Enhanced excitability compensates for high-pressure-induced depression of cortical inputs to the hippocampus

High pressure (>1.0 MPa) induces the high-pressure neurological syndrome (HPNS) characterized by increased excitability of the CNS and cognitive impairments involving memory disorders. The perforant-path transfer of cortical information to the hippocampal formation is important for memory acquisition. High pressure may alter information transfer in this connection. We used rat corticohippocampal slices for studying the effect of pressure on the transfer function between synaptic inputs from the medial perforant path (MPP) and spike generation by granule cells (GC) of the dentate gyrus. High pressure (10.1 MPa) reduced single MPP field excitatory postsynaptic potential (fEPSP) amplitude and slope by nearly 50%. Field antidromic action potentials (AAPs) elicited by stimulation of GC axons, and population spike (PS) generation by the pressure-depressed MPP fEPSP were not significantly altered at hyperbaric conditions. Nevertheless the relationship PS/fEPSP increased at high pressure, indicating dendritic hyperexcitability in the GC. PSs elicited by paired-pulse MPP fEPSPs at 10- to 200-ms interstimulus intervals and PS generated by trains of five fEPSPs at 25 Hz were also not affected in spite of severe pressure-induced synaptic depression. Similarly, trains of AAPs at 25-50 Hz were not significantly changed. Trains of fEPSPs at higher frequency (50 Hz), however, induced additional spikes at high pressure, indicating pressure disruption of the regular low-pass filter properties of the DG. Such effect was closely mimicked by partial blockade of GABAA inhibition. High pressure depresses synaptic activity while increases excitability in the neuronal dendrites but not in the axons. This mechanism, allowing neuronal communication at low input signals, may partially cope with pressure effects at the low frequency range (<25 Hz) but losses reliability at higher frequencies (>50 Hz).