Recreational Diving Practice for Stress Management: An Exploratory Trial.

Background: Within the components of Scuba diving there are similarities with meditation and mindfulness techniques by training divers to be in a state of open monitoring associated with slow and ample breathing. Perceived stress is known to be diminished during meditation practice. This study evaluates the benefits of scuba diving on perceived stress and mindful functioning. Method: A recreational diving group (RDG; n = 37) was compared with a multisport control group (MCG; n = 30) on perceived stress, mood, well-being and mindfulness by answering auto-questionnaires before and after a 1-week long UCPA course. For the diving group, stability of the effects was evaluated 1 month later using similar auto-questionnaires. Results: Perceived stress did not decrease after the course for the MCG [ The divers showed a significant reduction on the perceived stress score (p < 0.05) with a sustainable effect (p = 0.01)]. An improvement in mood scale was observed in both groups. This was associated to an increase in mindfulness abilities. Conclusions: The practice of a recreational sport improves the mood of subjects reporting the thymic benefits of a physical activity performed during a vacation period. The health benefits of recreational diving appear to be greater than the practice of other sports in reducing stress and improving well-being.

Examination of the Role of NMDA and GABAA Receptors in the Effects of Hyperbaric Oxygen on Striatal Dopamine Levels in Rats.

Hyperbaric oxygen induced in rats a decrease in striatal dopamine levels. Such decrease could be a result of changes in glutamatergic and GABAergic controls of the dopaminergic neurons into the Substantia Nigra Pars Compacta. The aim of this study was to determine the role of gluatamatergic and Gama-Amino-Butyric-Acid neurotransmissions in this alteration. Dopamine-sensitive electrodes were implanted into the striatum under general anesthesia. After one week rest, awaked rats were exposed to oxygen-nitrogen mixture at a partial pressure of oxygen of 3 absolute atmospheres. Dopamine level was monitored continuously (every 3 min) by in vivo voltammetry with multifiber carbon electrodes before and during hyperbaric oxygen exposure. Hyperbaric oxygen induced a decrease in dopamine level in relationship with the increase in partial pressure of oxygen (-40% at 3 ATA). The used of N-Methyl-D-Aspartate, agonist of glutamatergic N-Methyl-D-Aspartate receptors did not improve considerably this change and gabazine antagonist of Gama-Amino-Butyric-Acid-a receptors induced some little alteration of this change. These results suggest the involvement of other mechanisms.

A new biophysical decompression model for estimating the risk of articular bends during and after decompression.

The biophysical models that intend to predict the risk of decompression sickness after a change of pressure are not numerous. Few approaches focus in particular on joints as target tissues, with the aim to describe properly the mechanisms inducing pain. Nevertheless, for this type of decompression incidents, called articular bends, no model proved to fit the empirical results for a broad range of exposures and decompression procedures. We present here an original biophysical decompression model for describing the occurrence of articular bends. A target joint is broken down into two parts that exchange inert gases with the blood by perfusion and with each other by diffusion over distances of a few millimetres. This diffusion pathway allows the slow amplification of microbubbles growing during and after decompression, consistent with the possible delayed occurrence of bends. The diffusion coefficients introduced into this model are larger than those introduced into most modern decompression models. Their value remains physical (#10(-9)m(2)/s). Inert gas exchanges and the formation, amplification and resorption of microbubbles during and after decompression were simulated. We used a critical gas volume criterion for predicting the occurrence of bends. A risk database extracted from COMEX experience and other published studies were used for the correlation of model parameters not known a priori. We considered a large range of exposure, and the commonly used inert gases nitrogen and helium. This correlation phase identified the worst biophysical conformations most likely to lead to the formation, in tissues such as tendons, of a large number of microbubbles recruited from pre-existing gas nuclei during decompression. The risk of bends occurrence was found to be linked to the total separated gas volume generated during and after decompression. A clamping phenomenon occurs soon after the start of decompression, greatly slowing the gas exchanges controlled especially by the oxygen window. This model, which reproduces many empirical findings, may be considered both descriptive and predictive.

A review of recent neurochemical data on inert gas narcosis.

Nitrogen narcosis occurs in humans at around 0.4 MPa (4 ATA). Hydrogen narcosis occurs between 2.6 and 3.0 MPa. In rats, nitrogen disturbances occur from 1 MPa and a loss of righting reflex around 4 MPa. Neurochemical studies in striatum of rats with nitrogen at 3 MPa (75% of anesthesia threshold) with differential pulse voltammetry have demonstrated a decrease in dopamine (DA) release by neurons originated from the substantia nigra pars compacta (SNc). Such a decrease is found also with compressed argon, which is more narcotic than nitrogen and with the anesthetic gas nitrous oxide. Inversely, compressed helium with its very low narcotic potency induces DA increase. Microdialysis studies in the striatum have indicated that nitrogen also induces a decrease of glutamate concentration. Nitrogen pressure did not modify NMDA glutamate receptor activities in SNc or striatum but enhanced GABAA receptors activities in SNc. Repetitive exposures to nitrogen narcosis suppressed the DA decrease and induced an increase. This fact and the lack of improvement of motor disturbances did not support the hypothesis of a physiological adaptation. The desensitization of the GABAA receptors on DA cells during recurrent exposures and the parallel long-lasting decrease of glutamate coupled to the increase in NMDA receptor sensitivity suggest a nitrogen neurotoxicity or addiction induced by recurrent exposures. The differential changes produced by inert gases indifferent neurotransmitter receptors would support the binding protein theory.

Dopaminergic control of striatal 5-HT level at normobaric condition and at pressure.

High pressure of helium-oxygen (He-O2) increases the extracellular levels in both serotonine and dopamine in the rat striatum. Some motor symptoms evoked by high pressure (i.e., LMA) are known to be reduced by intrastriatal infusions of D1-like (SCH23390, 1 microM) or D2-like (Sulpiride, 1 microM) dopaminergic antagonists. Other studies have also reported that serotoninergic antagonists reduce the motor perturbation at pressure. However, it remains unknown whether the changes in serotoninergic neurotransmission may contribute to the beneficial effects of intrastriatal administration of a dopaminergic antagonist. The present study reports the effects of SCH23390 and sulpiride on serotonin levels in the striatum of rats exposed to 8 MPa of He-O2. Both sulpiride and SCH23390 reduced pressure-induced striatal 5-HT increase. Our data suggest that D1-like and D2-like receptors have similar effects on a pressure-evoked striatal 5-HT increase. Thus, reduction in serotoninergic neurotransmission may be one mechanism by which dopaminergic antagonists reduce motor symptoms at pressure.

The pathway to drive decompression microbubbles from the tissues to the blood and the lymphatic system as a part of this transfer.

The formation sites of the microbubbles that are routinely detected in the bloodstream at precordial level by Doppler after a decompression are reviewed and discussed here. First, microbubbles could form on the endothelium lumen wall of the capillaries, at specific nanometric sites, but the release mechanism of such small emerging entities remains puzzling. They could be also formed from pre-existing gas nuclei present in the blood when favorable local hydrodynamic/supersaturation conditions generate microcavitation and tribonucleation phenomena. Finally, tissues could represent large pools for microbubble formation and amplification. Nevertheless, it remains to explain what the potential pathways are to drive them to the blood. Knowing that the permeability of most of the blood capillary network is quite low, an alternative is proposed for such transport. The lymphatic system, which drains the interstitial fluid to guarantee the fluid balance of tissues, could allow the transfer of micrometric elements like stabilized microbubbles formed in tissues on long distances. A final rejection in the bloodstream at the termination of both right lymphatic and thoracic ducts can be expected. The characteristics of this slow transport, activated by the muscular pump, could explain the detection on long periods of massive venous gas emboli.

Post effect of repetitive exposures to pressure nitrogen-induced narcosis on the dopaminergic activity at atmospheric pressure.

Nitrogen at pressure produces a neurological syndrome called nitrogen narcosis. Neurochemical experiments indicated that a single exposure to 3 MPa of nitrogen reduced the concentration of dopamine by 20% in the striatum, a structure involved in the control of extrapyramidal motor activity. This effect of nitrogen was explained by enhanced GABAergic neurotransmission through GABAA receptors and, to a lesser extent, by a decreased glutamatergic input to DA cells through NMDA receptors. The aim of this study was to study, under normobaric conditions, possible alterations of NMDA receptor activity in the substantia nigra pars compacta (SNc) induced by repetitive exposures to nitrogen pressure. Under general anesthesia, male Sprague-Dawley rats were implanted in the striatum with multifiber carbon dopamine-sensitive electrodes and in the SNc with guide cannulae for drug injections. After recovery from surgery, the striatal dopamine level was recorded by voltammetry in freely-moving rats, in normobaric conditions, before and after 5 repetitive exposures to 1MPa of nitrogen (threshold of nitrogen narcosis occurrence in rat). The effect of NMDA receptor activity on DA concentration was investigated using agonist (NMDA) and specific antagonist (AP7) SNc administration. Following repetitive nitrogen exposures, the ability of NMDA to elevate DA concentrations was enhanced. In contrast, after nitrogen exposure AP7 produced a paradoxical increase in DA concentration compared to its inhibitory effect before any exposure. Similar responses were obtained after a single exposure to 3MPa nitrogen. Thus, repetitive exposures to nitrogen narcosis produced a sensitization of postsynaptic NMDA receptors on DA cells, related to a decreased glutamatergic input in SNc. Consequently, successive nitrogen narcosis exposures disrupted ion-channel receptor activity revealing a persistent nitrogen-induced neurochemical change underlying the pathologic process.

Effects of NMDA administration in the substantia nigra pars compacta on the striatal dopamine release before and after repetitive exposures to nitrogen narcosis in rats.

Hyperbaric nitrogen-oxygen exposure developed in rats a decrement of the striatal dopamine release, which was reversed by repetitive exposures. This dopamine decrease could be the result of the antagonistic effect of nitrogen on NMDA receptors. The increment of the dopamine release, following repetitive exposures to nitrogen, could be attributed to a desensitisation of NMDA receptors to the effects of nitrogen. To test these hypotheses, male Sprague-Dawley rats were implanted with electrodes in the striatum to measure dopamine release by voltammetry and cannula in the substantia nigra pars compacta for NMDA injection. Free-moving rats were exposed up to 3MPa of nitrogen-oxygen mixture before and after 5 exposures to 1MPa. At the first exposure to 3MPa, the dopamine level decreased (-15%) but is counteracted by NMDA administration. In contrast, after repetitive exposure, the second exposure to 3MPa, induces a 10% dopamine increase. NMDA administration significantly potentiated this increase. Our results neither support the hypothesis of an antagonist effect of nitrogen on NMDA receptors at the first exposure, nor that of a NMDA receptor desensitization following repetitive exposures to hyperbaric nitrogen.

Recent neurochemical basis of inert gas narcosis and pressure effects.

Compressed air or a nitrogen-oxygen mixture produces from 0.3 MPa nitrogen narcosis. The traditional view was that anaesthesia or narcosis occurs when the volume of a hydrophobic site is caused to expand beyond a critical amount by the absorption of molecules of a narcotic gas. The observation of the pressure reversal effect on general anaesthesia has for a long time supported the lipid theory. However, recently, protein theories are in increasing consideration since results have been interpreted as evidence for a direct anaesthetic-protein interaction. The question is to know whether inert gases act by binding processes on proteins of neurotransmitter receptors. Compression with breathing mixtures where nitrogen is replaced by helium which has a low narcotic potency induces from 1 MPa, the high pressure nervous syndrome which is related to neurochemical disturbances including changes of the amino-acid and monoamine neurotransmissions. The use of narcotic gas (nitrogen or hydrogen) added to a helium-oxygen mixture, reduced some symptoms of the HPNS but also had some effects due to an additional effect of the narcotic potency of the gas. The researches performed at the level of basal ganglia of the rat brain and particularly the nigro-striatal pathway involved in the control of the motor, locomotor and cognitive functions, disrupted by narcosis or pressure, have indicated that GABAergic neurotransmission is implicated via GABAa receptors.

Alteration of striatal dopaminergic function induced by glioma development: a microdialysis and immunohistological study in the rat striatum.

Tumoral growth effects on brain circuitry and neurochemical activities remain poorly documented. This study evaluates C6 graft effects on striatal dopaminergic afferent projections at both anatomical and functional levels. Immunohistochemistry was performed to investigate changes in neurofilament (NF), tyrosine hydroxylase (TH) and dopamine transporter (DAT) expression. Dopaminergic turnover was assessed using multiprobe microdialysis in freely-moving rat. In C6 graft striatum, dopamine (DA) catabolites were reduced in glioblastoma (DOPAC: -61%, HVA: -62%). In contrast, the DA level remained unchanged. Staining for NF, TH and DAT was drastically decreased inside the tumor. Our histological data report that striatal tumoral growth is associated with a decrease in the density of dopaminergic endings which can explain, at least in part, the decrease in DA turnover. The decrease in DAT transporter expression and the lack of change in DA level may result from an increase in DA diffusion from the peripheral areas of the tumor. In conclusion, glioblastoma growth has major consequences on the local neuronal circuitry and its neurochemistry. Changes in inter-connections and neurotransmitter turnover may result in abnormal neuronal firing activity and participate in clinical disorders associated with glioblastoma diagnosis.

Pallidal administrations of gabazine and 5-AVA affect pressure-induced behavioral disorders in rats.

The aim of this work was to study the role of pallidal GABAa and GABAb neurotransmission in the behavioral disorders induced by pressure. The effects of GABAb antagonist 5-aminovalleric acid (5-AVA) or GABAa antagonist gabazine administrations in the globus pallidus (GP) on locomotor and motor hyperactivity (LMA) and myoclonia expressions in the model of the rat submitted to 8 MPa of helium-oxygen breathing mixture were analyzed. The administration of GABAa antagonist gabazine enhances the occurrence of the epileptic seizures, slightly increases LMA but decreases myoclonia. In contrast, the administration of GABAb antagonist 5-AVA decreases both LMA and myoclonia during the compression and the beginning of the holding time at 8 MPa. These data indicate that some behavioral disorders induced by pressure are in relation with GABAergic neurotransmission and establish clearly that GABAa and GABAb receptor mediations have distinct functions in the GP of the rat.

Nitrogen at raised pressure interacts with the GABA(A) receptor to produce its narcotic pharmacological effect in the rat.

BACKGROUND: Strong evidence supports the concept that conventional anesthetics, including inhalational agents and inert gases, such as xenon and nitrous oxide, interact directly with ion channel neurotransmitter receptors. However, there is no evidence that nitrogen, which only exhibits narcotic potency at increased pressure, may act by a similar mechanism. METHODS: We compared the inhibitory and sedative effects of gamma-aminobutyric acid (GABA) and nitrogen pressure on locomotor activity and striatal dopamine release in freely moving rats and investigated the pharmacologic properties of the GABA-induced and nitrogen pressure-induced narcotic action using the highly selective competitive GABA(A) receptor antagonist bicuculine. RESULTS: Intracerebroventricular GABA infusion up to 60 micromol or exposure to nitrogen pressure up to 3 MPa decreased to a similar extent striatal dopamine release (r2= 0.899, df = 4, P < 0.01) and locomotor activity (r2 = 0.996, df = 28, P < 0.001). However, both agents only showed small effects on striatal dopamine release, reducing dopamine currents by only 12-13% at sedative concentrations. Pretreatment with bicuculline at 0.5, 1, and 2.5 pmol reduced the sedative action of GABA on locomotor activity by 10, 20, and 41%, respectively. Bicuculline in the nanomole range at 1, 2.5, and 5 nmol but not in the picomole range reduced the sedative action of nitrogen pressure by 5, 37, and 73%, respectively. Schild plot analysis is consistent with the fact that bicuculline is a competitive antagonist of both GABA and nitrogen at pressure. CONCLUSIONS: These results suggest (1) that the presynaptic effects of both GABA and nitrogen pressure on striatal dopamine transmission are modest and not mainly involved in their sedative action and (2) that nitrogen at increased pressure may interact directly with the GABA(A) receptor. However, because the antagonistic effect of bicuculline on nitrogen sedation only occurred at much higher bicuculline concentrations than seen with GABA, it is suggested that nitrogen does not compete for the same site as GABA.

Helium-oxygen pressure induces striatal glutamate increase: a microdialysis study in freely-moving rats.

In rat, helium pressures induce locomotor and motor activity which requires dopaminergic and N-methyl-D-aspartate (NMDA) receptor activities at striatal level. However, biochemical studies have suggested that pressure exposure may increase striatal glutamate level. We used microdialysis technique to study the effects of pressure on glutamate level in the striatum and the effects of local administration of D1 (SCH23390) or D2 (sulpiride) on these changes. Pressures increase both glutamate and glutamine levels in striatal microdialysates. Administration of sulpiride (1 microM) or SCH23390 (1 microM) by reverse microdialysis did not affect significantly pressure induced glutamate increase. So, protective effects of D1 and D2 antagonists against locomotor and motor hyperactivity (LMA) are probably independent of the processes involved in the striatal glutamate increase evoked by pressure.

In vivo study of tumor metabolism: an application of new multi-probe microdialysis system in the striatum of freely moving rats grafted with C6 cells.

The purpose of this study is to investigate the in vivo tumoral brain metabolism in free moving rats using microdialysis. Cells from C6 glioma cell line were inoculated in one striatum 15 days before the microdialysis experimentation. Then, using a new system allowing perfusion of several microdialysis probes in free moving rat, normalised dialysate levels of glucose, lactate and pyruvate were monitored in both glioma and control striatum. At the end of the procedure, animals were sacrificed for histological study. Data shows that probe functioning is similar in both tissues. The results for normalised glucose level were in striatum control: 2.14 mM, in tumoral striatum: 1.71 mM (P>0.1); for lactate, respectively, 0.86 and 1.65 mM (P<0.05) and for pyruvate, respectively, 65.56 and 140. 94 microM (P<0.05). This data clearly shows a significant increase of pyruvate and lactate in tumoral striatum compared to normal striatum, correlating previous in vitro studies on glioma metabolism. We conclude that this microdialysis technique is of value in tumoral brain and could constitute an interesting tool for a better understanding of glioma metabolism.

High pressure enhanced NMDA activity in the striatum and the globus pallidus: relationships with myoclonia and locomotor and motor activity in rat.

In mammals high pressure of helium-oxygen (He-O2) breathing mixture leads to the high pressure neurological syndrome (HPNS) which includes a set of behavioural disorders such as locomotor and motor hyperactivity (LMA) and myoclonia. In rats, i.c.v. administrations of competitive NMDA antagonists decrease some of these symptoms suggesting that He-O2 pressure could enhance NMDA neurotransmission within the central nervous system. More recently, we have shown using microdialysis that the extracellular glutamate level is increased in the striatum by He-O2 pressure. Neurochemical data have suggested that this structure is probably involved in the LMA development but not in the myoclonia expression. When considering myoclonia, recent neuropathological studies performed at normal pressure in humans suggest that the globus pallidus extern (equivalent to the globus pallidus in the rat) could be involved in this behavioural disorder. The aim of this study was to compare the role of striatal and pallidal NMDA activity on the LMA development and the myoclonia expression in the model of rat exposed to 8 MPa of He-O2 mixture. The intrastriatal administration of D(-)-2-amino-7-phosphonoheptanoic acid (2-APH) (10 nmol/slide) reduced the LMA development but only slightly reduced myoclonia. In contrast, the intrapallidal administration of 2-APH (10 nmol/slide) reduced both LMA and myoclonia. These results suggest that the LMA development requires NMDA activity at both striatal and pallidal level. In contrast, the myoclonia expression mainly requires NMDA activity at pallidal level. Consequently, NMDA neurotransmission at input and output levels of the striato-pallidal pathway play different roles in some of the behavioural disorders induced by He-O2 pressure.

Sigmoidal admission rate-dependence of toluene narcotic potency in rats: comparison with nitrous oxide.

Aromatic solvents, such as toluene, can cause depression of the central nervous system functions in both solvent-exposed workers and abusers. The mechanism by which toluene produces its effects is generally thought to be similar to that produced by general anaesthetics, including inert gases and alcohols. However, whether lipophilic compounds indirectly influence activity by perturbing membrane lipids or bind directly to proteins remains a major question. In a recent study, the sigmoidal admission rate-dependence of inert gas anaesthetic potency has been suggested to possibly reflect a direct narcotic-protein interaction. Therefore, experiments have been carried out using seven input toluene flows of 0.5, 1, 2, 3, 4, 5 and 6 l/min. Our results indicate that as the rate of toluene delivery increased, the concentration of toluene required to produce anaesthetic effects increased. Although this was fitted relatively well with linear regression, this fitted better when using a sigmoidal model (r = 0.998 vs. r = 0.971, P < 0.01). In addition, comparison with previous data on nitrous oxide shows a striking similarity between plots (r = 0.991) which appears consistent with a similar site of action for both agents. We suggest that all classes of lipophilic agents could produce their inhibitory effects at similar 'non-specific' sites of action of finite size and limited occupancy.

The full expression of locomotor and motor hyperactivities induced by pressure requires both striatal dopaminergic and N-methyl-D-aspartate receptor activities in the rat.

High pressure induced locomotor and motor hyperactivities (LMA), tremor and myoclonia in rat. The LMA has been reported to be reduced by intracerebroventricular (i.c.v.) administration of dopaminergic receptor antagonists. Moreover, the LMA but not myoclonia correlate with pressure induced striatal dopamine increase. Nevertheless the role of dopaminergic and NMDA receptor activities at striatal level in the development of LMA remained unclear. In this study, the microdialysis technique associated to a behavioural device was used to test the effects of intra-striatal administration of D1 antagonist SCH23390 (1 microM), D2 antagonist sulpiride (1 microM) and NMDA antagonist AP-5 (10 microM) on LMA, tremor and myoclonia expression. Data clearly showed that LMA was drastically reduced by each treatment. In contrast, tremor and myoclonia were poorly affected. These data suggest that both dopaminergic and NMDA receptor activities at striatal level are needed for the full expression of the pressure-induced LMA and confirm that striatal neurotransmission changes are principally involved in this behavioural disorders. At the light of recent studies on dopaminergic neurotransmission and glutamate evoked-NMDA activity, we suggest that blockage of D1 or D2 receptors should reduced the LMA by reducing glutamate-evoked activity.

Administration of the glutamate uptake inhibitor L-trans-PDC in the globus pallidus and the substantia nigra, but not in the striatum, attenuates the psychostimulant effect of high helium pressure on locomotor activity in the rat.

High helium pressure of more than 2 MPa produces central neuroexcitatory motor behavior. In rodents, symptoms comprise locomotor and motor activity (LMA), myoclonia, and, at pressure greater than 9-10 MPa, convulsions and tonic-clonic seizures. We studied the behavioral effects of bilateral injection of the glutamate uptake inhibitor L-trans-pyrollidine-2,4-dicarboxylic acid (L-trans-PDC), in either the substantia nigra reticulata (SNr), the globus pallidus (GP), or the striatum on high helium pressure-induced LMA and myoclonia. Injection of L-trans-PDC in the GP and the SNr attenuated LMA, whereas injection in the striatum enhanced it. Alternatively, injection of L-trans-PDC in the SNr increased myoclonia, whereas injection in the GP or the striatum showed no effects on myoclonia. These results confirm that helium pressure-induced LMA and myoclonia have different neural origins. According to current thinking on basal ganglia function and previous data, it is suggested that high helium pressure would lead to a reduction of glutamate transmission in the SNr that could contribute to a reduction in activity of the nigrothalamic GABA pathway and then to the occurrence of LMA. It is further suggested that glutamate and DA transmissions in the striatum could have synergistic, rather than antagonistic, influences on motor activity.

Administration of either non-NMDA receptor agonists or NMDA receptor antagonists into the substantia nigra or the globus pallidus reduces the psychostimulant effect of high helium pressure on locomotor activity in rats.

Helium pressure of >2 MPa is a well known factor underlying pressure-dependent central neuroexcitatory disorders that include locomotor and motor activity (LMA) and myoclonia. We investigated the effects of bilateral injection in either the substantia nigra (SN) or the globus pallidus (GP) of the AMPA receptor agonist (+/-)AMPA, the kainate receptor agonist kainic acid, the NMDA receptor agonist (+/-)-cis-piperidine-2,3-dicarboxylic acid (PDA), and the NMDA receptor antagonist (+/-)-2-amino-7-phosphono-heptanoic acid (AP-7) in the occurrence of helium pressure-induced LMA and myoclonia. Administration of AMPA, kainate, or AP-7 in either the SN or the GP significantly reduced high helium pressure-induced LMA, whereas the NMDA receptor agonist showed no significant effect. Injection in the SN of the non-NMDA receptor agonist AMPA and the NMDA receptor agonist PDA increased the development of high helium pressure-induced myoclonia, whereas injection of the NMDA receptor antagonist AP-7 into the SN or the GP decreased it. This confirms that NMDA transmission in the SN and the GP would play a major role in the development of helium pressure-induced LMA; manipulation of AMPA and kainate systems may have therapeutic potential. The opposite effects of AMPA on LMA and myoclonia also confirm the neural substrates involved in the motor disorder produced by helium pressure differ substantially between LMA and myoclonia.