Neuropharmacological Dynamics of Hyperbaric Oxygen Effects

Summary

Hyperbaric oxygen (HBO₂) exposure profoundly alters central nervous system function by elevating tissue oxygen partial pressures and thereby modulating neurochemical and redox signalling pathways. At therapeutic pressures, HBO₂ promotes angiogenesis, neurogenesis and anti‐inflammatory responses, underpinning its clinical use in wound healing, stroke rehabilitation and certain neurodegenerative conditions. However, at higher pressures or prolonged exposures, excessive reactive oxygen species accumulation disrupts the balance of inhibitory and excitatory neurotransmission, precipitating central nervous system oxygen toxicity (CNS‐OT). Key targets include the GABAergic and glutamatergic systems, whose activity is reshaped by oxidant‐mediated modifications of receptors, transporters and downstream second-messenger cascades. Mitochondrial dynamics are equally affected: altered mitophagy and biogenesis signals reflect an adaptive response to oxidative stress but can also contribute to neuroexcitation and seizure onset. The interplay between neurotransmitter availability, cerebral blood flow regulation and mitochondrial quality control defines the therapeutic window of HBO₂ and the threshold for toxicity. Understanding these neuropharmacological dynamics is critical for optimising dosing regimens, mitigating adverse effects in diving and clinical settings, and exploring novel combinatorial strategies that harness redox preconditioning or targeted receptor modulation.

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Neuropharmacological Dynamics of Hyperbaric Oxygen Effects publication trend

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Technical terms

Hyperbaric oxygen (HBO₂): Breathing of pure oxygen at pressures above one atmosphere to increase tissue oxygenation.

Central nervous system oxygen toxicity (CNS-OT): A set of neurological symptoms and seizures triggered by excessive oxygen levels under pressure.

Gamma-aminobutyric acid (GABA): The principal inhibitory neurotransmitter in the brain, modulation of which influences seizure susceptibility.

Glutamatergic system: The network of excitatory synapses using glutamate as neurotransmitter, critical for synaptic plasticity and excitotoxicity.

Mitophagy: The selective removal of damaged mitochondria by autophagy, a process that maintains cellular energy homeostasis under oxidative stress.

References

  1. GAT inhibition preserves cerebral blood flow and reduces oxidant damage to mitochondria in rodents exposed to extreme hyperbaric oxygen. Frontiers in Molecular Neuroscience (2023).
  2. CNS function and dysfunction during exposure to hyperbaric oxygen in operational and clinical settings. Redox Biology (2019).
  3. Тhe role of the glutamatergic system in the mechanism of development of hyperbaric oxygen seizures. Marine Medicine (2022).

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