hypoxia-treated neurons, even when expressed relative to total cellular protein, which correlated with the reduced activities of the measured mitochondrial enzymes. The results suggest that surviving neurons adapt to prolonged hypoxia by up-regulation of glycolysis and downregulation of oxidative energy metabolism, similar to certain other cell types. The factors leading to adaptation and survival for some neurons but not others remains to be determined.

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“…In particular, the cerebral neuron excitability critically depends on sufficient O 2 supply, but hypoxia may not only compromise ion channels but also signaling pathways and neurotransmitter function (22,35). So far, most of our knowledge about the processes underlying hypoxia-induced alterations of neuronal excitability and synaptic neurotransmission has been gained from in vitro patchclamped studies.…”

mentioning

confidence: 99%

The effects of short-term hypoxia on motor cortex excitability and neuromuscular activation

Szubski¹,

Burtscher²,

Löscher³

2006

Journal of Applied Physiology

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Szubski, Christoph, Martin Burtscher, and Wolfgang N. Lö scher. The effects of short-term hypoxia on motor cortex excitability and neuromuscular activation. J Appl Physiol 101: 1673-1677, 2006. First published August 17, 2006 doi:10.1152/japplphysiol.00617.2006.-The effects of acute hypoxia on motor cortex excitability, force production, and voluntary activation were studied using single-and double-pulse transcranial magnetic stimulation techniques in 14 healthy male subjects. Electrical supramaximal stimulations of the right ulnar nerve were performed, and transcranial magnetic stimulations were delivered to the first dorsal interosseus motor cortex area during short-term hypoxic (HX) and normoxic (NX) condition. M waves, voluntary activation, F waves, resting motor threshold (rMT), recruitment curves (100 -140% of rMT), and short-interval intracortical inhibition and intracortical facilitation were measured. Moreover, motor-evoked potentials (MEPs) and cortical silent periods were determined during brief isometric maximum right index finger abductions. Hypoxia was induced by breathing a fraction of inspired oxygen of 12% via a face mask. M waves, voluntary activation, and F waves did not differ between NX and HX. The rMT was significantly lower in HX (55.79 Ϯ 9.40%) than in NX (57.50 Ϯ 10.48%) (P Ͻ 0.01), whereas MEP recruitment curve, short-interval intracortical inhibition, intracortical facilitation, maximum right index finger abduction, and MEPs were unaffected by HX. In contrast, the cortical silent periods in HX (158.21 Ϯ 33.96 ms) was significantly shortened compared with NX (169.42 Ϯ 39.69 ms) (P Ͻ 0.05). These data demonstrate that acute hypoxia results in increased cortical excitability and suggest that acute hypoxia alters motor cortical ion-channel function and GABAergic transmission. transcranial magnetic stimulation; voluntary activation; cortical silent period STUDIES OF HYPOXIA-INDUCED CHANGES in central nervous system function have primarily focused on behavioral parameters and revealed impairments in psychomotor skills (25, 43) and cognitive performances (24,29,32). In addition to these deteriorations in performance, evidence of slowed visual and auditory reaction time has been demonstrated in experimental conditions corresponding to an altitude of ϳ6,100 m (15, 16).Numerous in vitro studies on central neurons strongly suggested that reduced arterial oxygen saturation impairs central nervous system function (34). In particular, the cerebral neuron excitability critically depends on sufficient O 2 supply, but hypoxia may not only compromise ion channels but also signaling pathways and neurotransmitter function (22,35). So far, most of our knowledge about the processes underlying hypoxia-induced alterations of neuronal excitability and synaptic neurotransmission has been gained from in vitro patchclamped studies.As yet, in vivo studies addressing the functional consequences of reduced O 2 supply to the neuromuscular system have primarily focused on effects on muscle force generation (13), endu...

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O2 deprivation in the central nervous system: On mechanisms of neuronal response, differential sensitivity and injury

Cited by 297 publications

References 194 publications

Impaired cognitive function and mental performance in mild dehydration

Impaired cognitive function and mental performance in mild dehydration

Effects of continuous hypoxia on energy metabolism in cultured cerebro-cortical neurons

The effects of short-term hypoxia on motor cortex excitability and neuromuscular activation

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