Excitatory and inhibitory amino acids involved in the high pressure nervous syndrome: Epileptic activity and hyperexcitability

Abstract

Epileptic-like activities are observed in mammals exposed to ambient pressures higher than 20 atm. These symptoms are part of the so called "high pressure nervous syndrome". In the search of the cellular mechanisms of this syndrome, we examined synaptic and intrinsic pressure-induced changes in the in vitro hippocampal slice preparation in the rat. We found that pressure (80 atm) depresses the efficiency of excitatory amino acidergic and inhibitory GABA synaptic transmissions, while it increases the intrinsic excitability of the CA1 pyramidal cells and induced multiple population spikes. The changes were associated with a selective increase in the effects of NMDA andL-homocysteate, while the postsynaptic effects of GABA was unchanged. NMDA antagonists and GABA synergistic drugs antagonized the pressure-induced hyperexcitability and multiple population spikes. These results suggest that pressure would decrease transmitter release at the tested excitatory and inhibitory synapses and would facilitate NMDA postsynaptic mechanisms. Thus, changes in both NMDA and GABA processes might be involved in the development of the high pressure nervous syndrome.