Helium pressure potentiates the decreases of field potentials in the rat hippocampal slice preparation

Fagni, Laurent; Zinebi, Fatiha; Hugon, M

doi:10.1016/0304-3940(87)90397-1

Cited by 27 publications

(31 citation statements)

References 11 publications

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“…The evidence accumulated to date indicates that at HP the NMDAR response is increased (Fagni et al, 1987; Mor and Grossman, 2006, 2007, 2010). This augmentation is thought to be one of the key elements causing HPNS and possibly long-term irreversible CNS impairment.…”

Section: Discussionmentioning

confidence: 99%

“…The glutamate N -methyl-D-aspartate receptor (NMDAR) has been implicated with CNS hyperexcitability as part of HPNS (Fagni et al, 1987; Daniels and Grossman, 2010). We have recently demonstrated in rat hippocampal brain slices that, under HP conditions, NMDAR synaptic responses are significantly augmented and less susceptible to Mg 2+ blockade.…”

Section: Introductionmentioning

confidence: 99%

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Pressure-selective modulation of NMDA receptor subtypes may reflect 3D structural differences

Mor¹,

Kuttner²,

Levy³

et al. 2012

Front. Cell. Neurosci.

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Professional deep-water divers exposed to high pressure (HP) above 1.1 MPa suffer from High Pressure Neurological Syndrome (HPNS), which is associated with CNS hyperexcitability. We have previously reported that HP augments N-methyl-D-aspartate receptor (NMDAR) synaptic responses, increases neuronal excitability, and potentially causes irreversible neuronal damage. We now report that HP (10.1 MPa) differentially affects eight specific NMDAR subtypes. GluN1(1a or 1b) was co-expressed with one of the four GluN2(A–D) subunits in Xenopus laevis oocytes. HP increased ionic currents (measured by two electrode voltage clamps) of one subtype, reduced the current in four others, and did not affect the current in the remaining three. 3D theoretical modeling was aimed at revealing specific receptor domains involved with HP selectivity. In light of the information on the CNS spatial distribution of the different NMDAR subtypes, we conclude that the NMDAR's diverse responses to HP may lead to selective HP effects on different brain regions. These discoveries call for further and more specific investigation of deleterious HP effects and suggest the need for a re-evaluation of deep-diving safety guidelines.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pressure-selective modulation of NMDA receptor subtypes may reflect 3D structural differences

Mor¹,

Kuttner²,

Levy³

et al. 2012

Front. Cell. Neurosci.

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“…The threshold pressure for HPNS is variable and affected by the rate of compression (18). Details regarding the cellular mechanism(s) underlying HPNS are unclear (114), but it appears that both synaptic (74,76,85,228,229) and intrinsic membrane properties are involved (72,73,191,192,216). Several excellent reviews on HPNS exist elsewhere (18,100,104,114).…”

Section: Hydrostatic Compression Of the Brainmentioning

confidence: 99%

“…At that time, making intracellular recordings of mammalian neurons proved to be technically challenging due to the comparatively small size of the neurons, inaccessibility of the tissue preparation and microelectrode once the pressure vessel was sealed, and the challenge of maintaining mechanical stability of the electrophysiological recording while "diving" and "surfacing" (191,192). Consequently, the majority of in vitro hyperbaric studies of the mCNS have selected more robust electrophysiological techniques, such as extracellular recording of evoked population spikes in the hippocampus (76,118,191,192,229), macropatch clamp recordings in the cerebellar cortex (72)(73)(74), and cervical nerve recordings of respiratory-related neural activity (197,198). Compared with intracellular recordings, extracellular recordings are easier to initiate once the chamber is sealed and to maintain during the ensuing compression and decompression periods.…”

Section: Appendix C: Comparison Of Electrophysiology Recording Technimentioning

confidence: 99%

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Dean¹,

Mulkey²,

Garcia³

et al. 2003

Journal of Applied Physiology

175

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III. Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures. J Appl Physiol 95: 883-909, 2003; 10.1152/japplphysiol.00920.2002.-As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired PO 2, PCO2, and N2 partial pressure, has deleterious effects on neuronal function, resulting in O 2 toxicity, CO2 toxicity, N2 narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures Ͻ5 atmospheres absolute (ATA). Here we summarize these methods, the physiologically relevant test pressures, potential research applications, and results of previous research, focusing on the significance of electrophysiological studies at Ͻ5 ATA. Intracellular recordings and tissue PO 2 measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (Յ3 ATA O 2) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system. anesthesia; carbon dioxide toxicity; free radicals; high-pressure nervous syndrome; membrane potential; nitrogen narcosis; oxidative stress; oxygen toxicity; polarographic oxygen electrode MOST HUMANS ARE PHYSIOLOGICALLY adapted to live and work near sea level, where ambient pressure is ϳ1 atmosphere absolute (ATA).1 Nonetheless, we exploit a continuum of barometric pressure (PB) ranging from the near vacuum of outer space, which we survive during Space Shuttle extravehicular activity by wearing a 4.3 lb./in.2 absolute (psia) pressure suit (30,300 ft. pressure equivalent, 0.29 ATA) (120, 220), down to the summit of Mt. Everest at 29,029 ft., where PB is 0.31 ATA (221), to ocean depths as great as 2,300 ft. of sea water (fsw), where PB increases to ϳ70 ATA (18). These situations are the pressure extremes of our inhabitable environment, which only relatively few highly trained individuals have ever occupied.Military personnel, medical personnel, and other humans, however, frequently encounter levels of hyperbaric pressure (i.e., Ͼ1 ATA) of lesser degrees in their normal work environments. Examples of moderate hyperbaric environments (e.g., Ͻ5 ATA) include the following: patients and medical attendants undergoing hyperbaric O 2 therapy (HBOT) (38,203); diving with an underwater breathing apparatus for recreational, professional (oil and salvage companies), and combat purposes (89); simulated dry and wet dives for hyperbaric research and dive training (217); and working in the compressed atmosphere of a subterranean environment (117). Abnormal work environments resulting from catastrophic accident...

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“…How can this be reconciled with the observation that strychnine and pressure act strictly additively? There are two possibilities that might account for a common mechanism between the two treatments: (i) There is evidence that increased hydrostatic pressure directly potentiates NMDA receptor-mediated responses (Fagni et al, 1987;Zinebi et al, 1988). In addition, NMDA receptor gated channels are indirectly regulated by the state of GABAergic (and presumably glycinergic) inhibition which affects the voltage-dependent Mg2" block of the channels (Nowak et al, 1984;Collingridge et al, 1988).…”

Section: Mechanism Of Effect Ofpressurementioning

confidence: 99%

Possible NMDA antagonist properties of drugs that affect high pressure neurological syndrome

Shuker

Bowser-Riley

Davies

1994

British J Pharmacology

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1 Previous studies have suggested that a series of drugs modelled on part of the strychnine molecule interfere with the development of high pressure neurological syndrome (HPNS) and it was presumed that this effect was via an action on inhibitory glycinergic transmission. We have now used the rat hippocampal slice preparation to examine the possibility that some of these drugs might instead have an action at the strychnine-insensitive (SI) glycine binding site associated with the NMDA receptor. 2 D-2-Amino-5-phosphonovalerate (AP5) and 7-chlorokynurenate (7CK) had no significant effect on the height of the population spike recorded from the CAl region in 1 mM Mg2' medium, but both blocked the multiple population spikes recorded in Mg2+-free medium. The effect of 7CK, but not AP5, was reversed by 200fLM D-serine which is consistent with the known antagonist action of 7CK at the SI-glycine site. 3 A derivative of benzimidazole, which shows the clearest structural similarities to known SI-glycine site antagonists and ameliorates HPNS, mirrored the effects of 7CK although it was considerably less potent. 4 Gramine, which exacerbates HPNS, significantly increased the number of population spikes evoked in Mg2+-free medium. 5 Mephenesin, which is the most potent known drug in ameliorating HPNS, had no significant effect on the response recorded in 1 mM Mg2' and significantly reduced the number of population spikes recorded in Mg2+-free medium, but this effect was only partially reversed by the addition of D-serine.6 The results are consistent with the benzimidazole derivative, but not gramine, being an antagonist at the SI-glycine receptor. The results with mephenesin are equivocal but leave open the possibility that some of the drugs which are effective against HPNS act via an effect on excitatory NMDA receptormediated transmission, rather than on inhibitory glycine-mediated transmission.

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Helium pressure potentiates the decreases of field potentials in the rat hippocampal slice preparation

Cited by 27 publications

References 11 publications

Pressure-selective modulation of NMDA receptor subtypes may reflect 3D structural differences

Pressure-selective modulation of NMDA receptor subtypes may reflect 3D structural differences

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Possible NMDA antagonist properties of drugs that affect high pressure neurological syndrome

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